scholarly journals Gut–neuroimmune interactions: the unexpected role of the immune system in brain development

2019 ◽  
Vol 41 (1) ◽  
pp. 36-41 ◽  
Author(s):  
Simon Spichak ◽  
Timothy G. Dinan ◽  
John F. Cryan
Keyword(s):  
Immune System ◽  
Brain Development ◽  
Neuronal Development ◽  
Inflammatory Responses ◽  
Later Life ◽  
Innate Immune ◽  
Brain Health ◽  
Cytokines And Chemokines ◽  
The Brain

How does the immune system impact brain development? The exciting and somewhat unexpected relationship between the immune system and the brain has become one of the most fascinating topics in neuroscience. Even though the immune system was initially implicated in resolving viral and bacterial threats, it is now becoming more evident that it also plays a role in processes in the brain, both under healthy and pathological conditions. This novel role of the immune system in brain health has been implicated in various psychopathologies where neurodevelopment, stress and mood are central. In particular, its role in healthy brain development is becoming more evident, and understanding neuroimmune communication is becoming crucial in treating neurodevelopmental and mood disorders in later life. In the brain, glia function as part of the innate immune system and are programmed to respond to pathogens and physical injury. They also play an important role in neuronal development and pruning. These cells communicate with and respond to chemical signals, such as cytokines and chemokines, which can then initiate or downregulate inflammatory responses. Finally, the trillions of microbes residing in the gut can also stimulate cytokine and chemokine responses in the periphery and play an important role in both immunity and brain development.

Immune and Inflammatory Responses to Stroke: Good Or Bad?

2008 ◽  
Vol 3 (4) ◽  
pp. 254-265 ◽  
Author(s):  
P. A. McCombe ◽  
S. J. Read
Keyword(s):  
Immune Response ◽  
Immune System ◽  
Immune Responses ◽  
Inflammatory Responses ◽  
Tissue Injury ◽  
Therapeutic Option ◽  
Regulatory Lymphocytes ◽  
The Brain ◽  
Pro Inflammatory Cytokines

Inflammatory and immune responses play important roles following ischaemic stroke. Inflammatory responses contribute to damage and also contribute to repair. Injury to tissue triggers an immune response. This is initiated through activation of the innate immune system. In stroke there is microglial activation. This is followed by an influx of lymphocytes and macrophages into the brain, triggered by production of pro-inflammatory cytokines. This inflammatory response contributes to further tissue injury. There is also a systemic immune response to stroke, and there is a degree of immunosuppression that may contribute to the stroke patient's risk of infection. This immunosuppressive response may also be protective, with regulatory lymphocytes producing cytokines and growth factors that are neuroprotective. The specific targets of the immune response after stroke are not known, and the details of the immune and inflammatory responses are only partly understood. The role of inflammation and immune responses after stroke is twofold. The immune system may contribute to damage after stroke, but may also contribute to repair processes. The possibility that some of the immune response after stroke may be neuroprotective is exciting and suggests that deliberate enhancement of these responses may be a therapeutic option.

scholarly journals The Many Faces of Innate Immunity in SARS-CoV-2 Infection

Vaccines ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 596
Author(s):  
Nicholas Hanan ◽  
Ronnie L. Doud ◽  
In-Woo Park ◽  
Harlan P. Jones ◽  
Stephen O. Mathew
Keyword(s):  
Immune System ◽  
Innate Immune System ◽  
Inflammatory Responses ◽  
Innate Immune ◽  
System A ◽  
Genetic Risks ◽  
Poor Outcomes ◽  
The Many ◽  
Lung Tissue Damage

The innate immune system is important for initial antiviral response. SARS-CoV-2 can result in overactivity or suppression of the innate immune system. A dysregulated immune response is associated with poor outcomes; with patients having significant Neutrophil-to-Lymphocyte ratios (NLR) due to neutrophilia alongside lymphopenia. Elevated interleukin (IL)-6 and IL-8 leads to overactivity and is a prominent feature of severe COVID-19 patients. IL-6 can result in lymphopenia; where COVID-19 patients typically have significantly altered lymphocyte subsets. IL-8 attracts neutrophils; which may play a significant role in lung tissue damage with the formation of neutrophil extracellular traps leading to cytokine storm or acute respiratory distress syndrome. Several factors like pre-existing co-morbidities, genetic risks, viral pathogenicity, and therapeutic efficacy act as important modifiers of SARS-CoV-2 risks for disease through an interplay with innate host inflammatory responses. In this review, we discuss the role of the innate immune system at play with other important modifiers in SARS-CoV-2 infection.

scholarly journals NLRP3 Inflammasome in the Pathophysiology of Hemorrhagic Stroke: A Review

2019 ◽  
Vol 17 (7) ◽  
pp. 582-589 ◽  
Author(s):  
Yujie Luo ◽  
Cesar Reis ◽  
Sheng Chen
Keyword(s):  
Immune System ◽  
Brain Injury ◽  
Nlrp3 Inflammasome ◽  
Innate Immune System ◽  
Hemorrhagic Stroke ◽  
Innate Immune ◽  
High Morbidity ◽  
Pyrin Domain ◽  
Cytokines And Chemokines

Hemorrhagic stroke is a devastating disease with high morbidity and mortality. There is still a lack of effective therapeutic approach. The recent studies have shown that the innate immune system plays a significant role in hemorrhagic stroke. Microglia, as major components in innate immune system, are activated and then can release cytokines and chemokines in response to hemorrhagic stroke, and ultimately led to neuroinflammation and brain injury. The NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome is predominantly released by microglia and is believed as the main contributor of neuroinflammation. Several studies have focused on the role of NLRP3 inflammasome in hemorrhagic stroke-induced brain injury, however, the specific mechanism of NLRP3 activation and regulation remains unclear. This review summarized the mechanism of NLRP3 activation and its role in hemorrhagic stroke and discussed the translational significance.

Role of Innate Immune System in Environmental Lung Diseases

2021 ◽  
Vol 21 (5) ◽  
Author(s):  
Marissa A. Guttenberg ◽  
Aaron T. Vose ◽  
Robert M. Tighe
Keyword(s):  
Immune System ◽  
Innate Immune System ◽  
Lung Diseases ◽  
Innate Immune

scholarly journals Terminal uridyltransferase 7 regulates TLR4-triggered inflammation by controlling Regnase-1 mRNA uridylation and degradation

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Chia-Ching Lin ◽  
Yi-Ru Shen ◽  
Chi-Chih Chang ◽  
Xiang-Yi Guo ◽  
Yun-Yun Young ◽  
...  
Keyword(s):  
Posttranscriptional Regulation ◽  
Inflammatory Responses ◽  
Rna Stability ◽  
Innate Immune ◽  
Stem Loop ◽  
Stem Loop Structure ◽  
Tlr4 Activation ◽  
Harmful Effects ◽  
Different Levels

AbstractDifferent levels of regulatory mechanisms, including posttranscriptional regulation, are needed to elaborately regulate inflammatory responses to prevent harmful effects. Terminal uridyltransferase 7 (TUT7) controls RNA stability by adding uridines to its 3′ ends, but its function in innate immune response remains obscure. Here we reveal that TLR4 activation induces TUT7, which in turn selectively regulates the production of a subset of cytokines, including Interleukin 6 (IL-6). TUT7 regulates IL-6 expression by controlling ribonuclease Regnase-1 mRNA (encoded by Zc3h12a gene) stability. Mechanistically, TLR4 activation causes TUT7 to bind directly to the stem-loop structure on Zc3h12a 3′-UTR, thereby promotes Zc3h12a uridylation and degradation. Zc3h12a from LPS-treated TUT7-sufficient macrophages possesses increased oligo-uridylated ends with shorter poly(A) tails, whereas oligo-uridylated Zc3h12a is significantly reduced in Tut7-/- cells after TLR4 activation. Together, our findings reveal the functional role of TUT7 in sculpting TLR4-driven responses by modulating mRNA stability of a selected set of inflammatory mediators.

scholarly journals Role of the Innate Immune System in Acute Viral Myocarditis

2009 ◽  
Vol 104 (3) ◽  
pp. 228-237 ◽  
Author(s):  
Chien-Hua Huang ◽  
Jesus G. Vallejo ◽  
George Kollias ◽  
Douglas L. Mann
Keyword(s):  
Immune System ◽  
Innate Immune System ◽  
Viral Myocarditis ◽  
Innate Immune ◽  
Acute Viral Myocarditis

Neuroinflammatory Signaling in the Pathogenesis of Alzheimer’s Disease

2021 ◽  
Vol 19 ◽  
Author(s):  
Md. Sahab Uddin ◽  
Md. Tanvir Kabir ◽  
Maroua Jalouli ◽  
Md. Ataur Rahman ◽  
Philippe Jeandet ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Innate Immune ◽  
Misfolded Proteins ◽  
Inflammatory Signaling ◽  
Genome Wide Analysis ◽  
Genome Wide ◽  
Immunological Mechanisms ◽  
The Brain

: Alzheimer’s disease (AD) is a chronic neurodegenerative disease characterized by the formation of intracellular neurofibrillary tangles (NFTs) and extracellular amyloid plaques. Growing evidence has suggested that AD pathogenesis is not only limited to the neuronal compartment but also strongly interacts with immunological processes in the brain. On the other hand, aggregated and misfolded proteins can bind with pattern recognition receptors located on astroglia and microglia and can in turn induce an innate immune response, characterized by the release of inflammatory mediators, ultimately playing a role in both the severity and the progression of the disease. It has been reported by genome-wide analysis that several genes which elevate the risk for sporadic AD encode for factors controlling the inflammatory response and glial clearance of misfolded proteins. Obesity and systemic inflammation are examples of external factors which may interfere with the immunological mechanisms of the brain and can induce disease progression. In this review, we discussed the mechanisms and essential role of inflammatory signaling pathways in AD pathogenesis. Indeed, interfering with immune processes and modulation of risk factors may lead to future therapeutic or preventive AD approaches.

scholarly journals Distribution of leukocyte subpopulation among students threatened by failure

2020 ◽  
Vol 11 (3) ◽  
pp. 3807-3812
Author(s):  
Aziez Chettoum ◽  
Kamilia Guedri ◽  
Zouhir Djerrou ◽  
Rachid Mosbah ◽  
Latifa Khattabi ◽  
...  
Keyword(s):  
Immune System ◽  
White Blood Cells ◽  
Significant Development ◽  
Biological Assays ◽  
Cell Counts ◽  
Student Volunteers ◽  
White Blood Cell Counts ◽  
Academic Year ◽  
The Brain

Psychoneuroimmunology or the study of the relationships between the brain and the immune system is an area of research that has experienced significant development over the decade. Stress does not appear without consequences on the state of health, the role of fears, emotions and significant constraints in the appearance of organic and mental diseases. In this research, we studied the effect of stress and anxiety during exams at the end of the academic year (2018/2019) on the distribution of leukocyte subpopulations and the immune system, questionnaires has been completed by student volunteers, to estimate the anxio-depressive comorbidities through the (HADS) test during and outside exams, and in the same time we asked them for a blood sample the next morning day to carry out some biological assays (CBC). We also found that stress during exams caused a change in the distribution of different types of white blood cells, a total decrease in white blood cell counts with neutropenia and lymphopenia were found in students during exams compared to controls, and an increase in monocyte and other types of polymorphonuclear levels in students during exams compared to controls. Other tests measuring the effects of stress on specific functions of the immune system can be used.

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