Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 20 de 2.387
Filtrar
1.
Front Immunol ; 11: 1997, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32983141

RESUMO

Obesity is a major independent risk factor for increased morbidity and mortality upon infection with Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV-2), which is responsible for the current coronavirus disease pandemic (COVID-19). Therefore, there is a critical need to identify underlying metabolic factors associated with obesity that could be contributing toward increased susceptibility to SARS-CoV-2 in this vulnerable population. Here, we focus on the critical role of potent endogenous lipid metabolites known as specialized pro-resolving mediators (SPMs) that are synthesized from polyunsaturated fatty acids. SPMs are generated during the transition of inflammation to resolution and have a vital role in directing damaged tissues to homeostasis; furthermore, SPMs display anti-viral activity in the context of influenza infection without being immunosuppressive. We cover evidence from rodent and human studies to show that obesity, and its co-morbidities, induce a signature of SPM deficiency across immunometabolic tissues. We further discuss how the effects of obesity upon SARS-CoV-2 infection are likely exacerbated with environmental exposures that promote chronic pulmonary inflammation and augment SPM deficits. Finally, we highlight potential approaches to overcome the loss of SPMs using dietary and pharmacological interventions. Collectively, this mini-review underscores the need for mechanistic studies on how SPM deficiencies driven by obesity and environmental exposures may exacerbate the response to SARS-CoV-2.


Assuntos
Betacoronavirus , Infecções por Coronavirus/epidemiologia , Ácidos Docosa-Hexaenoicos/deficiência , Ácido Eicosapentaenoico/metabolismo , Ácido Linoleico/deficiência , Lipoxinas/deficiência , Obesidade/epidemiologia , Obesidade/imunologia , Pneumonia Viral/epidemiologia , Comorbidade , Infecções por Coronavirus/dietoterapia , Infecções por Coronavirus/virologia , Suscetibilidade a Doenças , Ácidos Docosa-Hexaenoicos/uso terapêutico , Ácido Eicosapentaenoico/uso terapêutico , Humanos , Inflamação/metabolismo , Ácido Linoleico/uso terapêutico , Lipoxinas/uso terapêutico , Morbidade , Obesidade/metabolismo , Pandemias , Pneumonia Viral/dietoterapia , Pneumonia Viral/virologia , Fatores de Risco
2.
PLoS One ; 15(9): e0237496, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32881912

RESUMO

BACKGROUND: Obesity is often associated with inflammation in adipose tissue (AT) with release of mediators of atherogenesis. We postulated that it would be feasible to collect sufficient abdominal AT to quantify changes in a broad array of adaptive and innate mononuclear white cells in obese non-diabetic adults in response to a dipeptidyl protease inhibitor (DPP4i), known to inhibit activation of immune white cells. METHODS: Adults 18-55 years-of-age were screened for abdominal obesity and insulin resistance or impaired glucose tolerance but without known inflammatory conditions. Twenty-one eligible participants consented for study and were randomized 3:1 to receive sitagliptin (DPP4i) at 100mg or matching placebo daily for 28 days. Abdominal AT collected by percutaneous biopsy and peripheral blood mononuclear cell fractions were evaluated before and after treatment; plasma was stored for batch testing. RESULTS: Highly sensitive C-reactive protein, a global marker of inflammation, was not elevated in the study population. Innate lymphoid cells (ILC) type 3 (ILC-3) in abdominal AT decreased with active treatment compared with placebo (p = 0.04). Other immune white cells in AT and peripheral blood mononuclear cell (PBMC) fractions did not change with treatment compared to placebo (p>0.05); although ILC-2 declined in PBMCs (p = 0.007) in the sitagliptin treatment group. Two circulating biomarkers of atherogenesis, interferon-inducible protein-10 (IP-10) and sCD40L declined in plasma (p = 0.02 and p = 0.07, respectively) in the active treatment group, providing indirect validation of a net reduction in inflammation. CONCLUSIONS: In this pilot study, two cell types of the innate lymphoid system, ILC-3 in AT and ILC-2 PBMCs declined during treatment and as did circulating biomarkers of atherogenesis. Changes in other immune cells were not demonstrable. The study showed that sufficient abdominal AT could be obtained to quantify white cells of both innate and adaptive immunity and to demonstrate changes during therapy with an immune inhibitor. TRIAL REGISTRATION: ClinicalTrials.gov identifier (NCT number): NCT02576.


Assuntos
Gordura Abdominal/patologia , Imunidade Inata , Leucócitos Mononucleares/patologia , Obesidade/imunologia , Adulto , Biomarcadores/sangue , Estudos de Viabilidade , Feminino , Citometria de Fluxo , Humanos , Linfócitos/patologia , Masculino , Pessoa de Meia-Idade , Obesidade/sangue , Fosfato de Sitagliptina/farmacologia , Resultado do Tratamento
3.
Front Immunol ; 11: 1714, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32793244

RESUMO

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the third coronavirus leading to a global health outbreak. Despite the high mortality rates from SARS-CoV-1 and Middle-East respiratory syndrome (MERS)-CoV infections, which both sparked the interest of the scientific community, the underlying physiopathology of the SARS-CoV-2 infection, remains partially unclear. SARS-CoV-2 shares similar features with SARS-CoV-1, notably the use of the angiotensin conversion enzyme 2 (ACE2) as a receptor to enter the host cells. However, some features of the SARS-CoV-2 pandemic are unique. In this work, we focus on the association between obesity, metabolic syndrome, and type 2 diabetes on the one hand, and the severity of COVID-19 infection on the other, as it seems greater in these patients. We discuss how adipocyte dysfunction leads to a specific immune environment that predisposes obese patients to respiratory failure during COVID-19. We also hypothesize that an ACE2-cleaved protein, angiotensin 1-7, has a beneficial action on immune deregulation and that its low expression during the SARS-CoV-2 infection could explain the severity of infection. This introduces angiotensin 1-7 as a potential candidate of interest in therapeutic research on CoV infections.


Assuntos
Adipocinas/imunologia , Angiotensina I/imunologia , Betacoronavirus/imunologia , Infecções por Coronavirus/patologia , Fragmentos de Peptídeos/imunologia , Pneumonia Viral/patologia , Síndrome Respiratória Aguda Grave/patologia , Adipocinas/sangue , Diabetes Mellitus Tipo 2/imunologia , Humanos , Síndrome Metabólica/imunologia , Obesidade/imunologia , Pandemias , Peptidil Dipeptidase A/metabolismo
4.
Front Immunol ; 11: 1582, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32793223

RESUMO

Metabolic abnormalities such as dyslipidemia, hyperinsulinemia, or insulin resistance and obesity play key roles in the induction and progression of type 2 diabetes mellitus (T2DM). The field of immunometabolism implies a bidirectional link between the immune system and metabolism, in which inflammation plays an essential role in the promotion of metabolic abnormalities (e.g., obesity and T2DM), and metabolic factors, in turn, regulate immune cell functions. Obesity as the main inducer of a systemic low-level inflammation is a main susceptibility factor for T2DM. Obesity-related immune cell infiltration, inflammation, and increased oxidative stress promote metabolic impairments in the insulin-sensitive tissues and finally, insulin resistance, organ failure, and premature aging occur. Hyperglycemia and the subsequent inflammation are the main causes of micro- and macroangiopathies in the circulatory system. They also promote the gut microbiota dysbiosis, increased intestinal permeability, and fatty liver disease. The impaired immune system together with metabolic imbalance also increases the susceptibility of patients to several pathogenic agents such as the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Thus, the need for a proper immunization protocol among such patients is granted. The focus of the current review is to explore metabolic and immunological abnormalities affecting several organs of T2DM patients and explain the mechanisms, whereby diabetic patients become more susceptible to infectious diseases.


Assuntos
Diabetes Mellitus Tipo 2/imunologia , Diabetes Mellitus Tipo 2/patologia , Hiperglicemia/imunologia , Síndrome Metabólica/imunologia , Obesidade/imunologia , Betacoronavirus/imunologia , Infecções por Coronavirus/imunologia , Suscetibilidade a Doenças/imunologia , Disbiose/imunologia , Microbioma Gastrointestinal , Humanos , Sistema Imunitário/metabolismo , Inflamação/imunologia , Estresse Oxidativo/imunologia , Pandemias , Pneumonia Viral/imunologia
5.
Int J Mol Sci ; 21(16)2020 Aug 12.
Artigo em Inglês | MEDLINE | ID: mdl-32806722

RESUMO

The coronavirus disease 2019 COVID-19 pandemic is rapidly spreading worldwide and is becoming a major public health crisis. Increasing evidence demonstrates a strong correlation between obesity and the COVID-19 disease. We have summarized recent studies and addressed the impact of obesity on COVID-19 in terms of hospitalization, severity, mortality, and patient outcome. We discuss the potential molecular mechanisms whereby obesity contributes to the pathogenesis of COVID-19. In addition to obesity-related deregulated immune response, chronic inflammation, endothelium imbalance, metabolic dysfunction, and its associated comorbidities, dysfunctional mesenchymal stem cells/adipose-derived mesenchymal stem cells may also play crucial roles in fueling systemic inflammation contributing to the cytokine storm and promoting pulmonary fibrosis causing lung functional failure, characteristic of severe COVID-19. Moreover, obesity may also compromise motile cilia on airway epithelial cells and impair functioning of the mucociliary escalators, reducing the clearance of severe acute respiratory syndrome coronavirus (SARS-CoV-2). Obese diseased adipose tissues overexpress the receptors and proteases for the SARS-CoV-2 entry, implicating its possible roles as virus reservoir and accelerator reinforcing violent systemic inflammation and immune response. Finally, anti-inflammatory cytokines like anti-interleukin 6 and administration of mesenchymal stromal/stem cells may serve as potential immune modulatory therapies for supportively combating COVID-19. Obesity is conversely related to the development of COVID-19 through numerous molecular mechanisms and individuals with obesity belong to the COVID-19-susceptible population requiring more protective measures.


Assuntos
Infecções por Coronavirus/epidemiologia , Citocinas/metabolismo , Obesidade/epidemiologia , Pneumonia Viral/epidemiologia , Adipócitos/metabolismo , Animais , Infecções por Coronavirus/imunologia , Citocinas/genética , Humanos , Obesidade/imunologia , Pandemias , Pneumonia Viral/imunologia
6.
Obes Facts ; 13(4): 439-452, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32791497

RESUMO

Accumulating evidence suggests that obesity is a major risk factor for the initiation, progression, and outcomes of coronavirus disease 2019 (COVID-19). The European Association for the Study of Obesity (EASO), as a scientific and medical society dedicated to the promotion of health and well-being, is greatly concerned about the concomitant obesity and COVID-19 pandemics and their impact on health and society at large. In this perspective, we will address the inherent immunological perturbations and alterations in the renin-angiotensin-aldosterone system in patients with obesity and COVID-19, and discuss how these impairments may underlie the increased susceptibility and more detrimental outcomes of COVID-19 in people with obesity. Clearly, this has important implications for preventive measures, vaccination, and future therapeutic strategies to combat COVID-19. Furthermore, we will highlight important knowledge gaps and provide suggestions for future research and recommendations for policy actions. Since many new reports on COVID-19 rapidly appear, the present perspective should be seen as a focus for discussion to drive forward further understanding, research initiatives, and clinical management of COVID-19.


Assuntos
Betacoronavirus/imunologia , Infecções por Coronavirus/imunologia , Obesidade/complicações , Obesidade/imunologia , Pneumonia Viral/imunologia , Coronavirus , Infecções por Coronavirus/terapia , Suscetibilidade a Doenças , Humanos , Tolerância Imunológica/imunologia , Imunocompetência/imunologia , Pandemias , Peptidil Dipeptidase A , Pneumonia Viral/terapia , Prognóstico , Sistema Renina-Angiotensina/fisiologia , Fatores de Risco
7.
Eur J Pharmacol ; 882: 173329, 2020 Sep 05.
Artigo em Inglês | MEDLINE | ID: mdl-32615182

RESUMO

Coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is a newly discovered highly pathogenic virus that was declared pandemic in March 2020 by the World Health Organization. The virus affects the respiratory system, produces an inflammatory storm that causes lung damage and respiratory dysfunction. It infects humans of all ages. The Covid-19 takes a more severe course in individuals with chronic metabolic diseases such as obesity, diabetes mellitus, and hypertension. This category of persons exhibits weak immune activity and decreased levels of endogenous antioxidants. Melatonin is a multifunctional signaling hormone synthesized and secreted primarily by the pineal gland. It is a potent antioxidant with immunomodulatory action and has remarkable anti-inflammatory effects under a variety of circumstances. Regarding Covid-19 and metabolic syndrome, adequate information about the relationship between these two comorbidities is required for better management of these patients. Since Covid-19 infection and complications involve severe inflammation and oxidative stress in people with obesity and diabetes, we anticipated the inclusion of melatonin, as powerful antioxidant, within proposed treatment protocols. In this context, melatonin is a potential and promising agent to help overcome Covid-19 infection and boost the immune system in healthy persons and obese and diabetic patients. This review summarizes some evidence from recently published reports on the utility of melatonin as a potential adjuvant in Covid-19-infected individuals with diabetes and obesity.


Assuntos
Betacoronavirus/imunologia , Infecções por Coronavirus/tratamento farmacológico , Diabetes Mellitus/imunologia , Melatonina/farmacologia , Obesidade/imunologia , Pneumonia Viral/tratamento farmacológico , Adjuvantes Imunológicos/farmacologia , Adjuvantes Imunológicos/uso terapêutico , Antioxidantes/farmacologia , Antioxidantes/uso terapêutico , Antivirais/farmacologia , Antivirais/uso terapêutico , Betacoronavirus/patogenicidade , Ensaios Clínicos como Assunto , Comorbidade , Infecções por Coronavirus/epidemiologia , Infecções por Coronavirus/imunologia , Infecções por Coronavirus/virologia , Diabetes Mellitus/epidemiologia , Interações entre Hospedeiro e Microrganismos/efeitos dos fármacos , Interações entre Hospedeiro e Microrganismos/imunologia , Humanos , Sistema Imunitário/efeitos dos fármacos , Pulmão , Melatonina/uso terapêutico , Obesidade/epidemiologia , Estresse Oxidativo/efeitos dos fármacos , Estresse Oxidativo/imunologia , Pandemias , Pneumonia Viral/epidemiologia , Pneumonia Viral/imunologia , Pneumonia Viral/virologia , Fatores de Risco , Resultado do Tratamento
8.
J Popul Ther Clin Pharmacol ; 27(S Pt 1): e31-e36, 2020 Jun 29.
Artigo em Inglês | MEDLINE | ID: mdl-32650354

RESUMO

The coronavirus disease 2019 (COVID-19) pandemic has spread around the globe, infecting more than ten million individuals, with more than 500,000 dead; about one half of the infected people have recovered. Despite this fact, a subgroup of individuals affected by COVID-19 is at greater risk of developing worse outcomes and experience a high rate of mortality. Data on the association between obesity and COVID-19 are growing; the available studies, have reported a high prevalence of overweight and obesity in patients experiencing a severe COVID-19 course, with serious complications requiring hospitalization and admission to intensive care units. This paper attempts to highlight potential mechanisms behind the greater vulnerability to COVID-19 of individuals with obesity. The presence of uncontrolled chronic obesity-related comorbidities, particularly pulmonary diseases, can present a primary fertile soil for respiratory tract infection. Combined with immune system impairments, such as alteration in the T-cell proliferation and macrophage differentiation, and the high pro-inflammatory cytokine production by the adipose organ, this may worsen the general condition toward a systemic diffusion of infection. Prevention remains the first line of intervention in these patients that can be achieved by adhering to social distancing and adopting hygiene precautions, combined with a healthy lifestyle. Patients with obesity require preferential access dedicated to primary care services to ensure they are regularly taking their medications for the treatment of any concurrent chronic diseases. Finally, their physicians must promptly manage any medical signs or symptoms in the case of suspected severe acute respiratory syndrome coronavirus-2 (SARS-CoV2) infection to prevent the risk of severe outcomes.


Assuntos
Infecções por Coronavirus/complicações , Obesidade/complicações , Pneumonia Viral/complicações , Betacoronavirus , Humanos , Obesidade/imunologia , Obesidade/virologia , Pandemias , Fatores de Risco , Índice de Gravidade de Doença
9.
Proc Natl Acad Sci U S A ; 117(28): 16616-16625, 2020 07 14.
Artigo em Inglês | MEDLINE | ID: mdl-32601203

RESUMO

Enhanced inflammation is believed to contribute to overnutrition-induced metabolic disturbance. Nutrient flux has also been shown to be essential for immune cell activation. Here, we report an unexpected role of nutrient-sensing O-linked ß-N-acetylglucosamine (O-GlcNAc) signaling in suppressing macrophage proinflammatory activation and preventing diet-induced metabolic dysfunction. Overnutrition stimulates an increase in O-GlcNAc signaling in macrophages. O-GlcNAc signaling is down-regulated during macrophage proinflammatory activation. Suppressing O-GlcNAc signaling by O-GlcNAc transferase (OGT) knockout enhances macrophage proinflammatory polarization, promotes adipose tissue inflammation and lipolysis, increases lipid accumulation in peripheral tissues, and exacerbates tissue-specific and whole-body insulin resistance in high-fat-diet-induced obese mice. OGT inhibits macrophage proinflammatory activation by catalyzing ribosomal protein S6 kinase beta-1 (S6K1) O-GlcNAcylation and suppressing S6K1 phosphorylation and mTORC1 signaling. These findings thus identify macrophage O-GlcNAc signaling as a homeostatic mechanism maintaining whole-body metabolism under overnutrition.


Assuntos
Macrófagos/imunologia , N-Acetilglucosaminiltransferases/imunologia , Obesidade/imunologia , Proteínas Quinases S6 Ribossômicas 90-kDa/imunologia , Acetilglucosamina/imunologia , Tecido Adiposo/imunologia , Animais , Humanos , Ativação de Macrófagos , Macrófagos/enzimologia , Camundongos , Camundongos Knockout , N-Acetilglucosaminiltransferases/genética , Obesidade/enzimologia , Obesidade/genética , Obesidade/metabolismo , Fosforilação , Proteínas Quinases S6 Ribossômicas 90-kDa/genética , Transdução de Sinais
12.
Obes Res Clin Pract ; 14(4): 295-300, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32660813

RESUMO

BACKGROUND: Obesity is a global disease with at least 2.8 million people dying each year as a result of being overweight or obese according to the world health organization figures. This paper aims to explore the links between obesity and mortality in COVID-19. METHODS: Electronic search was made for the papers studying obesity as a risk factor for mortality following COVID-19 infection. Three authors independently selected the papers and agreed for final inclusion. The outcomes were the age, gender, body mass index, severe comorbidities, respiratory support and the critical illness related mortality in COVID-19. 572 publications were identified and 42 studies were selected including one unpublished study data. Only 14 studies were selected for quantitative analysis. RESULTS: All the primary points but the gender are significantly associated with COVID-19 mortality. The age >70, [odd ratio (OR): 0.17, CI; 95%, P-value: <0.00001], gender [OR: 0.89; CI: 95%, P-value: 0.32], BMI > 25 kg/m2 [OR: 3.68, CI: 95%, P-value: <0.003], severe comorbidities [OR: 1.84, CI:95%, P-value: <0.00001], advanced respiratory support [OR: 6.98, CI: 95%, P-value: <0.00001], and critical illness [OR: 2.03, CI: 95%, P-value: <0.00001]. CONCLUSIONS: Patients with obesity are at high risk of mortality from COVID-19 infection.


Assuntos
Betacoronavirus , Infecções por Coronavirus/mortalidade , Obesidade/complicações , Pneumonia Viral/mortalidade , Adulto , Idoso , Idoso de 80 Anos ou mais , Índice de Massa Corporal , Infecções por Coronavirus/etiologia , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Obesidade/imunologia , Pandemias , Peptidil Dipeptidase A/fisiologia , Pneumonia Viral/etiologia
13.
Int J Obes (Lond) ; 44(9): 1810-1817, 2020 09.
Artigo em Inglês | MEDLINE | ID: mdl-32647360

RESUMO

Overweight and obesity are major risk factors for diabetes, cardiovascular disease, and lung disease. These diseases are the most commonly reported health conditions that predispose individuals with SARS-CoV-2 infection to require hospitalization including intensive care unit admissions. The innate immune response is the host's first line of defense against a human coronavirus infection. However, most coronaviruses are armed with one strategy or another to overcome host antiviral defense, and the pathogenicity of the virus is related to its capacity to suppress host immunity. The multifaceted nature of obesity including its effects on immunity can fundamentally alter the pathogenesis of acute respiratory distress syndrome and pneumonia, which are the major causes of death due to SARS-CoV-2 infection. Elevated circulating leptin concentrations are a hallmark of obesity, which is associated with a leptin-resistant state. Leptin is secreted by adipocytes in proportion to body fat and regulates appetite and metabolism through signaling in the hypothalamus. However, leptin also signals through the Jak/STAT and Akt pathways, among others, to modulate T cell number and function. Thus, leptin connects metabolism with the immune response. Therefore, it seems appropriate that its dysregulation would have serious consequences during an infection. We propose that leptin may be the link between obesity and its high prevalence as a comorbidity of the SARS-CoV-2 infection. In this article, we present a synthesis of the mechanisms underpinning susceptibility to respiratory viral infections and the contribution of the immunomodulatory effects of obesity to the outcome.


Assuntos
Infecções por Coronavirus , Leptina , Obesidade , Pandemias , Pneumonia Viral , Betacoronavirus , Comorbidade , Infecções por Coronavirus/epidemiologia , Infecções por Coronavirus/imunologia , Infecções por Coronavirus/metabolismo , Interações Hospedeiro-Patógeno/imunologia , Humanos , Leptina/sangue , Leptina/imunologia , Leptina/metabolismo , Obesidade/epidemiologia , Obesidade/imunologia , Obesidade/metabolismo , Pneumonia Viral/epidemiologia , Pneumonia Viral/imunologia , Pneumonia Viral/metabolismo , Transdução de Sinais/imunologia
14.
Diabetes ; 69(9): 1857-1863, 2020 09.
Artigo em Inglês | MEDLINE | ID: mdl-32669390

RESUMO

Coronavirus disease 2019 (COVID-19) is a novel threat that seems to result from the collusion between a new pandemic of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and an existing pandemic of metabolic disease driven by obesity. This Perspective explores the evolving epidemiological, clinical, biological, and molecular evidence to propose an unfolding paradigm in which old age, chronic metabolic disease (such as obesity, type 2 diabetes, and metabolic syndrome), and male biological sex produce a deadly symbiosis of dysregulated immunometabolism and chronic systemic inflammation that intensifies virally induced hyperinflammation associated with SARS-CoV-2 infection. It is intended to inspire new research directions and stimulate funding in this field.


Assuntos
Envelhecimento/imunologia , Infecções por Coronavirus/imunologia , Diabetes Mellitus Tipo 2/imunologia , Inflamação/imunologia , Síndrome Metabólica/imunologia , Obesidade/imunologia , Pneumonia Viral/imunologia , Adiposidade/imunologia , Afro-Americanos , Fatores Etários , Betacoronavirus , Síndrome da Liberação de Citocina/imunologia , Citocinas/imunologia , Grupos Étnicos , Feminino , Hispano-Americanos , Humanos , Masculino , Pandemias , Racismo , Fatores Sexuais , Estresse Psicológico/imunologia
16.
Allergol. immunopatol ; 48(3): 306-312, mayo-jun. 2020. ilus
Artigo em Inglês | IBECS | ID: ibc-192034

RESUMO

Over the past three decades, the number of obese people has risen steadily. The chronic low-grade inflammatory state and the non-specific activation of the immune system have contributed greatly to the development of obesity-related immunology. Food allergy as a kind of inflammatory disease with abnormal immune response may be associated with obesity. This review begins with the pro-inflammatory immunological effects of adipose tissue in obesity, and explains the possible effects of obesity on food allergy. In short, obesity not only directly causes imbalance of allergic-related immune cells in adipose tissue, but also indirectly causes this consequence through affecting expression of adipocytokines and peroxisome proliferator-activated receptor gamma (PPARγ) in adipose tissue. As a result, circulating levels of pro-inflammatory factors which are partly derived from adipose tissue increase, which might cause intestinal barrier injury. Therefore, obesity may increase the risk of food allergy


No disponible


Assuntos
Humanos , Tecido Adiposo/imunologia , Hipersensibilidade Alimentar/diagnóstico , Obesidade/complicações , Hipersensibilidade Alimentar/metabolismo , Inflamação/etiologia , Hipersensibilidade Alimentar/imunologia , Obesidade/imunologia , Tecido Adiposo/patologia
17.
Heart Fail Clin ; 16(3): 357-368, 2020 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-32503758

RESUMO

Obesity is very common in patients with heart failure with preserved ejection fraction (HFpEF). Obesity and increased adiposity have multiple adverse effects on the cardiovascular system, including hemodynamic, inflammatory, mechanical, and neurohormonal effects. Obesity and increased adiposity may be a promising target for therapy in HFpEF. This review summarizes the current understanding of the pathophysiology of obesity-related HFpEF, diagnostic evaluation of HFpEF among obese patients with dyspnea, and potential therapeutic options for the HFpEF obesity phenotype.


Assuntos
Insuficiência Cardíaca , Obesidade , Gerenciamento Clínico , Insuficiência Cardíaca/etiologia , Insuficiência Cardíaca/fisiopatologia , Insuficiência Cardíaca/terapia , Hemodinâmica , Humanos , Obesidade/complicações , Obesidade/imunologia , Obesidade/fisiopatologia , Volume Sistólico
18.
Clin Immunol ; 217: 108486, 2020 08.
Artigo em Inglês | MEDLINE | ID: mdl-32479985

RESUMO

The lymphopenia exhibited in patients with COVID-19 has been associated with a worse prognosis in the development of the disease. To understand the factors associated with a worse evolution of COVID-19, we analyzed comorbidities, indicators of inflammation such as CRP and the ratio of neutrophils/lymphocytes, as well as the count of blood cells with T-lymphocyte subtypes in 172 hospitalized patients with COVID-19 pneumonia. Patients were grouped according to their needs for mechanical ventilation (ICU care) or not. Within the comorbidities studied, obesity was the only associated with greater severity and ICU admission. Both the percentage and the absolute number of neutrophils were higher in patients needing ICU care than non-ICU patients, whereas absolute lymphocyte count, and especially the percentage of lymphocytes, presented a deep decline in critical patients. There was no difference between the two groups of patients for CD4 T-lymphocytes, neither in percentage of lymphocyte nor in absolute number, however for CD8 T-cells the differences were significant for both parameters which were in decline in ICU patients. There was a firm correlation between the highest values of inflammation indicators with the decrease in percentage of CD8 T-lymphocytes. This effect was not seen with CD4 cells. Obesity together with lymphopenia, especially whether preferentially affects to CD8 T- lymphocytes, are factors that can predict a poor prognosis in patients with COVID-19.


Assuntos
Betacoronavirus/patogenicidade , Linfócitos T CD8-Positivos/patologia , Infecções por Coronavirus/imunologia , Linfopenia/imunologia , Neutrófilos/patologia , Obesidade/imunologia , Pneumonia Viral/imunologia , Idoso , Idoso de 80 Anos ou mais , Betacoronavirus/imunologia , Biomarcadores/sangue , Proteína C-Reativa/metabolismo , Linfócitos T CD4-Positivos/imunologia , Linfócitos T CD4-Positivos/patologia , Linfócitos T CD4-Positivos/virologia , Linfócitos T CD8-Positivos/imunologia , Linfócitos T CD8-Positivos/virologia , Estudos de Casos e Controles , Infecções por Coronavirus/complicações , Infecções por Coronavirus/mortalidade , Infecções por Coronavirus/terapia , Feminino , Humanos , Unidades de Terapia Intensiva , Contagem de Linfócitos , Linfopenia/complicações , Linfopenia/mortalidade , Linfopenia/terapia , Masculino , Pessoa de Meia-Idade , Neutrófilos/imunologia , Neutrófilos/virologia , Obesidade/complicações , Obesidade/mortalidade , Obesidade/terapia , Pandemias , Pneumonia Viral/complicações , Pneumonia Viral/mortalidade , Pneumonia Viral/terapia , Prognóstico , Respiração Artificial , Estudos Retrospectivos , Índice de Gravidade de Doença , Análise de Sobrevida
19.
Diabetes Metab Syndr ; 14(4): 655-659, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32438328

RESUMO

BACKGROUND AND AIMS: COVID-19 is an emerging pandemic due to droplet infection of 2019-novel coronavirus (2019-nCoV). Due to its rapid transmission and high case-fatality rate, recognition of its risk and prognostic factor is important. Obesity has been associated with impaired immune system, increasing the susceptibility for 2019-nCoV infection. We aimed to study the impact of obesity to the prognosis and disease severity of COVID-19. METHODS: A systematic search and handsearching was conducted in four databases: Cochrane, MEDLINE, EMBASE, and PubMed. The identified articles were screened using the chosen eligibility criteria. We obtained three retrospective cohort studies (Wu J et al., Lighter J et al., and Simonnet A et al.) to be critically appraised using Newcastle Ottawa Scale. RESULTS: The findings of all included studies were consistent in stating the contribution of obesity as a risk factor to increase the requirement for advanced medical care. Study with the highest quality, Simonnet A et al., reported an increase need of invasive mechanical ventilation in COVID-19 patients with body mass index higher than 35 kg/m2, OR: 7.36 (1.63-33.14; p = 0.021). This is associated with a higher mortality rate in obese population infected with COVID-19. CONCLUSION: Obesity is an independent risk and prognostic factor for the disease severity and the requirement of advanced medical care in COVID-19. This systematic review highlights a particularly vulnerable group - obese, and emphasises on the importance of treatment aggression and disease prevention in this population group.


Assuntos
Infecções por Coronavirus/complicações , Infecções por Coronavirus/fisiopatologia , Obesidade/complicações , Obesidade/fisiopatologia , Pneumonia Viral/complicações , Pneumonia Viral/fisiopatologia , Betacoronavirus/patogenicidade , Infecções por Coronavirus/imunologia , Infecções por Coronavirus/mortalidade , Humanos , Obesidade/imunologia , Obesidade/mortalidade , Pandemias , Pneumonia Viral/imunologia , Pneumonia Viral/mortalidade , Prognóstico
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA