Differential gene expressions of NLRC5 signaling pathway in chicken macrophages cells response to Salmonella Enteritidisderived lipopplysaccharides stimulation

2016 ◽  
Author(s):  
Guobin Chang ◽  
Lingling Qiu ◽  
Xiangping Liu ◽  
Zhiteng Li ◽  
Wei Lu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Host Defense ◽  
Inflammatory Responses ◽  
Cell Types ◽  
Innate Immune ◽  
Gene Expressions ◽  
Mhc I ◽  
Chicken Macrophage ◽  
Differential Gene ◽  
Molecular Patterns

As we all known, NLRC5 recognizes intracellular pathogen-associated molecular patterns (PAMPs) and provokes innate immune system. Its role in innate immune response, NF-kB activation and MHC-I expression remains controversial. In the present study, it was detected that differential gene expressions in NLRC5 signaling pathway at 2, 4, 6 and 8 hours after exposure to LPS using qRT-PCR technology, then analyzed its roles in host defense. The results showed that, comparing to control groups, the expression of NLRC5, MHC-I and IL-18 in LPS-treated groups were significantly up-regulated at 2 hours post stimulation (hps), TLR4 and NF-kB showed conspicuously up-regulated at 4 hps, while STAT1 was significantly down-regulated at 8 hps. Collectively, LPS did evoke inflammatory responses and NLRC5 may negatively regulate NF-kB and critically regulate MHC-I to control intracellular PAMPs in chicken macrophage cell line but the specific role of NLRC5 in host defense relates to cell types and species tested.

scholarly journals Activated Platelets Induce an Anti-Inflammatory Response of Monocytes/Macrophages through Cross-Regulation of PGE2and Cytokines

2017 ◽  
Vol 2017 ◽  
pp. 1-14 ◽  
Author(s):  
Bona Linke ◽  
Yannick Schreiber ◽  
Bettina Picard-Willems ◽  
Patrick Slattery ◽  
Rolf M. Nüsing ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Cell Types ◽  
Inhibitory Effect ◽  
Innate Immune ◽  
Prostaglandin E ◽  
Murine Bone Marrow ◽  
Activated Platelets ◽  
Monocytes And Macrophages ◽  
Inflammatory Processes ◽  
Necrosis Factor

Platelets are well known for their role in hemostasis and are also increasingly recognized for their roles in the innate immune system during inflammation and their regulation of macrophage activation. Here, we aimed to study the influence of platelets on the production of inflammatory mediators by monocytes and macrophages. Analyzing cocultures of platelets and murine bone marrow-derived macrophages or human monocytes, we found that collagen-activated platelets release high amounts of prostaglandin E2(PGE2) that leads to an increased interleukin- (IL-) 10 release and a decreased tumor necrosis factor (TNF)αsecretion out of the monocytes or macrophages. Platelet PGE2mediated the upregulation of IL-10 in both cell types via the PGE2receptor EP2. Notably, PGE2-mediated IL-10 synthesis was also mediated by EP4 in murine macrophages. Inhibition of TNFαsynthesis via EP2 and EP4, but not EP1, was mediated by IL-10, since blockade of the IL-10 receptor abolished the inhibitory effect of both receptors on TNFαrelease. This platelet-mediated cross-regulation between PGE2and cytokines reveals one mechanism how monocytes and macrophages can attenuate excessive inflammatory responses induced by activated platelets in order to limit inflammatory processes.

scholarly journals microRNA-210 and microRNA-3570 Negatively Regulate NF-κB-Mediated Inflammatory Responses by Targeting RIPK2 in Teleost Fish

2021 ◽  
Vol 12 ◽  
Author(s):  
Hui Su ◽  
Renjie Chang ◽  
Weiwei Zheng ◽  
Yuena Sun ◽  
Tianjun Xu
Keyword(s):  
Immune Response ◽  
Signaling Pathway ◽  
Innate Immune Response ◽  
Inflammatory Responses ◽  
Innate Immune ◽  
Regulatory Role ◽  
Inflammatory Cytokine Production ◽  
Immune Genes ◽  
Lower Vertebrates ◽  
Antimicrobial Immunity

Pathogen infection can cause the production of inflammatory cytokines, which are key mediators that cause the host’s innate immune response. Therefore, proper regulation of immune genes associated with inflammation is essential for immune response. Among them, microRNAs (miRNAs) as gene regulator have been widely reported to be involved in the innate immune response of mammals. However, the regulatory network in which miRNAs are involved in the development of inflammation is largely unknown in lower vertebrates. Here, we identified two miRNAs from miiuy croaker (Miichthys miiuy), miR-210 and miR-3570, which play a negative regulatory role in host antibacterial immunity. We found that the expressions of miR-210 and miR-3570 were significantly upregulated under the stimulation of Gram-negative bacterium vibrio harveyi and LPS (lipopolysaccharide). Induced miR-210 and miR-3570 inhibit inflammatory cytokine production by targeting RIPK2, thereby avoiding excessive inflammation. In particular, we found that miR-210 and miR-3570 negatively regulate antimicrobial immunity by regulating the RIPK2-mediated NF-κB signaling pathway. The collective results indicated that both miRNAs are used as negative feedback regulators to regulate RIPK2-mediated NF-κB signaling pathway and thus play a regulatory role in bacteria-induced inflammatory response.

scholarly journals Inflammation and the Gut-Liver Axis in the Pathophysiology of Cholangiopathies

2018 ◽  
Vol 19 (10) ◽  
pp. 3003 ◽  
Author(s):  
Debora Giordano ◽  
Claudio Pinto ◽  
Luca Maroni ◽  
Antonio Benedetti ◽  
Marco Marzioni
Keyword(s):  
Immune Responses ◽  
Inflammatory Responses ◽  
Enterohepatic Circulation ◽  
Intestinal Barrier ◽  
Cell Types ◽  
Innate Immune ◽  
Primary Biliary Cholangitis ◽  
Innate Immune Responses ◽  
Adaptive Immune Cells ◽  
Bacterial Products

Cholangiocytes, the epithelial cells lining the bile ducts, represent the unique target of a group of progressive diseases known as cholangiopathies whose pathogenesis remain largely unknown. In normal conditions, cholangiocytes are quiescent and participate to the final bile volume and composition. Following exogenous or endogenous stimuli, cholangiocytes undergo extensive modifications of their phenotype. Reactive cholangiocytes actively proliferate and release a set of proinflammatory molecules, which act in autocrine/paracrine manner mediating the cross-talk with other liver cell types and innate and adaptive immune cells. Cholangiocytes themselves activate innate immune responses against gut-derived microorganisms or bacterial products that reach the liver via enterohepatic circulation. Gut microbiota has been implicated in the development and progression of the two most common cholangiopathies, i.e., primary sclerosing cholangitis (PSC) and primary biliary cholangitis (PBC), which have distinctive microbiota composition compared to healthy individuals. The impairment of intestinal barrier functions or gut dysbiosis expose cholangiocytes to an increasing amount of microorganisms and may exacerbate inflammatory responses thus leading to fibrotic remodeling of the organ. The present review focuses on the complex interactions between the activation of innate immune responses in reactive cholangiocytes, dysbiosis, and gut permeability to bacterial products in the pathogenesis of PSC and PBC.

scholarly journals Diverse Functions of Pulmonary Collectins in Host Defense of the Lung

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Shigeru Ariki ◽  
Chiaki Nishitani ◽  
Yoshio Kuroki
Keyword(s):  
Pattern Recognition ◽  
Growth Inhibition ◽  
Host Defense ◽  
Pulmonary Surfactant ◽  
Inflammatory Responses ◽  
Biological Activities ◽  
Innate Immune ◽  
The Other ◽  
Surfactant Proteins ◽  
Specific Proteins

Pulmonary surfactant is a mixture of lipids and proteins that covers alveolar surfaces and keeps alveoli from collapsing. Four specific proteins have been identified in surfactant. Among them, two C-type lectins, surfactant proteins A and D (SP-A and SP-D), are known to be implicated in host defense and regulation of inflammatory responses of the lung. These host defense lectins are structurally characterized by N-terminal collagen-like domains and lectin domains and are called pulmonary collectins. They prevent dissemination of infectious microbes by their biological activities including agglutination and growth inhibition. They also promote clearance of microbes by enhancing phagocytosis in macrophages. In addition, they interact with the other pattern-recognition molecules, including Toll-like receptors (TLRs) and TLR-associated molecules, CD14 and MD-2, and regulate inflammatory responses. Furthermore, recent studies have demonstrated that these collectins modulate functions of neutrophil-derived innate immune molecules by interacting with them. These findings indicate that pulmonary collectins play critical roles in host defense of the lung.

scholarly journals The Role of Toll-Like Receptors in Skin Host Defense, Psoriasis, and Atopic Dermatitis

2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Lixiang Sun ◽  
Wenjie Liu ◽  
Ling-juan Zhang
Keyword(s):  
Atopic Dermatitis ◽  
Human Body ◽  
Lupus Erythematosus ◽  
Mammalian Cells ◽  
Skin Diseases ◽  
Inflammatory Responses ◽  
Innate Immune ◽  
Host Responses ◽  
Molecular Patterns

As the key defense molecules originally identified in Drosophila, Toll-like receptor (TLR) superfamily members play a fundamental role in detecting invading pathogens or damage and initiating the innate immune system of mammalian cells. The skin, the largest organ of the human body, protects the human body by providing a critical physical and immunological active multilayered barrier against invading pathogens and environmental factors. At the first line of defense, the skin is constantly exposed to pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs), and TLRs, expressed in a cell type-specific manner by various skin cells, serve as key molecules to recognize PAMPs and DAMPs and to initiate downstream innate immune host responses. While TLR-initiated inflammatory responses are necessary for pathogen clearance and tissue repair, aberrant activation of TLRs will exaggerate T cell-mediated autoimmune activation, leading to unwanted inflammation, and the development of several skin diseases, including psoriasis, atopic dermatitis, systemic lupus erythematosus, diabetic foot ulcers, fibrotic skin diseases, and skin cancers. Together, TLRs are at the interface between innate immunity and adaptive immunity. In this review, we will describe current understanding of the role of TLRs in skin defense and in the pathogenesis of psoriasis and atopic dermatitis, and we will also discuss the development and therapeutic effect of TLR-targeted therapies.

Stimulator of Interferon Genes Signaling Pathway and its Role in Anti-tumor Immune Therapy

2020 ◽  
Vol 26 (26) ◽  
pp. 3085-3095 ◽  
Author(s):  
Yuanjin Gong ◽  
Chang Chang ◽  
Xi Liu ◽  
Yan He ◽  
Yiqi Wu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Immune Therapy ◽  
Signal Transduction Pathway ◽  
The Body ◽  
Innate Immune ◽  
Type I ◽  
Innate Immune Signaling ◽  
Critical Problems ◽  
Molecular Patterns ◽  
Damage Associated Molecular Patterns

Stimulator of interferon genes is an important innate immune signaling molecule in the body and is involved in the innate immune signal transduction pathway induced by pathogen-associated molecular patterns or damage-associated molecular patterns. Stimulator of interferon genes promotes the production of type I interferon and thus plays an important role in the innate immune response to infection. In addition, according to a recent study, the stimulator of interferon genes pathway also contributes to anti-inflammatory and anti-tumor reactions. In this paper, current researches on the Stimulator of interferon genes signaling pathway and its relationship with tumor immunity are reviewed. Meanwhile, a series of critical problems to be addressed in subsequent studies are discussed as well.

scholarly journals Toll-Like Receptors, Their Ligands, and Atherosclerosis

2011 ◽  
Vol 11 ◽  
pp. 437-453 ◽  
Author(s):  
Conrad P. Hodgkinson ◽  
Shu Ye
Keyword(s):  
Arterial Wall ◽  
Cell Types ◽  
Innate Immune ◽  
Toll Like Receptors ◽  
Increased Risk ◽  
Inflammatory Proteins ◽  
Endogenous Proteins ◽  
Molecular Patterns ◽  
Microbial Agents

Atherosclerosis is a disease characterized by inflammation in the arterial wall. Atherogenesis is dependent on the innate immune response involving activation of Toll-like receptors (TLRs) and the expression of inflammatory proteins. TLRs, which recognize various pathogen-associated molecular patterns, are expressed in various cell types within the atherosclerotic plaque. Microbial agents are associated with an increased risk of atherosclerosis and this is, in part, due to activation of TLRs. Recently considerable evidence has been provided suggesting that endogenous proteins promote atherosclerosis by binding to TLRs. In this review, we describe the role of TLRs in atherosclerosis with particular emphasis on those atherogenic endogenous proteins that have been implicated as TLR ligands.

Cytokine release from innate immune cells: association with diverse membrane trafficking pathways

Blood ◽  
2011 ◽  
Vol 118 (1) ◽  
pp. 9-18 ◽  
Author(s):  
Paige Lacy ◽  
Jennifer L. Stow
Keyword(s):  
Membrane Trafficking ◽  
Immune Cells ◽  
Inflammatory Responses ◽  
Cell Types ◽  
Innate Immune ◽  
Innate Immune Cells ◽  
Cytokine Release ◽  
Research Findings ◽  
Specific Receptors ◽  
Different Cell Types

AbstractCytokines released from innate immune cells play key roles in the regulation of the immune response. These intercellular messengers are the source of soluble regulatory signals that initiate and constrain inflammatory responses to pathogens and injury. Although numerous studies describe detailed signaling pathways induced by cytokines and their specific receptors, there is little information on the mechanisms that control the release of cytokines from different cell types. Indeed, the pathways, molecules, and mechanisms of cytokine release remain a “black box” in immunology. Here, we review research findings and new approaches that have begun to generate information on cytokine trafficking and release by innate immune cells in response to inflammatory or infectious stimuli. Surprisingly complex machinery, multiple organelles, and specialized membrane domains exist in these cells to ensure the selective, temporal, and often polarized release of cytokines in innate immunity.

scholarly journals Multi-omics approach to COVID-19: a domain-based literature review

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Chiara Montaldo ◽  
Francesco Messina ◽  
Isabella Abbate ◽  
Manuela Antonioli ◽  
Veronica Bordoni ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Integrated Approach ◽  
Cell Types ◽  
Innate Immune ◽  
Domain Model ◽  
Molecular Signature ◽  
Omics Data ◽  
Innate Immune Responses ◽  
Expert Working Group ◽  
Different Levels

Abstract Background Omics data, driven by rapid advances in laboratory techniques, have been generated very quickly during the COVID-19 pandemic. Our aim is to use omics data to highlight the involvement of specific pathways, as well as that of cell types and organs, in the pathophysiology of COVID-19, and to highlight their links with clinical phenotypes of SARS-CoV-2 infection. Methods The analysis was based on the domain model, where for domain it is intended a conceptual repository, useful to summarize multiple biological pathways involved at different levels. The relevant domains considered in the analysis were: virus, pathways and phenotypes. An interdisciplinary expert working group was defined for each domain, to carry out an independent literature scoping review. Results The analysis revealed that dysregulated pathways of innate immune responses, (i.e., complement activation, inflammatory responses, neutrophil activation and degranulation, platelet degranulation) can affect COVID-19 progression and outcomes. These results are consistent with several clinical studies. Conclusions Multi-omics approach may help to further investigate unknown aspects of the disease. However, the disease mechanisms are too complex to be explained by a single molecular signature and it is necessary to consider an integrated approach to identify hallmarks of severity.

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