Nuclear factor-κB activation and innate immune response in microbial pathogen infection

2000 ◽  
Vol 60 (8) ◽  
pp. 1109-1114 ◽  
Author(s):  
Michael Naumann
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Nuclear Factor Κb ◽  
Innate Immune ◽  
Nuclear Factor ◽  
Pathogen Infection ◽  
Microbial Pathogen

scholarly journals Manipulation of the nuclear factor-κB pathway and the innate immune response by viruses

Oncogene ◽  
2006 ◽  
Vol 25 (51) ◽  
pp. 6844-6867 ◽  
Author(s):  
J Hiscott ◽  
T-L A Nguyen ◽  
M Arguello ◽  
P Nakhaei ◽  
S Paz
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Nuclear Factor Κb ◽  
Innate Immune ◽  
Nuclear Factor

Role of miRNA-146a in the regulation of the innate immune response and cancer

2008 ◽  
Vol 36 (6) ◽  
pp. 1211-1215 ◽  
Author(s):  
Andrew E. Williams ◽  
Mark M. Perry ◽  
Sterghios A. Moschos ◽  
Hanna M. Larner-Svensson ◽  
Mark A. Lindsay
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Mammalian Cells ◽  
Mrna Translation ◽  
Nuclear Factor Κb ◽  
Causal Link ◽  
Innate Immune ◽  
Major Function ◽  
Biological Responses

In mammalian cells, miRNAs (microRNAs) are the most abundant family of small non-coding RNAs that regulate mRNA translation through the RNA interference pathway. In general, it appears that the major function of miRNAs is in development, differentiation and homoeostasis, which is indicated by studies showing aberrant miRNA expression during the development of cancer. Interestingly, changes in the expression of miR-146a have been implicated in both the development of multiple cancers and in the negative regulation of inflammation induced via the innate immune response. Furthermore, miR-146a expression is driven by the transcription factor NF-κB (nuclear factor κB), which has been implicated as an important causal link between inflammation and carcinogenesis. In the present article, we review the evidence for a role of miR-146a in innate immunity and cancer and assess whether changes in miR-146a might link these two biological responses.

scholarly journals The Metabolic Phenotype Associated with Mounting an Immune Response to a Systemic Infection of Listeria Monocytogenes (FS12-07-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Robert Johnson ◽  
Adesola Olatunde ◽  
Lauren Woodie ◽  
Michael Greene ◽  
Elizabeth Schwartz
Keyword(s):  
Immune Response ◽  
Bacterial Infection ◽  
Innate Immune Response ◽  
Adaptive Immune Response ◽  
Innate Immune ◽  
Metabolic Phenotype ◽  
Metabolic Demand ◽  
Pathogen Infection ◽  
Full Spectrum ◽  
Adaptive Immune

Abstract Objectives Our goal in these studies was to quantitatively determine the metabolic phenotype of intracellular bacterial infection, immune response, and clearance. Mounting an immune response to a bacterial infection is metabolically taxing to the host. During infection, the host exhibits sickness syndrome characterized by fever, lethargy and anorexia. Cells of the immune system also shift cellular metabolic pathways, which alters the metabolic and nutritional needs of the host. Previous studies of the metabolic demands of sickness have used model antigens, mitogens or pattern associated molecular patterns, which do not represent the full spectrum of response to a live pathogen infection. Thus, our study is the first of its kind to assess the full spectrum of metabolic, nutritional, immunological, and behavioral demands of live pathogen infection. Methods Mice were administered either a mock intraperitoneal (ip) injection of PBS (Control) or ip dose of Listeria and individually housed over the course of 12 days in Promethion metabolic cages to monitor their metabolic phenotype. In a parallel study, groups of mice were equivalently treated, yet conventionally housed and sacrificed at 3, 5, 7 and 10 days over the course of infection to determine splenic bacterial burden, Listeria-specific T cell response, and cellular metabolic status. Results We observed that the period of the innate immune response (days 1–4) had the most metabolic demand, indicated by weight loss (P < 0.05), reduced activity (P < 0.05), increased sleep (P < 0.05), and decreased energy expenditure (P < 0.05). During the period of the adaptive immune response (days 5–10), there was little to no metabolic impact in the infected animals when compared to the uninfected control animals. We also observed increased GLUT1 expression (P < 0.05) on the membranes of myeloid cells during the period of highest metabolic demand, indicating shifts in cellular metabolism of innate immune cells during the early stages of infection. Conclusions The innate immune response is more metabolically taxing on the host compared to the adaptive immune response and places an increased metabolic demand on infected animals. Funding Sources Departmental startup funds to Elizabeth Hiltbold Schwartz.

scholarly journals Mycobacterial infection induces a specific human innate immune response

2015 ◽  
Author(s):  
John D Blischak ◽  
Ludovic Tailleux ◽  
Amy Mitrano ◽  
Luis B Barreiro ◽  
Yoav Gilad
Keyword(s):  
Immune Response ◽  
Immune System ◽  
Innate Immune Response ◽  
Transcriptional Response ◽  
Adaptive Immune System ◽  
Mycobacterial Infection ◽  
Innate Immune ◽  
Pathogen Infection ◽  
General Response ◽  
Candidate Loci

The innate immune system provides the first response to pathogen infection and orchestrates the activation of the adaptive immune system. Though a large component of the innate immune response is common to all infections, pathogen-specific responses have been documented as well. The innate immune response is thought to be especially critical for fighting infection with Mycobacterium tuberculosis (MTB), the causative agent of tuberculosis (TB). While TB can be deadly, only 5-10% of individuals infected with MTB develop active disease. The risk for disease susceptibility is, at least partly, heritable. Studies of inter-individual variation in the innate immune response to MTB infection may therefore shed light on the genetic basis for variation in susceptibility to TB. Yet, to date, we still do not know which properties of the innate immune response are specific to MTB infection and which represent a general response to pathogen infection. To begin addressing this gap, we infected macrophages with eight different bacteria, including different MTB strains and related mycobacteria, and studied the transcriptional response to infection. Although the ensued gene regulatory responses were largely consistent across the bacterial infection treatments, we were able to identify a novel subset of genes whose regulation was affected specifically by infection with mycobacteria. Genetic variants that are associated with regulatory differences in these genes should be considered candidate loci for explaining inter-individual susceptibility TB.

scholarly journals Oral streptococci subvert the host innate immune response through hydrogen peroxide

2022 ◽  
Vol 12 (1) ◽  
Author(s):  
Yi Ling Tang ◽  
Tiow Suan Sim ◽  
Kai Soo Tan
Keyword(s):  
Hydrogen Peroxide ◽  
Immune Response ◽  
Innate Immune Response ◽  
Mammalian Cells ◽  
Innate Immune ◽  
Related Factor ◽  
Dependent Manner ◽  
Nuclear Factor ◽  
Oral Streptococci ◽  
Periodontal Health

AbstractIn periodontal health, oral streptococci constitute up to 80% of the plaque biofilm. Yet, destructive inflammatory events of the periodontium are rare. This observation suggests that oral streptococci may possess mechanisms to co-exist with the host. However, the mechanisms employed by oral streptococci to modulate the innate immune response have not been well studied. One of the key virulence factors produced by oral streptococci is hydrogen peroxide (H2O2). In mammalian cells, H2O2 triggers the activation of nuclear factor erythroid 2-related factor 2 (Nrf2), a key pathway mediating antioxidant defence. This study aimed to determine (1) if H2O2 producing oral streptococci activated the Nrf2 pathway in macrophages, and (2) if the activation of Nrf2 influenced the innate immune response. We found that oral streptococci downregulated the innate immune response in a H2O2 dependent manner through the activation of the Nrf2. The activation of the Nrf2 signalling pathway led to the inhibition of nuclear factor kappa-light-chain-enhancer of activated B cells (NFĸB), the key transcription factor regulating pro-inflammatory response. This study showed for the first time that oral streptococci are unlikely passive bystanders but could play an active role in the maintenance of periodontal health by preventing overt inflammation.

scholarly journals Long Non-Coding RNAs and the Innate Immune Response

2019 ◽  
Vol 5 (2) ◽  
pp. 34 ◽  
Author(s):  
Hadjicharalambous ◽  
Lindsay
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Nuclear Factor Κb ◽  
Innate Immune ◽  
Rapid Induction ◽  
Transcription Process ◽  
Heterogeneous Nuclear Ribonucleoproteins ◽  
In Trans ◽  
Non Coding Rnas

Innate immunity provides the initial defence against infection and it is now clear that long non-coding RNAs (lncRNAs) are important regulators of this response. Following activation of the innate response, we commonly see rapid induction of these lncRNAs and this is often mediated via the pro-inflammatory transcription factor, nuclear factor-κB (NF-κB). Knockdown studies have shown that lncRNAs tend to act in trans to regulate the expression of multiple inflammatory mediators and other responses. Mechanistically, many lncRNAs have demonstrated acting through heterogeneous nuclear ribonucleoproteins, complexes that are implicated chromatin re-modelling, transcription process and translation. In addition, these lncRNAs have also been shown to interact with multiple other proteins involved in the regulation of chromatin re-modelling, as well as those proteins involved in intracellular immune signalling, which include NF-κB. In this review, we will describe the evidence that supports this emerging role of lncRNA in the innate immune response.

Protein kinase networks that limit TLR signalling

2014 ◽  
Vol 42 (1) ◽  
pp. 11-24 ◽  
Author(s):  
Kristopher Clark
Keyword(s):  
Immune Response ◽  
Protein Kinase ◽  
Molecular Mechanisms ◽  
Inflammatory Diseases ◽  
Nuclear Factor Κb ◽  
Innate Immune ◽  
Nuclear Factor ◽  
Chronic Inflammatory Diseases ◽  
Micro Organisms ◽  
Tlr Signalling

TLRs (Toll-like receptors) detect invading micro-organisms which triggers the production of pro-inflammatory mediators needed to combat infection. Although these signalling networks are required to protect the host against invading pathogens, dysregulation of TLR pathways contributes to the development of chronic inflammatory diseases and autoimmune disorders. Molecular mechanisms have therefore evolved to restrict the strength of TLR signalling. In the present review, I highlight recent advances in our understanding of the protein kinase networks required to suppress the innate immune response by negatively regulating TLR signalling and/or promoting the secretion of anti-inflammatory cytokines. I present my discoveries on the key roles of the IKK (inhibitor of nuclear factor κB kinase)-related kinases and the SIKs (salt-inducible kinases) in limiting innate immunity within the greater context of the field.

Oral Immune Activation by Disgust and Disease-Related Pictures

2015 ◽  
Vol 29 (3) ◽  
pp. 119-129 ◽  
Author(s):  
Richard J. Stevenson ◽  
Deborah Hodgson ◽  
Megan J. Oaten ◽  
Luba Sominsky ◽  
Mehmet Mahmut ◽  
...  
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Innate Immune Response ◽  
Negative Control ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Immune Markers ◽  
Before And After ◽  
Secondary Analyses ◽  
Image Set

Abstract. Both disgust and disease-related images appear able to induce an innate immune response but it is unclear whether these effects are independent or rely upon a common shared factor (e.g., disgust or disease-related cognitions). In this study we directly compared these two inductions using specifically generated sets of images. One set was disease-related but evoked little disgust, while the other set was disgust evoking but with less disease-relatedness. These two image sets were then compared to a third set, a negative control condition. Using a wholly within-subject design, participants viewed one image set per week, and provided saliva samples, before and after each viewing occasion, which were later analyzed for innate immune markers. We found that both the disease related and disgust images, relative to the negative control images, were not able to generate an innate immune response. However, secondary analyses revealed innate immune responses in participants with greater propensity to feel disgust following exposure to disease-related and disgusting images. These findings suggest that disgust images relatively free of disease-related themes, and disease-related images relatively free of disgust may be suboptimal cues for generating an innate immune response. Not only may this explain why disgust propensity mediates these effects, it may also imply a common pathway.

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