scholarly journals IL-4 Inhibits IL-1β-Induced Depressive-Like Behavior and Central Neurotransmitter Alterations

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Hyun-Jung Park ◽  
Hyun-Soo Shim ◽  
Kyungeh An ◽  
Angela Starkweather ◽  
Kyung Soo Kim ◽  
...  
Keyword(s):  
Tryptophan Hydroxylase ◽  
Total Activity ◽  
Innate Immune ◽  
Behavioral Changes ◽  
Depressive Behavior ◽  
Neurotransmitter Systems ◽  
Social Exploration ◽  
Inflammatory Activation ◽  
Th Mrna

It has been known that activation of the central innate immune system or exposure to stress can disrupt balance of anti-/proinflammatory cytokines. The aim of the present study was to investigate the role of pro- and anti-inflammatory cytokines in the modulation of depressive-like behaviors, the hormonal and neurotransmitter systems in rats. We investigated whether centrally administered IL-1βis associated with activation of CNS inflammatory pathways and behavioral changes and whether treatment with IL-4 could modulate IL-1β-induced depressive-like behaviors and central neurotransmitter systems. Infusion of IL-4 significantly decreased IL-1β-induced anhedonic responses and increased social exploration and total activity. Treatment with IL-4 markedly blocked IL-1β-induced increase in PGE2and CORT levels. Also, IL-4 reduced IL-1β-induced 5-HT levels by inhibiting tryptophan hydroxylase (TPH) mRNA and activating serotonin transporter (SERT) in the hippocampus, and levels of NE were increased by activating tyrosine hydroxylase (TH) mRNA expression. These results demonstrate that IL-4 may locally contribute to the regulation of noradrenergic and serotonergic neurotransmission and may inhibit IL-1β-induced behavioral and immunological changes. The present results suggest that IL-4 modulates IL-1β-induced depressive behavior by inhibiting IL-1β-induced central glial activation and neurotransmitter alterations. IL-4 reduced central and systemic mediatory inflammatory activation, as well as reversing the IL-1β-induced alterations in neurotransmitter levels. The present findings contribute a biochemical pathway regulated by IL-4 that may have therapeutic utility for treatment of IL-1β-induced depressive behavior and neuroinflammation which warrants further study.

scholarly journals Scavenger receptor A1 participates in the phagocytosis of Leptospira interrogans and leads to subsequent high inflammatory responses and bacterial dissemination in leptospirosis

2020 ◽  
Author(s):  
Yanchun Wang ◽  
Xia Fan ◽  
Lin Du ◽  
Boyu Liu ◽  
Haihan Xiao ◽  
...  
Keyword(s):  
Immune Response ◽  
Cytokine Production ◽  
Inflammatory Responses ◽  
Scavenger Receptor ◽  
Severe Infection ◽  
Innate Immune ◽  
Bacterial Dissemination ◽  
Inflammatory Activation ◽  
Severe Jaundice

AbstractLeptospirosis, caused by pathogenic Leptospira species, has emerged as a widespread zoonotic disease worldwide. Macrophages mediate the elimination of pathogens through phagocytosis and cytokine production. Scavenger receptor A1 (SR-A1), one of the critical receptors mediating this process, plays a complicated role in innate immunity. However, the role of SR-A1 in the immune response against pathogenic Leptospira invasion is unknown. In the present study, we found that SR-A1 is an important nonopsonic phagocytic receptor on murine macrophages for Leptospira. We also found that leptospiral LPS is the ligand of SR-A1. However, intraperitoneal injection of leptospires into WT mice presented with more severe jaundice, subcutaneous hemorrhaging, and higher bacteria burdens in blood and tissues than that of SR-A1-/- mice. Exacerbated cytokine and inflammatory mediator levels were also observed in WT mice and higher recruited macrophages in the liver than those of SR-A1-/- mice. Our findings collectively reveal that although beneficial in the uptake of Leptospira by macrophage, SR-A1 might be exploited by Leptospira to promote bacterial dissemination and modulate inflammatory activation, which causes a more severe infection in the host. These results provide our new insights into the innate immune response during early infection by L. interrogans.

scholarly journals The role of innate immune pathway in repeated social defeat stress-induced behavioral changes in mice

2018 ◽  
Vol WCP2018 (0) ◽  
pp. PO3-1-20
Author(s):  
Shiho Kitaoka ◽  
Xiang Nie ◽  
Kohei Tanaka ◽  
Atsubumi Ogawa ◽  
Fumitake Nakano ◽  
...  
Keyword(s):  
Social Defeat ◽  
Innate Immune ◽  
Behavioral Changes ◽  
Social Defeat Stress ◽  
Immune Pathway ◽  
Innate Immune Pathway

scholarly journals A role of innate immune molecules in behavioral changes induced by repeated social defeat stress in mice

2019 ◽  
Vol 92 (0) ◽  
pp. 2-P-023
Author(s):  
Xiang Nie ◽  
Shiho Kitaoka ◽  
Kohei Tanaka ◽  
Atsubumi Ogawa ◽  
Fumitake Nakano ◽  
...  
Keyword(s):  
Social Defeat ◽  
Innate Immune ◽  
Behavioral Changes ◽  
Social Defeat Stress

Role of Innate Immune Sensors, TLRs, and NALP3 in Rheumatoid Arthritis and Osteoarthritis

2014 ◽  
Vol 24 (4) ◽  
pp. 243-251 ◽  
Author(s):  
Yuya Takakubo ◽  
G. Barreto ◽  
Yrjo T. Konttinen ◽  
H. Oki ◽  
Michiaki Takagi
Keyword(s):  
Rheumatoid Arthritis ◽  
Innate Immune

scholarly journals Primary and Memory Response of Human Monocytes to Vaccines: Role of Nanoparticulate Antigens in Inducing Innate Memory

Nanomaterials ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 931
Author(s):  
Mayra M. Ferrari Ferrari Barbosa ◽  
Alex Issamu Kanno ◽  
Leonardo Paiva Farias ◽  
Mariusz Madej ◽  
Gergö Sipos ◽  
...  
Keyword(s):  
Membrane Vesicles ◽  
Outer Membrane Vesicles ◽  
Innate Immune ◽  
Soluble Form ◽  
Neisseria Lactamica ◽  
Particulate Form ◽  
Future Challenges ◽  
Monocytes And Macrophages

Innate immune cells such as monocytes and macrophages are activated in response to microbial and other challenges and mount an inflammatory defensive response. Exposed cells develop the so-called innate memory, which allows them to react differently to a subsequent challenge, aiming at better protection. In this study, using human primary monocytes in vitro, we have assessed the memory-inducing capacity of two antigenic molecules of Schistosoma mansoni in soluble form compared to the same molecules coupled to outer membrane vesicles of Neisseria lactamica. The results show that particulate challenges are much more efficient than soluble molecules in inducing innate memory, which is measured as the production of inflammatory and anti-inflammatory cytokines (TNFα, IL-6, IL-10). Controls run with LPS from Klebsiella pneumoniae compared to the whole bacteria show that while LPS alone has strong memory-inducing capacity, the entire bacteria are more efficient. These data suggest that microbial antigens that are unable to induce innate immune activation can nevertheless participate in innate activation and memory when in a particulate form, which is a notion that supports the use of nanoparticulate antigens in vaccination strategies for achieving adjuvant-like effects of innate activation as well as priming for improved reactivity to future challenges.

scholarly journals The Role of Cell Metabolism in Innate Immune Memory

2020 ◽  
pp. 1-9
Author(s):  
Anaisa Valido Ferreira ◽  
Jorge Domiguéz-Andrés ◽  
Mihai Gheorghe Netea
Keyword(s):  
Metabolic Pathways ◽  
Tricarboxylic Acid Cycle ◽  
Cell Metabolism ◽  
Innate Immune ◽  
Immune Memory ◽  
Functional Changes ◽  
Trained Immunity ◽  
Health And Disease

Immunological memory is classically attributed to adaptive immune responses, but recent studies have shown that challenged innate immune cells can display long-term functional changes that increase nonspecific responsiveness to subsequent infections. This phenomenon, coined <i>trained immunity</i> or <i>innate immune memory</i>, is based on the epigenetic reprogramming and the rewiring of intracellular metabolic pathways. Here, we review the different metabolic pathways that are modulated in trained immunity. Glycolysis, oxidative phosphorylation, the tricarboxylic acid cycle, amino acid, and lipid metabolism are interplaying pathways that are crucial for the establishment of innate immune memory. Unraveling this metabolic wiring allows for a better understanding of innate immune contribution to health and disease. These insights may open avenues for the development of future therapies that aim to harness or dampen the power of the innate immune response.

scholarly journals Effects and Side Effects of Platelet Transfusion

2021 ◽  
Author(s):  
Fabrice Cognasse ◽  
Kathryn Hally ◽  
Sebastien Fauteux-Daniel ◽  
Marie-Ange Eyraud ◽  
Charles-Antoine Arthaud ◽  
...  
Keyword(s):  
Side Effects ◽  
Immune Responses ◽  
Platelet Transfusion ◽  
Biological Response ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Stress Injury ◽  
Processing And Storage ◽  
And Storage

AbstractAside from their canonical role in hemostasis, it is increasingly recognized that platelets have inflammatory functions and can regulate both adaptive and innate immune responses. The main topic this review aims to cover is the proinflammatory effects and side effects of platelet transfusion. Platelets prepared for transfusion are subject to stress injury upon collection, preparation, and storage. With these types of stress, they undergo morphologic, metabolic, and functional modulations which are likely to induce platelet activation and the release of biological response modifiers (BRMs). As a consequence, platelet concentrates (PCs) accumulate BRMs during processing and storage, and these BRMs are ultimately transfused alongside platelets. It has been shown that BRMs present in PCs can induce immune responses and posttransfusion reactions in the transfusion recipient. Several recent reports within the transfusion literature have investigated the concept of platelets as immune cells. Nevertheless, current and future investigations will face the challenge of encompassing the immunological role of platelets in the scope of transfusion.

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