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1.
Depress Anxiety ; 37(2): 179-193, 2020 02.
Artigo em Inglês | MEDLINE | ID: mdl-31995664

RESUMO

BACKGROUND: Depression rates increase markedly for girls across the adolescent transition, but the social-environmental and biological processes underlying this phenomenon remain unclear. To address this issue, we tested a key hypothesis from Social Signal Transduction Theory of Depression, which posits that individuals who mount stronger inflammatory responses to social stress should exhibit greater increases in depressive symptoms following interpersonal life stress exposure than those who mount weaker inflammatory responses to such stress. METHOD: Participants were 116 adolescent girls (Mage = 14.71) at risk for psychopathology, defined as having a history of mental health concerns (e.g., psychiatric treatment, significant symptoms) over the past 2 years. At baseline, we characterized their inflammatory reactivity to social stress by quantifying their salivary proinflammatory cytokine responses to a laboratory-based social stressor. Then, 9 months later, we assessed the interpersonal and noninterpersonal stressful life events that they experienced over the prior 9 months using an interview-based measure of life stress. RESULTS: As hypothesized, greater interpersonal life stress exposure was associated with significant increases in depression over time, but only for girls exhibiting stronger salivary tumor necrosis factor-α and interleukin-1ß reactivity to social stress. In contrast, noninterpersonal stress exposure was unrelated to changes in depression longitudinally, both alone and when combined with youths' cytokine reactivity scores. DISCUSSION: These results are consistent with Social Signal Transduction Theory of Depression and suggest that heightened inflammatory reactivity to social stress may increase adolescents' risk for depression. Consequently, it may be possible to reduce depression risk by modifying inflammatory responses to social stress.


Assuntos
Depressão/complicações , Depressão/imunologia , Inflamação/complicações , Inflamação/psicologia , Relações Interpessoais , Modelos Psicológicos , Estresse Psicológico/complicações , Estresse Psicológico/imunologia , Adolescente , Criança , Depressão/psicologia , Feminino , Humanos , Inflamação/imunologia , Interleucina-1beta/análise , Interleucina-1beta/imunologia , Entrevistas como Assunto , Masculino , Psicopatologia , Saliva/imunologia , Estresse Psicológico/psicologia , Fator de Necrose Tumoral alfa/análise , Fator de Necrose Tumoral alfa/imunologia
2.
Nat Med ; 25(9): 1428-1441, 2019 09.
Artigo em Inglês | MEDLINE | ID: mdl-31501614

RESUMO

Psychological distress has long been suspected to influence cancer incidence and mortality. It remains largely unknown whether and how stress affects the efficacy of anticancer therapies. We observed that social defeat caused anxiety-like behaviors in mice and dampened therapeutic responses against carcinogen-induced neoplasias and transplantable tumors. Stress elevated plasma corticosterone and upregulated the expression of glucocorticoid-inducible factor Tsc22d3, which blocked type I interferon (IFN) responses in dendritic cell (DC) and IFN-γ+ T cell activation. Similarly, close correlations were discovered among plasma cortisol levels, TSC22D3 expression in circulating leukocytes and negative mood in patients with cancer. In murine models, exogenous glucocorticoid injection, or enforced expression of Tsc22d3 in DC was sufficient to abolish therapeutic control of tumors. Administration of a glucocorticoid receptor antagonist or DC-specific Tsc22d3 deletion reversed the negative impact of stress or glucocorticoid supplementation on therapeutic outcomes. Altogether, these results indicate that stress-induced glucocorticoid surge and Tsc22d3 upregulation can subvert therapy-induced anticancer immunosurveillance.


Assuntos
Imunidade Celular , Neoplasias/imunologia , Estresse Psicológico/imunologia , Fatores de Transcrição/genética , Animais , Ansiedade/sangue , Ansiedade/induzido quimicamente , Ansiedade/imunologia , Ansiedade/psicologia , Comportamento Animal/fisiologia , Carcinógenos/toxicidade , Neoplasias Colorretais/sangue , Neoplasias Colorretais/genética , Neoplasias Colorretais/imunologia , Neoplasias Colorretais/psicologia , Corticosterona/sangue , Células Dendríticas/transplante , Regulação Neoplásica da Expressão Gênica , Glucocorticoides/farmacologia , Humanos , Hidrocortisona/sangue , Neoplasias Pulmonares/sangue , Neoplasias Pulmonares/genética , Neoplasias Pulmonares/imunologia , Neoplasias Pulmonares/psicologia , Ativação Linfocitária/genética , Camundongos , Monitorização Imunológica/métodos , Neoplasias/induzido quimicamente , Neoplasias/genética , Neoplasias/psicologia , Receptores de Glucocorticoides/antagonistas & inibidores , Transdução de Sinais/efeitos dos fármacos , Neoplasias Gástricas/sangue , Neoplasias Gástricas/genética , Neoplasias Gástricas/imunologia , Neoplasias Gástricas/psicologia , Estresse Psicológico/induzido quimicamente , Estresse Psicológico/genética , Estresse Psicológico/terapia , Fatores de Transcrição/imunologia
3.
Trans Am Clin Climatol Assoc ; 130: 235-245, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31516188

RESUMO

Significant adverse impact of various forms of psychological stress on susceptibility to infection, altered wound healing, increased prevalence and severity of hypersensitivity diseases, and even increased mortality in cancer patients has been well described. Yet these observations are limited by often unpredictable individual responses to various stressful situations. These associations are further clouded by natural variability among diverse forms of and responses to chronic life stressors and associated comorbid conditions. This is particularly true for inflammatory diseases where gene/external environmental interactions are well-described. What is much less understood is gene-internal environmental (i.e., psychological) interactions that commonly affect disease activity and possible susceptibility. We have used selected single nucleotide polymorphisms of stress hormone and regulatory cytokine receptors to categorize both baseline and stress-associated immune parameters for the a priori classification of individuals with the most stress susceptible immune systems to identify those most responsive to a stress reduction/management-based intervention.


Assuntos
Hipersensibilidade/genética , Estresse Psicológico/genética , Suscetibilidade a Doenças , Predisposição Genética para Doença , Humanos , Hipersensibilidade/imunologia , Hipersensibilidade/psicologia , Polimorfismo de Nucleotídeo Único , Receptores Adrenérgicos beta 2/genética , Receptores Adrenérgicos beta 2/imunologia , Receptores de Glucocorticoides/genética , Receptores de Glucocorticoides/imunologia , Estresse Psicológico/imunologia , Estresse Psicológico/psicologia
4.
Psychiatr Danub ; 31(Suppl 3): 381-385, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31488756

RESUMO

BACKGROUND: Psychiatric disorders may be correlated with a low-grade systemic inflammation but the origin of this inflammatory response remains unclear and both genetics and environmental factors seems to be concerned. Recent researches observed that gut microbiota seems to have an impact on the brain and immune processes. METHOD: We review recent literature to a better understanding of how microbiota interacts with brain, immunity and psychiatric disorders. We search on Pubmed, PsycINFO, PsycARTICLES and Sciencedirect articles with the keywords "gastrointestinal microbiota" and "mental disorders" or "psychological stress". RESULTS: We showed links between gut microbiota and brain-gut axis regulation, immune and endocrine system activity, neurophysiological changes, behavior variations and neuropsychiatric disorders. Communications between brain and gut are bidirectional via neural, endocrine and immune pathway. Microbiota dysbiosis and increase gut permeability with subsequent immune challenges seems to be the source of the chronic mild inflammation associated with neuropsychiatric disorders. Repeated immune or stress events early in life may lead to neurodevelopmental disorders or sickness behavior later in life. CONCLUSIONS: Psychological stress impact gut microbiota with subsequent immune activation leading to neurodevelopmental disorders or sickness behavior and altering neurophysiology and reactivity to stress or lifestyle.


Assuntos
Encéfalo/imunologia , Encéfalo/fisiopatologia , Microbioma Gastrointestinal/imunologia , Microbioma Gastrointestinal/fisiologia , Inflamação/imunologia , Inflamação/psicologia , Transtornos Mentais/imunologia , Transtornos Mentais/microbiologia , Disbiose/imunologia , Disbiose/microbiologia , Disbiose/psicologia , Sistema Endócrino/imunologia , Sistema Endócrino/metabolismo , Sistema Endócrino/microbiologia , Humanos , Inflamação/microbiologia , Neuropsiquiatria , Estresse Psicológico/imunologia , Estresse Psicológico/microbiologia
5.
Int J Mol Sci ; 20(14)2019 Jul 17.
Artigo em Inglês | MEDLINE | ID: mdl-31319604

RESUMO

Altered adaptive immunity involving T lymphocytes has been found in depressed patients and in stress-induced depression-like behavior in animal models. Peripheral T cells play important roles in homeostasis and function of the central nervous system and thus modulate behavior. However, the T cell phenotype and function associated with susceptibility and resilience to depression remain largely unknown. Here, we characterized splenic T cells in susceptible and resilient mice after 10 days of social defeat stress (SDS). We found equally decreased T cell frequencies and comparably altered expression levels of genes associated with T helper (Th) cell function in resilient and susceptible mice. Interleukin (IL)-17 producing CD4+ and CD8+ T cell numbers in the spleen were significantly increased in susceptible mice. These animals further exhibited significantly reduced numbers of regulatory T cells (Treg) and decreased gene expression levels of TGF-ß. Mice with enhanced Th17 differentiation induced by conditional deletion of PPARγ in CD4+ cells (CD4-PPARγKO), an inhibitor of Th17 development, were equally susceptible to SDS when compared to CD4-PPARγWT controls. These data indicate that enhanced Th17 differentiation alone does not alter stress vulnerability. Thus, SDS promotes Th17 cell and suppresses Treg cell differentiation predominantly in susceptible mice with yet unknown effects in immune responses after stress exposure.


Assuntos
Diferenciação Celular/imunologia , Estresse Psicológico/imunologia , Linfócitos T Reguladores/imunologia , Células Th17/imunologia , Animais , Suscetibilidade a Doenças , Masculino , Camundongos , Estresse Psicológico/patologia , Linfócitos T Reguladores/patologia , Células Th17/patologia
6.
Cells ; 8(7)2019 06 30.
Artigo em Inglês | MEDLINE | ID: mdl-31262067

RESUMO

Inflammatory bowel disease (IBD) is a chronic and relapsing intestinal inflammatory condition, hallmarked by a disturbance in the bidirectional interaction between gut and brain. In general, the gut/brain axis involves direct and/or indirect communication via the central and enteric nervous system, host innate immune system, and particularly the gut microbiota. This complex interaction implies that IBD is a complex multifactorial disease. There is increasing evidence that stress adversely affects the gut/microbiota/brain axis by altering intestinal mucosa permeability and cytokine secretion, thereby influencing the relapse risk and disease severity of IBD. Given the recurrent nature, therapeutic strategies particularly aim at achieving and maintaining remission of the disease. Alternatively, these strategies focus on preventing permanent bowel damage and concomitant long-term complications. In this review, we discuss the gut/microbiota/brain interplay with respect to chronic inflammation of the gastrointestinal tract and particularly shed light on the role of stress. Hence, we evaluated the therapeutic impact of stress management in IBD.


Assuntos
Encéfalo/imunologia , Sistema Nervoso Entérico/imunologia , Microbioma Gastrointestinal/imunologia , Doenças Inflamatórias Intestinais/imunologia , Estresse Psicológico/imunologia , Terapia Comportamental/métodos , Doença Crônica/psicologia , Ensaios Clínicos como Assunto , Retroalimentação Psicológica , Humanos , Doenças Inflamatórias Intestinais/psicologia , Doenças Inflamatórias Intestinais/terapia , Mucosa Intestinal/imunologia , Mucosa Intestinal/inervação , Vias Neurais/imunologia , Qualidade de Vida , Estresse Psicológico/psicologia , Estresse Psicológico/terapia , Resultado do Tratamento
7.
Psychopharmacology (Berl) ; 236(10): 3063-3079, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31359117

RESUMO

Social Signal Transduction Theory of Depression is a biologically plausible, multi-level theory that describes neural, physiologic, molecular, and genomic mechanisms that link experiences of social-environmental adversity with internal biological processes that drive depression pathogenesis, maintenance, and recurrence. Central to this theory is the hypothesis that interpersonal stressors involving social threat (e.g., social conflict, evaluation, rejection, isolation, and exclusion) upregulate inflammatory processes that can induce several depressive symptoms, including sad mood, anhedonia, fatigue, psychomotor retardation, and social-behavioral withdrawal. The original article describing this formulation (Psychol Bull 140:774-815, 2014) addressed critical questions involving depression onset and recurrence, as well as why depression is strongly predicted by early life stress and comorbid with anxiety disorders and certain physical disease conditions, such as asthma, rheumatoid arthritis, chronic pain, and cardiovascular disease. Here, we extend the theory to help explain sex differences in depression prevalence, which is a defining feature of this disorder. Central to this extension is research demonstrating that ovarian hormone fluctuations modulate women's susceptibility to stress, brain structure and function, and inflammatory activity and reactivity. These effects are evident at multiple levels and are highly context-dependent, varying as a function of several factors including sex, age, reproductive state, endogenous versus exogenous hormones, and hormone administration mode and dose. Together, these effects help explain why women are at greater risk for developing inflammation-related depressed mood and other neuropsychiatric, neurodevelopmental, and neurodegenerative disorders during the reproductive years, especially for those already at heightened risk for depression or in the midst of a hormonal transition period.


Assuntos
Transtorno Depressivo Maior/imunologia , Hormônios Esteroides Gonadais/imunologia , Transtornos do Humor/imunologia , Caracteres Sexuais , Transdução de Sinais/fisiologia , Estresse Psicológico/imunologia , Encéfalo/imunologia , Transtorno Depressivo Maior/diagnóstico , Transtorno Depressivo Maior/psicologia , Feminino , Humanos , Inflamação/diagnóstico , Inflamação/imunologia , Inflamação/psicologia , Masculino , Transtornos do Humor/diagnóstico , Transtornos do Humor/psicologia , Estresse Psicológico/diagnóstico , Estresse Psicológico/psicologia
8.
Int Immunopharmacol ; 73: 527-538, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31176083

RESUMO

The kynurenine pathway (KP), a major route of tryptophan catabolism, may be associated with the pathophysiology of depressive disorders. KP is responsible for ca. 99% of brain tryptophan metabolism via its degradation to kynurenine (KYN) catalyzed by indoleamine 2,3-dioxygenase (IDO). Some cytokines, such as interferon-γ (IFN-γ) and interleukin (IL)-6 are potent inducers of IDO. KYN is further converted by kynurenine aminotransferase (KAT) to the more neuroprotective kynurenic acid or by kynurenine 3-monooxygenase (KMO) to neurotoxic 3-hydroxykynurenine. The aim of the present study was to delineate whether the administration of imipramine (IMI) to rats subjected to chronic mild stress (CMS) may reverse behavioral changes induced by CMS in association with changes in immune-inflammatory markers and KP. We confirmed that the CMS procedure modeled one of the main symptoms of depression, i.e. anhedonia, and administration of IMI for 5 weeks resulted in a significant reduction in anhedonia in a majority of animals (CMS IMI-R animals), whereas 20% of animals did not respond to IMI treatment (CMS IMI-NR animals). We established that CMS procedure increased IFN-γ and IDO mRNA and decreased KAT II mRNA expression in the rat cortex. In the cortex and hippocampus, IMI treatment and non-responsiveness to IMI (in CMS IMI-NR animals) were associated with increased IL-6 mRNA expression. In the spleen, CMS increased production of IFN-γ and IL-6 proteins, while these cytokines were decreased by IMI in CMS IMI-R animals. Chronic IMI administration to CMS rats decreased IDO and KMO mRNA and protein expression and increased KAT II/KMO mRNA and protein ratio in IMI responders (CMS IMI-R) in comparison to CMS rats. In CMS IMI-NR rats, a significant increase in IDO mRNA expression and protein level in comparison with IMI responders was observed. Our findings indicate that resistance to therapeutic action of IMI could be explained by a deficiency of the inhibitory properties of IMI on IDO, KMO and KYN synthesis in the cortex. We conclude that the antidepressant activity of IMI may, at least in part, be explained by modulatory activities on the KAT II/KMO ratio in brain areas.


Assuntos
Depressão/imunologia , Resistência a Medicamentos/imunologia , Cinurenina/imunologia , Estresse Psicológico/imunologia , Animais , Antidepressivos/farmacologia , Antidepressivos/uso terapêutico , Comportamento Animal/efeitos dos fármacos , Proliferação de Células , Córtex Cerebral/efeitos dos fármacos , Córtex Cerebral/imunologia , Citocinas/genética , Depressão/tratamento farmacológico , Hipocampo/efeitos dos fármacos , Hipocampo/imunologia , Imipramina/farmacologia , Imipramina/uso terapêutico , Indolamina-Pirrol 2,3,-Dioxigenase/genética , Indolamina-Pirrol 2,3,-Dioxigenase/metabolismo , Masculino , Ratos Wistar , Baço/citologia , Estresse Psicológico/tratamento farmacológico
9.
Psychopharmacology (Berl) ; 236(5): 1653-1670, 2019 May.
Artigo em Inglês | MEDLINE | ID: mdl-31119329

RESUMO

RATIONALE: Mycobacterium vaccae (NCTC 11659) is an environmental saprophytic bacterium with anti-inflammatory, immunoregulatory, and stress resilience properties. Previous studies have shown that whole, heat-killed preparations of M. vaccae prevent allergic airway inflammation in a murine model of allergic asthma. Recent studies also demonstrate that immunization with M. vaccae prevents stress-induced exaggeration of proinflammatory cytokine secretion from mesenteric lymph node cells stimulated ex vivo, prevents stress-induced exaggeration of chemically induced colitis in a model of inflammatory bowel disease, and prevents stress-induced anxiety-like defensive behavioral responses. Furthermore, immunization with M. vaccae induces anti-inflammatory responses in the brain and prevents stress-induced exaggeration of microglial priming. However, the molecular mechanisms underlying anti-inflammatory effects of M. vaccae are not known. OBJECTIVES: Our objective was to identify and characterize novel anti-inflammatory molecules from M. vaccae NCTC 11659. METHODS: We have purified and identified a unique anti-inflammatory triglyceride, 1,2,3-tri [Z-10-hexadecenoyl] glycerol, from M. vaccae and evaluated its effects in freshly isolated murine peritoneal macrophages. RESULTS: The free fatty acid form of 1,2,3-tri [Z-10-hexadecenoyl] glycerol, 10(Z)-hexadecenoic acid, decreased lipopolysaccharide-stimulated secretion of the proinflammatory cytokine IL-6 ex vivo. Meanwhile, next-generation RNA sequencing revealed that pretreatment with 10(Z)-hexadecenoic acid upregulated genes associated with peroxisome proliferator-activated receptor alpha (PPARα) signaling in lipopolysaccharide-stimulated macrophages, in association with a broad transcriptional repression of inflammatory markers. We confirmed using luciferase-based transfection assays that 10(Z)-hexadecenoic acid activated PPARα signaling, but not PPARγ, PPARδ, or retinoic acid receptor (RAR) α signaling. The effects of 10(Z)-hexadecenoic acid on lipopolysaccharide-stimulated secretion of IL-6 were prevented by PPARα antagonists and absent in PPARα-deficient mice. CONCLUSION: Future studies should evaluate the effects of 10(Z)-hexadecenoic acid on stress-induced exaggeration of peripheral inflammatory signaling, central neuroinflammatory signaling, and anxiety- and fear-related defensive behavioral responses.


Assuntos
Anti-Inflamatórios/imunologia , Anti-Inflamatórios/isolamento & purificação , Mycobacterium/imunologia , Mycobacterium/isolamento & purificação , Estresse Psicológico/imunologia , Estresse Psicológico/prevenção & controle , Animais , Ansiedade/induzido quimicamente , Ansiedade/imunologia , Ansiedade/prevenção & controle , Colite/induzido quimicamente , Colite/imunologia , Colite/prevenção & controle , Medo/efeitos dos fármacos , Medo/fisiologia , Inflamação/imunologia , Inflamação/prevenção & controle , Lipopolissacarídeos/toxicidade , Macrófagos/efeitos dos fármacos , Macrófagos/imunologia , Masculino , Camundongos , Camundongos da Linhagem 129 , Camundongos Endogâmicos BALB C , Camundongos Endogâmicos C57BL , Microglia/efeitos dos fármacos , Microglia/imunologia , Microbiologia do Solo , Estresse Psicológico/induzido quimicamente
10.
Horm Behav ; 113: 76-84, 2019 07.
Artigo em Inglês | MEDLINE | ID: mdl-31054843

RESUMO

Early life stress leads to long lasting effects on behavior. Neuroimmune cells have been implicated as key mediators of experience-induced changes in brain and behavioral development, in that they are highly responsive to stress. Mast cells are one such type of neuroimmune cell, but little is known about their role in brain development or following early life stress. Here, we assessed the impact of three different early life stress exposure paradigms on mast cell dynamics in the developing brain of male and female rats, focusing on the hippocampus and hypothalamus, where most mast cells reside. We found that exposure to two weeks of chronic variable stress during gestation led to increased mast cell number and activation in the female offspring hypothalamus on the day of birth. Acute exposure to maternal separation stress on postnatal day (PN) 2 led to significant decreases in mast cells within the hypothalamus and hippocampus of females, but not males. In contrast, one week of exposure to brief daily maternal separation stress (e.g., handling), increased mast cell numbers in the female, but not male, hippocampus. We found significant sex differences in mast cell number and activation, including males having more mast cells than females in the hippocampus on the day of birth and males having significantly more degranulated mast cells on PN11. Thus, mast cells may be an unappreciated mediator of sex-specific brain development in response to early life perturbations.


Assuntos
Encéfalo/crescimento & desenvolvimento , Encéfalo/patologia , Mastócitos/patologia , Privação Materna , Estresse Psicológico , Animais , Animais Recém-Nascidos , Encéfalo/imunologia , Encéfalo/metabolismo , Contagem de Células , Feminino , Hipocampo/crescimento & desenvolvimento , Hipocampo/imunologia , Hipocampo/patologia , Hipotálamo/crescimento & desenvolvimento , Hipotálamo/imunologia , Hipotálamo/patologia , Masculino , Neuroimunomodulação/fisiologia , Ratos , Ratos Sprague-Dawley , Caracteres Sexuais , Estresse Psicológico/imunologia , Estresse Psicológico/metabolismo , Estresse Psicológico/fisiopatologia
11.
Biol Sex Differ ; 10(1): 20, 2019 04 16.
Artigo em Inglês | MEDLINE | ID: mdl-30992051

RESUMO

BACKGROUND: Antarctica challenges human explorers by its extreme environment. The effects of these unique conditions on the human physiology need to be understood to best mitigate health problems in Antarctic expedition crews. Moreover, Antarctica is an adequate Earth-bound analogue for long-term space missions. To date, its effects on human physiology have been studied mainly in male cohorts though more female expeditioners and applicants in astronaut training programs are selected. Therefore, the identification of sex differences in stress and immune reactions are becoming an even more essential aim to provide a more individualized risk management. METHODS: Ten female and 16 male subjects participated in three 1-year expeditions to the German Antarctic Research Station Neumayer III. Blood, saliva, and urine samples were taken 1-2 months prior to departure, subsequently every month during their expedition, and 3-4 months after return from Antarctica. Analyses included cortisol, catecholamine and endocannabinoid measurements; psychological evaluation; differential blood count; and recall antigen- and mitogen-stimulated cytokine profiles. RESULTS: Cortisol showed significantly higher concentrations in females than males during winter whereas no enhanced psychological stress was detected in both sexes. Catecholamine excretion was higher in males than females but never showed significant increases compared to baseline. Endocannabinoids and N-acylethanolamides increased significantly in both sexes and stayed consistently elevated during the confinement. Cytokine profiles after in vitro stimulation revealed no sex differences but resulted in significant time-dependent changes. Hemoglobin and hematocrit were significantly higher in males than females, and hemoglobin increased significantly in both sexes compared to baseline. Platelet counts were significantly higher in females than males. Leukocytes and granulocyte concentrations increased during confinement with a dip for both sexes in winter whereas lymphocytes were significantly elevated in both sexes during the confinement. CONCLUSIONS: The extreme environment of Antarctica seems to trigger some distinct stress and immune responses but-with the exception of cortisol and blood cell counts-without any major relevant sex-specific differences. Stated sex differences were shown to be independent of enhanced psychological stress and seem to be related to the environmental conditions. However, sources and consequences of these sex differences have to be further elucidated.


Assuntos
Ambientes Extremos , Caracteres Sexuais , Estresse Psicológico , Adulto , Regiões Antárticas , Antígenos de Fungos/imunologia , Catecolaminas/urina , Citocinas/imunologia , Endocanabinoides/sangue , Feminino , Testes Hematológicos , Humanos , Hidrocortisona/metabolismo , Masculino , Pessoa de Meia-Idade , Mitógenos da Erva-dos-Cancros/imunologia , Estresse Psicológico/sangue , Estresse Psicológico/imunologia , Estresse Psicológico/metabolismo , Estresse Psicológico/urina , Adulto Jovem
12.
Bull Exp Biol Med ; 166(6): 754-758, 2019 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-31028579

RESUMO

We studied immunocorrecting effects of Semax (Met-Glu-His-Phe-Pro-Gly-Pro) on the model of "social" stress caused by sensory contact and intermale confrontation. Functional activity of the immune system of laboratory animals was evaluated in standard immunopharmacological tests: delayed-type hypersensitivity reaction, direct agglutination test, latex test for studying phagocytic activity of peripheral blood neutrophils, changes in differential leukocyte count, and weight of immunocompetent organs. It was found that changes in the immune response caused by "social" stress are multidirectional, which confirms the theory of stress-induced "immune imbalance". Semax acted as effective immune corrector restoring cellular and humoral immunogenesis reactions and phagocytic activity of neutrophils. This attested to the presence of immunomodulating properties in Semax and necessitates further studies in this field.


Assuntos
Hormônio Adrenocorticotrópico/análogos & derivados , Fatores Imunológicos/farmacologia , Fármacos Neuroprotetores/farmacologia , Nootrópicos/farmacologia , Fragmentos de Peptídeos/farmacologia , Estresse Psicológico/tratamento farmacológico , Hormônio Adrenocorticotrópico/farmacologia , Agressão , Animais , Animais não Endogâmicos , Hipersensibilidade Tardia/tratamento farmacológico , Hipersensibilidade Tardia/imunologia , Imunidade Inata/efeitos dos fármacos , Testes de Fixação do Látex , Contagem de Leucócitos , Masculino , Neutrófilos/efeitos dos fármacos , Neutrófilos/imunologia , Fagocitose/efeitos dos fármacos , Estresse Psicológico/imunologia , Estresse Psicológico/fisiopatologia
13.
Nurs Res ; 68(2): 167-173, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-30829924

RESUMO

BACKGROUND: Allostatic load (AL) is a biopsychosocial model that suggests chronic psychosocial stress leads to physiological dysregulation and poor outcomes. The purpose of this study was to examine AL in pregnant women operationalized using proinflammatory cytokines and psychosocial indicators and perinatal outcomes. OBJECTIVES: The aim of the study was to identify relationships between circulating cytokines/chemokines and the Prenatal Distress Questionnaire, the Maternal Antenatal Attachment Scale, the Emotional Quotient Inventory, the Life Experiences Scale, and demographics in pregnant women. METHODS: A cross-sectional design was used to recruit pregnant women between 24 and 28 weeks of gestation. Blood and stress/emotional indicators were obtained after informed consent. Plasma was abstracted to simultaneously measure 29 cytokines/chemokines using a multiplex array. Cytokine/chemokine levels were compared with continuous variables using Spearman's rho and with categorical variables using Mann-Whitney U. RESULTS: Twenty-five women with medically high-risk (n = 16) and low-risk (n = 9) pregnancies consented. Most women were White (68%) with a mean age of 29 years (SD = 5.9). Although several cytokines and chemokines showed significant correlations with the stress/emotional indicators, only interleukin-17A (IL-17A) was significantly associated with all of the indicators (Prenatal Distress Questionnaire: rs = .528, p = .012; Maternal Antenatal Attachment Scale: rs = -.439, p = .036; Emotional Quotient Inventory total: rs = -.545, p = .007), Life Experiences Scale (rs = .458, p = .032), birth weight (rs = -.499, p = .013), and race (p = .01). DISCUSSION: Increased levels of IL-17A, a known cytokine associated with chronic stress and with poor perinatal outcomes, were associated with high prenatal distress, low maternal attachment, and lower emotional intelligence in pregnant women. Increased levels of IL-17A also were associated with lower birth weight and non-White race. Results support the model of AL in pregnant women and highlight IL-17A as a potential biomarker of AL during pregnancy.


Assuntos
Interleucina-17/sangue , Complicações na Gravidez/imunologia , Proteínas da Gravidez/sangue , Estresse Psicológico/imunologia , Adulto , Biomarcadores/sangue , Estudos Transversais , Citocinas/sangue , Feminino , Humanos , Gravidez , Segundo Trimestre da Gravidez/imunologia
14.
Med Sci Sports Exerc ; 51(8): 1635-1641, 2019 08.
Artigo em Inglês | MEDLINE | ID: mdl-30829964

RESUMO

Studies suggest that exercise can improve vaccination responses in humans. Chronic stress can lead to immunosuppression, and there may be a role for exercise in augmenting immune responses. PURPOSE: To investigate the effects of acute eccentric exercise (ECC) and voluntary wheel exercise training (VWR) on antibody and cell-mediated immune responses to vaccination in chronically stressed mice. We hypothesized that both ECC and VWR would attenuate chronic stress-induced reductions in vaccination responses. METHODS: Mice were randomized into four groups: control (CON), stress (S)-ECC, S-VWR, and S-sedentary (SED). Stressed groups received chronic restraint stress for 6 h·d, 5 d·wk for 3 wk. After the first week of stress, S-ECC were exercised at 17 m·min speed at -20% grade for 45 min on a treadmill and then intramuscularly injected with 100 µg of ovalbumin (OVA) and 200 µg of alum adjuvant. All other groups were also vaccinated at this time. Stress-VWR mice voluntarily ran on a wheel for the entire experiment. Plasma was collected before, and at 1, 2, and 4 wk postvaccination. Enzyme-linked immunosorbent assay was performed to analyze anti-OVA IgG and IgM antibodies. After 3 wk of chronic stress, all mice were injected with OVA into the ear to determine the delayed-type hypersensitivity. RESULTS: We found that chronic restraint stress significantly reduced body weight and caused adrenal hypertrophy. We also found both S-ECC and S-VWR groups had significantly elevated anti-OVA IgG (P < 0.05), whereas no significant differences between the two exercise groups. Neither S-ECC nor S-VWR altered anti-OVA IgM or delayed-type hypersensitivity responses compared with S-SED group. CONCLUSIONS: Acute eccentric exercise and voluntary exercise training alleviated the chronic stress-induced anti-OVA IgG reductions in vaccination responses.


Assuntos
Imunidade Celular , Imunoglobulina G/sangue , Imunoglobulina M/sangue , Condicionamento Físico Animal/fisiologia , Estresse Psicológico/imunologia , Vacinação , Glândulas Suprarrenais/patologia , Animais , Hipertrofia , Masculino , Camundongos Endogâmicos C57BL , Modelos Animais , Tamanho do Órgão , Ovalbumina/imunologia , Distribuição Aleatória , Baço/parasitologia , Perda de Peso
15.
J Fam Psychol ; 33(3): 338-348, 2019 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-30742465

RESUMO

We followed 402 African American young adults from ages 24 to 29, a period of emerging committed relationships, to examine the association of contextual stress (CS), for example, experiences of financial strain, victimization, and racial discrimination, with inflammation, and to test predictions that greater perceived relationship warmth and support (PRWS) at age 29 would moderate the association between earlier CS and inflammation, using a multiplex assessment of cytokines to construct an index of the ratio between predominantly proinflammatory cytokines versus predominantly anti-inflammatory cytokines. CS experienced at age 24 was associated with greater inflammation at age 29 in the full sample (b = .112, p = .004). PRWS at age 29 moderated the association of earlier CS with inflammation (b = -.114, p = .011), but there was no significant main effect of PRWS (b = -.053, p = .265). Finally, using an internal moderator approach, we compared the association of CS with inflammation among those not in a committed relationship to those in more or less supportive relationships, showing a significant and stronger association of CS with inflammation for those with low PRWS (-1 SD; b = .182, p < .001), a weaker and nonsignificant association of CS with inflammation among those with higher PRWS (+1 SD; b = -.002, p = .975), and an intermediate and nonsignificant association of CS with inflammation among those with no committed romantic relationship (b = .077, p = .227). Results were robust to number of cytokines included in the inflammation index. (PsycINFO Database Record (c) 2019 APA, all rights reserved).


Assuntos
Afro-Americanos/psicologia , Vítimas de Crime/psicologia , Inflamação/imunologia , Inflamação/psicologia , Racismo/psicologia , Parceiros Sexuais/psicologia , Apoio Social , Estresse Psicológico/imunologia , Adulto , Citocinas/imunologia , Citocinas/metabolismo , Economia , Feminino , Humanos , Mediadores da Inflamação/imunologia , Estudos Longitudinais , Masculino , Percepção Social , Fatores Socioeconômicos , Estresse Psicológico/psicologia , Adulto Jovem
16.
Cancer ; 125(9): 1417-1431, 2019 05 01.
Artigo em Inglês | MEDLINE | ID: mdl-30768779

RESUMO

The range of psychosocial stress factors/processes (eg, chronic stress, distress states, coping, social adversity) were reviewed as they relate to immune variables in cancer along with studies of psychosocial interventions on these stress processes and immune measures in cancer populations. The review includes molecular, cellular, and clinical research specifically examining the effects of stress processes and stress-management interventions on immune variables (eg, cellular immune function, inflammation), which may or may not be changing directly in response to the cancer or its treatment. Basic psychoneuroimmunologic research on stress processes (using animal or cellular/tumor models) provides leads for investigating biobehavioral processes that may underlie the associations reported to date. The development of theoretically driven and empirically supported stress-management interventions may provide important adjuncts to clinical cancer care going forward.


Assuntos
Neoplasias/imunologia , Neoplasias/terapia , Estresse Psicológico , Adaptação Psicológica/fisiologia , Progressão da Doença , Humanos , Imunidade Inata/fisiologia , Metástase Neoplásica , Neoplasias/complicações , Neoplasias/patologia , Psicoterapia/métodos , Estresse Psicológico/complicações , Estresse Psicológico/imunologia , Estresse Psicológico/terapia , Evasão Tumoral/fisiologia
17.
Physiology (Bethesda) ; 34(2): 123-133, 2019 03 01.
Artigo em Inglês | MEDLINE | ID: mdl-30724127

RESUMO

Metabolic syndrome and major depression are two of the most common and debilitating disorders worldwide, occurring with significant rates of comorbidity. Recent studies have uncovered that each of these conditions is associated with chronic, low-grade inflammation. This is characterized by increased circulating pro-inflammatory cytokines, altered leukocyte population frequencies in blood, accumulation of immune cells in tissues including the brain, and activation of these immune cells. Cytokines that become elevated during obesity can contribute to the progression of metabolic syndrome by directly causing insulin resistance. During chronic stress, there is evidence that these cytokines promote depression-like behavior by disrupting neurotransmitter synthesis and signal transduction. Animal models of obesity and depression have revealed a bi-directional relationship whereby high-fat feeding and chronic stress synergize and exacerbate metabolic dysregulation and behavioral abnormalities. Although far from conclusive, emerging evidence suggests that inflammation in the central and peripheral immune system may link metabolic syndrome to major depressive disorder. In this review, we will synthesize available data supporting this view and identify critical areas for future investigation.


Assuntos
Transtorno Depressivo Maior/imunologia , Encefalite/imunologia , Mediadores da Inflamação/imunologia , Inflamação/imunologia , Síndrome Metabólica/imunologia , Animais , Citocinas/metabolismo , Transtorno Depressivo Maior/complicações , Encefalite/complicações , Humanos , Inflamação/complicações , Leucócitos/imunologia , Síndrome Metabólica/complicações , Obesidade/complicações , Obesidade/imunologia , Estresse Psicológico/complicações , Estresse Psicológico/imunologia
18.
Gen Comp Endocrinol ; 275: 30-37, 2019 05 01.
Artigo em Inglês | MEDLINE | ID: mdl-30721660

RESUMO

Stress-induced inhibition of innate immune activity has been observed in a variety of wild birds and may increase chances of infection because this activity constitutes the first line of defense against pathogens. We previously reported that the transient elevation of plasma corticosterone (CORT; the primary avian glucocorticoid) that occurs during stress is necessary for stress-induced suppression of natural antibody-mediated, complement-mediated, and bactericidal activity. Here, we further investigated the regulatory role of CORT during this suppression. To this end, we treated House Sparrows (Passer domesticus) with mitotane to block endogenous CORT production, administered CORT at one of three doses (HI: 1.34 mg/kg; LO: 1.00 mg/kg; CON: vehicle), and assessed natural antibody-mediated, complement-mediated, and bactericidal activity during acute stress induced by handling and restraint. Mitotane administration eliminated the endogenous plasma CORT increase that normally takes place during stress, and corticosterone treatment increased plasma CORT to levels similar to those measured in intact birds during acute stress. As predicted, mitotane-treated birds receiving CON injections did not exhibit stress-induced suppression of complement-mediated and bactericidal activity, and CORT administration at both LO and HI doses restored this suppression. Contrary to expectations, mitotane-treated birds receiving CON injections demonstrated stress-induced suppression of natural antibody-mediated activity. Furthermore, CORT administration did not influence this parameter. These results suggest that stress inhibits innate immune activity through both CORT-dependent and CORT-independent mechanisms, but the contribution of these mechanisms can vary. This variation may result from effects of environmental factors, the identity and role of which warrant further research.


Assuntos
Corticosterona/farmacologia , Imunidade Inata/efeitos dos fármacos , Pardais/imunologia , Estresse Psicológico/imunologia , Animais , Animais Selvagens , Relação Dose-Resposta a Droga , Glucocorticoides/farmacologia , Masculino , Mitotano/farmacologia , Distribuição Aleatória , Pardais/fisiologia , Estresse Fisiológico/efeitos dos fármacos , Estresse Psicológico/sangue , Estresse Psicológico/induzido quimicamente
19.
Bull Exp Biol Med ; 166(3): 344-347, 2019 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-30627910

RESUMO

The role of signaling molecules in synthesis of humoral regulators of granulocytopoiesis by the hematopoietic microenvironmental cells during stress was analyzed using specific inhibitors. The major role in stimulation of the synthesis of granulocytic CSF during stressful stimulation is played by PI3K/Akt signaling cascade. Nuclear transcription factor NF-κB plays an auxiliary role in the regulation of functional activity of the bone marrow mononuclears. However, this factor affects the synthesis of granulocytic CSF by CD4+ cells of the bone marrow in response to stressful stimulation. Different degree and specific character of involvement of the signaling proteins in the regulation of the production of humoral factors determining colony-stimulating activity are explained by changes in functional state of monocyte-derived macrophages in different periods of stress response.


Assuntos
Fator Estimulador de Colônias de Granulócitos/genética , Granulócitos/imunologia , NF-kappa B/genética , Fosfatidilinositol 3-Quinases/genética , Transdução de Sinais/imunologia , Estresse Psicológico/genética , Animais , Células da Medula Óssea/efeitos dos fármacos , Células da Medula Óssea/imunologia , Células da Medula Óssea/patologia , Cromonas/farmacologia , Flavonoides/farmacologia , Regulação da Expressão Gênica , Tiomalato Sódico de Ouro/farmacologia , Fator Estimulador de Colônias de Granulócitos/imunologia , Granulócitos/efeitos dos fármacos , Granulócitos/patologia , Imidazóis/farmacologia , Imobilização/métodos , Leucopoese/efeitos dos fármacos , Leucopoese/imunologia , Macrófagos/efeitos dos fármacos , Macrófagos/imunologia , Macrófagos/patologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Proteína Quinase 1 Ativada por Mitógeno/antagonistas & inibidores , Proteína Quinase 1 Ativada por Mitógeno/genética , Proteína Quinase 1 Ativada por Mitógeno/imunologia , Proteína Quinase 3 Ativada por Mitógeno/antagonistas & inibidores , Proteína Quinase 3 Ativada por Mitógeno/genética , Proteína Quinase 3 Ativada por Mitógeno/imunologia , Morfolinas/farmacologia , NF-kappa B/antagonistas & inibidores , NF-kappa B/imunologia , Fosfatidilinositol 3-Quinases/imunologia , Piridinas/farmacologia , Estresse Psicológico/imunologia , Estresse Psicológico/metabolismo , Estresse Psicológico/fisiopatologia , Proteínas Quinases p38 Ativadas por Mitógeno/antagonistas & inibidores , Proteínas Quinases p38 Ativadas por Mitógeno/genética , Proteínas Quinases p38 Ativadas por Mitógeno/imunologia
20.
Stress ; 22(2): 236-247, 2019 03.
Artigo em Inglês | MEDLINE | ID: mdl-30676166

RESUMO

The objective of this study was to assess the influence of prenatal stress (PNS) on innate immune responses to an endotoxin challenge in weaned bull calves. Altered innate immune response to lipopolysaccharide (LPS), as characterized by changes in a range of variables was hypothesized in PNS bull calves. Brahman cows (n = 96; 48 stressed by transportation at five stages of gestation and 48 Controls) produced 85 calves, from which 16 uncastrated male (bull) calves from each PNS and Control treatment were selected for an LPS challenge period. Rectal temperature (RT), sickness behavior score (SBS), serum concentrations of cortisol, interferon-gamma (IFN-γ), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and complete blood count (CBC) variables were assessed in response to intravenous LPS (0.25 µg/kg body weight) administration. Each reported variable increased or decreased following LPS administration. Prior to LPS, PNS bull calves exhibited increased TNF-α, IL-6, and monocyte counts, but decreased IFN-γ, eosinophils, and basophils (p < .05). Compared with Control, in response to LPS, PNS bull calves exhibited greater circulating concentrations of cortisol. PNS bull calves exhibited lower (p < .05) eosinophil and basophil counts at time 0 (time of LPS administration) but similar counts to Control bull calves 2 h after LPS. PNS bull calves exhibited a greater change from baseline for IFN-γ and monocytes in response to LPS administration. No other variables were influenced by prenatal treatment (p > .05). These findings suggest that PNS did not adversely affect basal or induced components of the innate immune response to an immunological challenge. Lay summary Our laboratory studied the influence of prenatal stress (i.e., transportation of pregnant cows) on immune function of bull calves at 8 months of age. This was accomplished by studying aspects of their innate immune response to an immunological challenge. Prenatal stress did not adversely affect basal or induced components of the innate immune response to an immunological challenge.


Assuntos
Imunidade Inata/fisiologia , Estresse Psicológico/imunologia , Transportes , Desmame , Animais , Bovinos , Endotoxinas , Hidrocortisona/sangue , Interleucina-6/sangue , Lipopolissacarídeos , Masculino , Estresse Psicológico/sangue , Fator de Necrose Tumoral alfa/sangue
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