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1.
Neuroimmunomodulation ; 31(1): 157-172, 2024.
Artículo en Inglés | MEDLINE | ID: mdl-39008963

RESUMEN

BACKGROUND: That neuroimmune interaction occurs in chronic pain conditions has been established for over a century, since the discovery of neurogenic inflammation in the periphery. However, the central aspects of neuroimmune interactions have not been fully appreciated until the late 1900s, when a growing interest in how cytokines in the cerebrospinal fluid (CSF) might be relevant in chronic pain conditions emerged. Since then, the field has evolved, and nowadays neuroinflammation is considered to be involved in the pathophysiology of chronic pain. Whether or not pain conditions can be called "neuroinflammatory" is a matter of debate. This review summarizes the results from studies investigating cytokines in the CSF in various pain conditions, and critically discusses neuroimmune aspects of pain conditions using previously proposed hallmarks of neuroinflammation as a framework. SUMMARY: Fifty-two papers were summarized and their results evaluated according to (a) the level of the measured cytokines in patients compared to controls, and (b) the correlation between cytokine level and pain intensity. A subdivision based on pain type was also conducted for each of the 52 studies. A total of 49 proteins have been studied in at least 5 studies, 21 of which were upregulated in a majority of studies. IL-8 was specifically upregulated in a majority of studies of nociceptive pain conditions. Regarding correlation to pain intensity, there is a scarcity of data but 31 proteins were upregulated and correlated with pain in at least one study. Of these, 24 proteins were negatively correlated with pain, and 7 were positively correlated. None of the most studied cytokines, such as TNF, IL-1b, IL-6, IL-8, CCL2/MCP1, BDNF, or bNGF, were consistently correlated to pain. KEY MESSAGES: There is sufficient evidence to say that chronic pain conditions come with an upregulation of several cytokines. However, the majority of correlations to symptomatology seem to be negative, indicating that the cytokines might play a protective role that has not been broadly considered. Calling chronic pain conditions neuroinflammatory seems wrong; instead, a more suitable term for depicting the findings would, perhaps, be to talk about neuroimmune activation.


Asunto(s)
Dolor Crónico , Citocinas , Humanos , Citocinas/líquido cefalorraquídeo , Citocinas/inmunología , Dolor Crónico/inmunología , Dolor Crónico/líquido cefalorraquídeo , Enfermedades Neuroinflamatorias/inmunología , Enfermedades Neuroinflamatorias/líquido cefalorraquídeo , Neuroinmunomodulación/fisiología , Neuroinmunomodulación/inmunología
2.
Neuroimmunomodulation ; 31(1): 143-156, 2024.
Artículo en Inglés | MEDLINE | ID: mdl-38934151

RESUMEN

BACKGROUND: Establishing causal relationships is essential in biology and medicine. However, various notions of causality have been operationalized at different times in various fields of the life and health sciences. While this is expected from a history or sociology of science point of view, as different accounts may correspond to what is valued in terms of establishing causal relationships at different times as well as in different fields of biology and medicine, this may come as a surprise for a present-day actor in those fields. If, over time, causal accounts have not been fully dismissed, then they are likely to invite some form of, potentially salutary, explanatory pluralism. SUMMARY: In the decades following WWII, psychosomatic medicine could propose that psychological factors cause somatic diseases. But today, most medicine has to meet the standard of a randomized clinical trial before any causal relationship can be proposed. Instead, in biology, mechanisms seem to be the most-valued causal discourse to explain how phenomena of interest are brought about. Here, the focus will be on how psychoneuroimmunology, an interdisciplinary research field addressing interactions between the nervous system and immune system, and between behavior and health, has considered causal relationships between psychological factors and cancer. KEY MESSAGES: When it comes to causal explanations of links between psychological factors and cancer, psychoneuroimmunology is invited to consider the question of the directionality of these links as well as what and how factors causally contribute to cancer.


Asunto(s)
Neoplasias , Neuroinmunomodulación , Psiconeuroinmunología , Medicina Psicosomática , Humanos , Neuroinmunomodulación/fisiología , Neuroinmunomodulación/inmunología , Neoplasias/inmunología , Neoplasias/psicología , Historia del Siglo XX , Causalidad
3.
Fluids Barriers CNS ; 21(1): 3, 2024 Jan 05.
Artículo en Inglés | MEDLINE | ID: mdl-38183042

RESUMEN

Many neuroscientists use the term Blood-Brain Barrier (BBB) to emphasize restrictiveness, often equating or reducing the notion of BBB properties to tight junction molecules physically sealing cerebral endothelial cells, rather than pointing out the complexity of this biological interface with respect to its selectivity and variety of exchange between the general blood circulation and the central nervous tissue. Several authors in the field find it unfortunate that the exquisitely dynamic interfaces between blood and brain continue to be viewed primarily as obstructive barriers to transport. Although the term blood-brain interface is an excellent descriptor that does not convey the idea of a barrier, it is important and preferable for the spreading of an idea beyond specialist communities to try to appeal to well-chosen metaphors. Recent evidence reviewed here indicates that blood-brain interfaces are more than selective semi-permeable membranes in that they display many dynamic processes and complex mechanisms for communication. They are thus more like 'geopolitical borders'. Furthermore, some authors working on blood-brain interface-relevant issues have started to use the word border, for example in border-associated macrophages. Therefore, we suggest adopting the term Blood-Brain Border to better communicate the flexibility of and movement across blood-brain interfaces.


Asunto(s)
Barrera Hematoencefálica , Sistema Cardiovascular , Células Endoteliales , Encéfalo , Uniones Estrechas
4.
Brain Behav Immun ; 115: 737-746, 2024 01.
Artículo en Inglés | MEDLINE | ID: mdl-37972881

RESUMEN

In medicine and science, one is typically taught the main theories in a discipline or field along with standard models before receiving more instructions on how to apply certain methods. The aim of this work is not to address one method, but rather methodology, the study and evaluation of methods, by taking a philosophy of science detour. In this, a critique of biomedicine will be used as a starting point to address some positions regarding reductionism, specifying notions such as systems and mechanisms, as well as regarding the mind-body problem discussing psychosomatic medicine and psychoneuroimmunology. Some recommendations to make science more pluralistic, robust and translationally-relevant will then be made as a way to foster constructive debates on reductionism and the mind-body problem and, in turn, favor more interdisciplinary research.


Asunto(s)
Filosofía
5.
Stud Hist Philos Sci ; 103: 123-136, 2024 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-38157672

RESUMEN

Evidence-Based Medicine has little consideration for mechanisms and philosophers of science and medicine have recently made pleas to increase the place of mechanisms in the medical evidence hierarchy. However, in this debate the notions of mechanisms seem to be limited to 'mechanistic processes' and 'complex-systems mechanisms,' understood as 'componential causal systems'. I believe that this will not do full justice to how mechanisms are used in biological, psychological and social sciences and, consequently, in a more biopsychosocial approach to medicine. Here, I propose, following (Kuorikoski, 2009), to pay more attention to 'abstract forms of interaction' mechanisms. The present work scrutinized review articles on depression and medically unexplained pain, which are considered to be of multifactorial pathogenesis, for their use of mechanisms. In review articles on these disorders there seemed to be a range of uses between more 'abstract forms of interaction' and 'componential causal system' mechanisms. I therefore propose to expand the notions of mechanisms considered in medicine to include that of more 'abstract forms of interaction' to better explain and manage biopsychosocial disorders.


Asunto(s)
Depresión , Medicina , Humanos , Depresión/diagnóstico , Dolor/diagnóstico , Ciencias Sociales
6.
Neurobiol Dis ; 185: 106231, 2023 09.
Artículo en Inglés | MEDLINE | ID: mdl-37468048

RESUMEN

Astrocytes are in contact with the vasculature, neurons, oligodendrocytes and microglia, forming a local network with various functions critical for brain homeostasis. One of the primary responders to brain injury are astrocytes as they detect neuronal and vascular damage, change their phenotype with morphological, proteomic and transcriptomic transformations for an adaptive response. The role of astrocytic responses in brain dysfunction is not fully elucidated in adult, and even less described in the developing brain. Children are vulnerable to traumatic brain injury (TBI), which represents a leading cause of death and disability in the pediatric population. Pediatric brain trauma, even with mild severity, can lead to long-term health complications, such as cognitive impairments, emotional disorders and social dysfunction later in life. To date, the underlying pathophysiology is still not fully understood. In this review, we focus on the astrocytic response in pediatric TBI and propose a potential immune role of the astrocyte in response to trauma. We discuss the contribution of astrocytes in the local inflammatory cascades and secretion of various immunomodulatory factors involved in the recruitment of local microglial cells and peripheral immune cells through cerebral blood vessels. Taken together, we propose that early changes in the astrocytic phenotype can alter normal development of the brain, with long-term consequences on neurological outcomes, as described in preclinical models and patients.


Asunto(s)
Lesiones Traumáticas del Encéfalo , Lesiones Encefálicas , Niño , Humanos , Astrocitos , Proteómica , Lesiones Traumáticas del Encéfalo/complicaciones , Encéfalo , Lesiones Encefálicas/complicaciones , Microglía
7.
Brain Behav Immun ; 113: 176-188, 2023 10.
Artículo en Inglés | MEDLINE | ID: mdl-37468114

RESUMEN

Children that survive leukemia are at an increased risk for cognitive difficulties. A better understanding of the neurobiological changes in response to early life chemotherapy will help develop therapeutic strategies to improve quality of life for leukemia survivors. To that end, we used a translationally-relevant mouse model consisting of leukemic cell line (L1210) injection into postnatal day (P)19 mice followed by methotrexate, vincristine, and leucovorin chemotherapy. Beginning one week after the end of chemotherapy, social behavior, recognition memory and executive function (using the 5 choice serial reaction time task (5CSRTT)) were tested in male and female mice. Prefrontal cortex (PFC) and hippocampus (HPC) were collected at the conclusion of behavioral assays for gene expression analysis. Mice exposed to early life cancer + chemotherapy were slower to progress through increasingly difficult stages of the 5CSRTT and showed an increase in premature errors, indicating impulsive action. A cluster of microglial-related genes in the PFC were found to be associated with performance in the 5CSRTT and acquisition of the operant response, and long-term changes in gene expression were evident in both PFC and HPC. This work identifies gene expression changes in PFC and HPC that may underlie cognitive deficits in survivors of early life exposure to cancer + chemotherapy.


Asunto(s)
Leucemia , Neoplasias , Ratones , Masculino , Femenino , Animales , Microglía , Calidad de Vida , Corteza Prefrontal/metabolismo , Cognición/fisiología , Neoplasias/metabolismo , Leucemia/metabolismo , Expresión Génica
8.
Front Neurosci ; 17: 1172783, 2023.
Artículo en Inglés | MEDLINE | ID: mdl-38260022

RESUMEN

Scientific and philosophical accounts of cognition and perception have traditionally focused on the brain and external sense organs. The extended view of embodied cognition suggests including other parts of the body in these processes. However, one organ has often been overlooked: the gut. Frequently conceptualized as merely a tube for digesting food, there is much more to the gut than meets the eye. Having its own enteric nervous system, sometimes referred to as the "second brain," the gut is also an immune organ and has a large surface area interacting with gut microbiota. The gut has been shown to play an important role in many physiological processes, and may arguably do so as well in perception and cognition. We argue that proposals of embodied perception and cognition should take into account the role of the "gut complex," which considers the enteric nervous, endocrine, immune, and microbiota systems as well as gut tissue and mucosal structures. The gut complex is an interface between bodily tissues and the "internalized external environment" of the gut lumen, involved in many aspects of organismic activity beyond food intake. We thus extend current embodiment theories and suggest a more inclusive account of how to "mind the gut" in studying cognitive processes.

9.
Pharmaceuticals (Basel) ; 15(2)2022 Jan 25.
Artículo en Inglés | MEDLINE | ID: mdl-35215252

RESUMEN

In spite of the brain-protecting tissues of the skull, meninges, and blood-brain barrier, some forms of injury to or infection of the CNS can give rise to cerebral cytokine production and action and result in drastic changes in brain function and behavior. Interestingly, peripheral infection-induced systemic inflammation can also be accompanied by increased cerebral cytokine production. Furthermore, it has been recently proposed that some forms of psychological stress may have similar CNS effects. Different conditions of cerebral cytokine production and action will be reviewed here against the background of neuroinflammation. Within this context, it is important to both deepen our understanding along already taken paths as well as to explore new ways in which neural functioning can be modified by cytokines. This, in turn, should enable us to put forward different modes of cerebral cytokine production and action in relation to distinct forms of neuroinflammation.

10.
Brain Behav Immun ; 99: 192-202, 2022 01.
Artículo en Inglés | MEDLINE | ID: mdl-34655730

RESUMEN

Survivors of acute lymphoblastic leukemia (ALL), the most common childhood cancer, are at increased risk for long-term cognitive problems, including executive function deficits. The chemotherapeutic agent methotrexate (MTX) is used to treat most ALL patients and is closely associated with cognitive deficits. To address how early life cancer chemotherapy leads to cognitive deficits, we developed a translationally relevant mouse model of leukemia survival that exposed mice to leukemic cells and chemotherapeutic drugs (vincristine and MTX, with leucovorin rescue) in early life. Male and female mice were tested several weeks later using novel object recognition (recognition memory) and 5-choice serial reaction time task (executive function). Gene expression of proinflammatory, white matter and synapse-associated molecules was assessed in the prefrontal cortex and small intestine both acutely after chemotherapy and chronically after cognitive testing. Early life cancer-chemotherapy exposure resulted in recognition memory and executive function deficits in adult male mice. Prefrontal cortex expression of the chemokine Ccl2 was increased acutely, while small intestine expression of the proinflammatory cytokine tumor necrosis factor-alpha was elevated both acutely (both sexes) and chronically (males only). Inflammation in the small intestine was correlated with prefrontal cortical proinflammatory and synaptic gene expression changes, as well as to executive function deficits. Collectively, these data indicate that the current protocol results in a robust mouse model in which to study cognitive deficits in leukemia survivors, and suggest that small intestine inflammation may represent a novel contributor to adverse CNS consequences of early life chemotherapy.


Asunto(s)
Citocinas , Leucemia-Linfoma Linfoblástico de Células Precursoras , Animales , Encéfalo/patología , Niño , Cognición , Femenino , Humanos , Intestino Delgado , Masculino , Ratones , Leucemia-Linfoma Linfoblástico de Células Precursoras/complicaciones , Leucemia-Linfoma Linfoblástico de Células Precursoras/tratamiento farmacológico , Leucemia-Linfoma Linfoblástico de Células Precursoras/patología
11.
Pharmaceuticals (Basel) ; 14(10)2021 Oct 11.
Artículo en Inglés | MEDLINE | ID: mdl-34681254

RESUMEN

Sickness behavior, characterized by on overall reduction in behavioral activity, is commonly observed after bacterial infection. Sickness behavior can also be induced by the peripheral administration of Gram-negative bacterial lipopolysaccharide (LPS) or interleukin-1beta (IL-1ß), a pro-inflammatory cytokine released by LPS-activated macrophages. In addition to the microglia, the brain contains perivascular macrophages, which express the IL-1 type 1 receptor (IL-1R1). In the present study, we assessed the role of brain perivascular macrophages in mediating IL-1ß-induced sickness behavior in rats. To do so, we used intracerebroventricular (icv) administration of an IL-1ß-saporin conjugate, known to eliminate IL-R1-expressing brain cells, prior to systemic or central IL-1ß injection. Icv IL-1ß-saporin administration resulted in a reduction in brain perivascular macrophages, without altering subsequent icv or ip IL-1ß-induced reductions in food intake, locomotor activity, and social interactions. In conclusion, the present work shows that icv IL-1ß-saporin administration is an efficient way to target brain perivascular macrophages, and to determine whether these cells are involved in IL-1ß-induced sickness behavior.

12.
Animal Model Exp Med ; 4(3): 249-260, 2021 09.
Artículo en Inglés | MEDLINE | ID: mdl-34557651

RESUMEN

Background: Magnetic resonance imaging (MRI) of rodents combined with histology allows to determine what mechanisms underlie functional and structural brain changes during sepsis-associated encephalopathy. However, the effects of MRI performed in isoflurane-anesthetized rodents on modifications of the blood-brain barrier and the production of vasoactive prostaglandins and glia cells, which have been proposed to mediate sepsis-associated brain dysfunction, are unknown. Methods: This study addressed the effect of MRI under isoflurane anesthesia on blood-brain barrier integrity, cyclooxygenase-2 expression, and glial cell activation during cecal ligature and puncture-induced sepsis-associated brain dysfunction in rats. Results: Cecal ligature and puncture reduced food intake and the righting reflex. MRI under isoflurane anesthesia reduced blood-brain barrier breakdown, decreased circularity of white matter astrocytes, and increased neuronal cyclooxygenase-2 immunoreactivity in the cortex 24 hours after laparotomy. In addition, it annihilated cecal ligature and puncture-induced increased circularity of white matter microglia. MRI under isoflurane anesthesia, however, did not alter sepsis-associated perivascular cyclooxygenase-2 induction. Conclusion: These findings indicate that MRI under isoflurane anesthesia of rodents can modify neurovascular and glial responses and should, therefore, be interpreted with caution.


Asunto(s)
Anestesia , Isoflurano , Sepsis , Animales , Ciclooxigenasa 2 , Isoflurano/farmacología , Imagen por Resonancia Magnética/métodos , Neuroglía , Ratas , Sepsis/complicaciones
13.
Front Psychiatry ; 12: 630331, 2021.
Artículo en Inglés | MEDLINE | ID: mdl-33716828

RESUMEN

Animals, including human beings, modify their behavior when they fall sick. Interestingly, sociology, biology, and psychology have at different times in their history developed constructs of illness or sickness behavior. The aims of the present paper are to consider sickness behavior in animals and humans and to evaluate to what extent the notions of sickness behavior would allow for interdisciplinary research. After distinguishing disease, illness, and sickness, the case will be made that illness behavior and sickness behavior can be considered heuristically as synonyms given the existence of some fluidity between the notion of illness and sickness. Based on this, different faces, phases, and facets of sickness behavior will be presented before addressing the question of how integration of constructs of sickness behaviors would be possible across biology, medicine, psychology, and sociology. It is concluded that interdisciplinary research on sickness behavior between biology, psychology, and sociology is possible and called for with regard to constructs, methods, and explanations, while keeping in mind differences in perspectives, for example between acute and chronic sickness behavior.

14.
Neurosci Biobehav Rev ; 115: 15-24, 2020 08.
Artículo en Inglés | MEDLINE | ID: mdl-32433924

RESUMEN

Increasing evidence from animal and human studies suggests that inflammation may be involved in mood disorders. Sickness behavior and emotional changes induced by experimental inflammatory stimuli have been extensively studied in humans and rodents to better understand the mechanisms underlying inflammation-driven mood alterations. However, research in animals and humans have remained compartmentalized and a comprehensive comparison of inflammation-induced sickness and depressive-like behavior between rodents and humans is lacking. Thus, here, we highlight similarities and differences in the effects of bacterial lipopolysaccharide administration on the physiological (fever and cytokines), behavioral and emotional components of the sickness response in rodents and humans, and discuss the translational challenges involved. We also emphasize the differences between observable sickness behavior and subjective sickness reports, and advocate for the need to obtain both subjective reports and objective measurements of sickness behavior in humans. We aim to provide complementary insights for translational clinical and experimental research on inflammation-induced behavioral and emotional changes, and their relevance for mood disorders such as depression.


Asunto(s)
Conducta de Enfermedad , Lipopolisacáridos , Animales , Ansiedad/inducido químicamente , Conducta Animal , Citocinas , Depresión/inducido químicamente , Humanos , Inflamación/inducido químicamente , Roedores
16.
Brain Behav Immun ; 83: 200-213, 2020 01.
Artículo en Inglés | MEDLINE | ID: mdl-31622656

RESUMEN

Sepsis-associated encephalopathy (SAE) refers to brain dysfunction, including delirium, occurs during severe infection and is associated with development of post-traumatic stress disorder. SAE has been proposed to be related to reduced cerebral blood flow (CBF), blood-brain barrier breakdown (BBB), white matter edema and disruption and glia cell activation, but their exact relationships remain to be determined. In the present work, we set out to study CBF using Arterial Spin Labeling (ASL) and grey and white matter structure with T2- and diffusion magnetic resonance imaging (dMRI) in rats with cecal ligation and puncture (CLP)-induced encephalopathy. Using immunohistochemistry, the distribution of the vasoactive prostaglandin-synthesizing enzyme cyclooxygenase-2 (COX-2), perivascular immunoglobulins G (IgG), aquaporin-4 (AQP4) and the morphology of glial cell were subsequently assessed in brains of the same animals. CLP induced deficits in the righting reflex and resulted in higher T2-weighted contrast intensities in the cortex, striatum and at the base of the brain, decreased blood perfusion distribution to the cortex and increased water diffusion parallel to the fibers of the corpus callosum compared to sham surgery. In addition, CLP reduced staining for microglia- and astrocytic-specific proteins in the corpus callosum, decreased neuronal COX-2 and AQP4 expression in the cortex while inducing perivascular COX-2 expression, but did not induce widespread perivascular IgG diffusion. In conclusion, our findings indicate that experimental SAE can occur in the absence of BBB breakdown and is accompanied by increased water diffusion anisotropy and altered glia cell morphology in brain white matter.


Asunto(s)
Barrera Hematoencefálica , Ciclooxigenasa 2/biosíntesis , Neuroglía/patología , Perfusión , Encefalopatía Asociada a la Sepsis , Agua/metabolismo , Animales , Acuaporina 4 , Ciclooxigenasa 2/genética , Difusión , Inmunoglobulina G , Masculino , Ratas , Ratas Wistar , Encefalopatía Asociada a la Sepsis/sangre , Encefalopatía Asociada a la Sepsis/enzimología , Encefalopatía Asociada a la Sepsis/metabolismo , Encefalopatía Asociada a la Sepsis/patología
17.
Brain Behav Immun ; 81: 560-573, 2019 10.
Artículo en Inglés | MEDLINE | ID: mdl-31310797

RESUMEN

A reduction in food intake is commonly observed after bacterial infection, a phenomenon that can be reproduced by peripheral administration of Gram-negative bacterial lipopolysaccharide (LPS) or interleukin-1beta (IL-1ß), a pro-inflammatory cytokine released by LPS-activated macrophages. The arcuate nucleus of the hypothalamus (ARH) plays a major role in food intake regulation and expresses IL-1 type 1 receptor (IL-1R1) mRNA. In the present work, we tested the hypothesis that IL-1R1 expressing cells in the ARH mediate IL-1ß and/or LPS-induced hypophagia in the rat. To do so, we developed an IL-1ß-saporin conjugate, which eliminated IL-R1-expressing neurons in the hippocampus, and micro-injected it into the ARH prior to systemic IL-1ß and LPS administration. ARH IL-1ß-saporin injection resulted in loss of neuropeptide Y-containing cells and attenuated hypophagia and weight loss after intraperitoneal IL-1ß, but not LPS, administration. In conclusion, the present study shows that ARH NPY-containing neurons express functional IL-1R1s that mediate peripheral IL-1ß-, but not LPS-, induced hypophagia. Our present and previous findings indicate that the reduction of food intake after IL-1ß and LPS are mediated by different neural pathways.


Asunto(s)
Peso Corporal/efectos de los fármacos , Ingestión de Alimentos/efectos de los fármacos , Interleucina-1beta/farmacología , Saporinas/farmacología , Animales , Núcleo Arqueado del Hipotálamo/efectos de los fármacos , Núcleo Arqueado del Hipotálamo/metabolismo , Citocinas/metabolismo , Hipotálamo/efectos de los fármacos , Hipotálamo/metabolismo , Proteína Antagonista del Receptor de Interleucina 1/metabolismo , Interleucina-1/metabolismo , Interleucina-1beta/química , Lipopolisacáridos/farmacología , Masculino , Vías Nerviosas/metabolismo , Neuronas/metabolismo , Neuropéptido Y/metabolismo , Ratas , Ratas Sprague-Dawley , Proteínas Recombinantes/farmacología
18.
Pharmaceuticals (Basel) ; 12(1)2019 Feb 14.
Artículo en Inglés | MEDLINE | ID: mdl-30769887

RESUMEN

The possibility that inflammation plays a causal role in major depression is an important claim in the emerging field of immunopsychiatry and has generated hope for new treatments. The aims of the present review are first to provide some historical background and to consider the evidence in favor of the claim that inflammation is causally involved in major depression. The second part discusses some of the possibilities allowed for by the use of broad 'umbrella' concepts, such as inflammation and stress, in terms of proposing new working hypotheses and potential mechanisms. The third part reviews proposed biomarkers of inflammation and depression and the final part addresses how elements discussed in the preceding sections are used in immunopsychiatry. The 'umbrella' concepts of inflammation and stress, as well as insufficiently-met criteria based inferences and reverse inferences are being used to some extent in immunopsychiatry. The field is therefore encouraged to specify concepts and constructs, as well as to consider potential alternative interpretations and explanations for findings obtained. The hope is that pointing out some of the potential problems will allow for a clearer picture of immunopsychiatry's current strengths and limitations and help the field mature.

19.
Behav Brain Sci ; 42: e60, 2018 Sep 12.
Artículo en Inglés | MEDLINE | ID: mdl-30207256

RESUMEN

Microbiota-gut-brain (MGB) research is a fast-growing field of inquiry with important implications for how human brain function and behaviour are understood. Researchers manipulate gut microbes ("microbiota") to reveal connections between intestinal microbiota and normal brain functions (e.g., cognition, emotion, and memory) or pathological states (e.g., anxiety, mood disorders, and neural developmental disorders such as autism). Many claims are made about causal relationships between gut microbiota and human behaviour. By uncovering these relationships, MGB research aims to offer new explanations of mental health and potential avenues of treatment.So far, limited evaluation has been made of MGB's methods and its core experimental findings, many of which are extensively reiterated in copious reviews of the field. These factors, plus the self-help potential of MGB, have combined to encourage uncritical public uptake of MGB discoveries. Both social and professional media focus on the potential for dietary intervention in mental health, and causal relationships are assumed to be established.Our target article has two main aims. One is to examine critically the core practices and findings of experimental MGB research and to raise questions about them for brain and behavioural scientists who may not be familiar with the field. The other is to challenge the way in which MGB findings are presented. Our positive goal is to suggest how current problems and weaknesses may be addressed, in order for both scientific and public audiences to gain a clearer picture of MGB research and its strengths and limitations.

20.
Clin Auton Res ; 28(3): 289-299, 2018 06.
Artículo en Inglés | MEDLINE | ID: mdl-29541878

RESUMEN

Although the immune and nervous systems have long been considered independent biological systems, they turn out to mingle and interact extensively. The present review summarizes recent insights into the neural pathways activated by and involved in infection-induced inflammation and discusses potential clinical applications. The simplest activation concerns a reflex action within C-fibers leading to neurogenic inflammation. Low concentrations of pro-inflammatory cytokines or bacterial fragments may also act on these afferent nerve fibers to signal the central nervous system and bring about early fever, hyperalgesia and sickness behavior. In the brain, the preoptic area and the paraventricular hypothalamus are part of a neuronal network mediating sympathetic activation underlying fever while brainstem circuits play a role in the reduction of food intake after systemic exposure to bacterial fragments. A vagally-mediated anti-inflammatory reflex mechanism has been proposed and, in turn, questioned because the major immune organs driving inflammation, such as the spleen, are not innervated by vagal efferent fibers. On the contrary, sympathetic nerves do innervate these organs and modulate immune cell responses, production of inflammatory mediators and bacterial dissemination. Noradrenaline, which is both released by these fibers and often administered during sepsis, along with adrenaline, may exert pro-inflammatory actions through the stimulation of ß1 adrenergic receptors, as antagonists of this receptor have been shown to exert anti-inflammatory effects in experimental sepsis.


Asunto(s)
Enfermedades del Sistema Nervioso Autónomo/fisiopatología , Infecciones/complicaciones , Inflamación/fisiopatología , Enfermedades del Sistema Nervioso/complicaciones , Vías Nerviosas/fisiopatología , Animales , Enfermedades del Sistema Nervioso Autónomo/etiología , Catecolaminas/metabolismo , Infecciones del Sistema Nervioso Central/complicaciones , Humanos , Inflamación/etiología
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