scholarly journals Importance of Lipopolysaccharide and Cyclicβ-1,2-Glucans inBrucella-Mammalian Infections

2010 ◽  
Vol 2010 ◽  
pp. 1-12 ◽  
Author(s):  
Andreas F. Haag ◽  
Kamila K. Myka ◽  
Markus F. F. Arnold ◽  
Paola Caro-Hernández ◽  
Gail P. Ferguson
Keyword(s):  
Immune System ◽  
Vaccine Development ◽  
Cell Envelope ◽  
Zoonotic Diseases ◽  
Innate Immune ◽  
Economic Losses ◽  
Biosynthesis Pathway ◽  
Host Interaction ◽  
Causative Agents

Brucellaspecies are the causative agents of one of the most prevalent zoonotic diseases: brucellosis. Infections byBrucellaspecies cause major economic losses in agriculture, leading to abortions in infected animals and resulting in a severe, although rarely lethal, debilitating disease in humans.Brucellaspecies persist as intracellular pathogens that manage to effectively evade recognition by the host's immune system. Sugar-modified components in theBrucellacell envelope play an important role in their host interaction.Brucellalipopolysaccharide (LPS), unlikeEscherichia coliLPS, does not trigger the host's innate immune system.Brucellaproduces cyclicβ-1,2-glucans, which are important for targeting them to their replicative niche in the endoplasmic reticulum within the host cell. This paper will focus on the role of LPS and cyclicβ-1,2-glucans inBrucella-mammalian infections and discuss the use of mutants, within the biosynthesis pathway of these cell envelope structures, in vaccine development.

scholarly journals Compromised Protein Prenylation as Pathogenic Mechanism in Mevalonate Kinase Deficiency

2021 ◽  
Vol 12 ◽  
Author(s):  
Frouwkje A. Politiek ◽  
Hans R. Waterham
Keyword(s):  
Immune System ◽  
Innate Immune System ◽  
Innate Immune ◽  
Mevalonate Kinase Deficiency ◽  
Mevalonate Kinase ◽  
Biosynthesis Pathway ◽  
Protein Prenylation ◽  
Pathogenic Variants ◽  
Essential Enzyme

Mevalonate kinase deficiency (MKD) is an autoinflammatory metabolic disorder characterized by life-long recurring episodes of fever and inflammation, often without clear cause. MKD is caused by bi-allelic pathogenic variants in the MVK gene, resulting in a decreased activity of the encoded enzyme mevalonate kinase (MK). MK is an essential enzyme in the isoprenoid biosynthesis pathway, which generates both non-sterol and sterol isoprenoids. The inflammatory symptoms of patients with MKD point to a major role for isoprenoids in the regulation of the innate immune system. In particular a temporary shortage of the non-sterol isoprenoid geranylgeranyl pyrophosphate (GGPP) is increasingly linked with inflammation in MKD. The shortage of GGPP compromises protein prenylation, which is thought to be one of the main causes leading to the inflammatory episodes in MKD. In this review, we discuss current views and the state of knowledge of the pathogenetic mechanisms in MKD, with particular focus on the role of compromised protein prenylation.

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 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

scholarly journals Adipocytes, Innate Immunity and Obesity: A Mini-Review

2021 ◽  
Vol 12 ◽  
Author(s):  
Alecia M. Blaszczak ◽  
Anahita Jalilvand ◽  
Willa A. Hsueh
Keyword(s):  
Adipose Tissue ◽  
Immune System ◽  
Immune Cells ◽  
Adaptive Immune System ◽  
Innate Immune ◽  
Lymphoid Cells ◽  
Innate Immune Cells ◽  
Adaptive Immune

The role of adipose tissue (AT) inflammation in obesity and its multiple related-complications is a rapidly expanding area of scientific interest. Within the last 30 years, the role of the adipocyte as an endocrine and immunologic cell has been progressively established. Like the macrophage, the adipocyte is capable of linking the innate and adaptive immune system through the secretion of adipokines and cytokines; exosome release of lipids, hormones, and microRNAs; and contact interaction with other immune cells. Key innate immune cells in AT include adipocytes, macrophages, neutrophils, and innate lymphoid cells type 2 (ILC2s). The role of the innate immune system in promoting adipose tissue inflammation in obesity will be highlighted in this review. T cells and B cells also play important roles in contributing to AT inflammation and are discussed in this series in the chapter on adaptive immunity.

scholarly journals Mitochondria surveillance systems trigger innate immune responses to bacterial pathogens via AMPK pathway in C. elegans

2020 ◽  
Author(s):  
Shouyong Ju ◽  
Hanqiao Chen ◽  
Shaoying Wang ◽  
Jian Lin ◽  
Raffi V Aroian ◽  
...  
Keyword(s):  
Immune System ◽  
Immune Responses ◽  
Innate Immune ◽  
Surveillance Systems ◽  
Innate Immune Responses ◽  
Energy Status ◽  
Microbial Infection ◽  
C Elegans ◽  
Host Interaction ◽  
Intracellular Energy

AbstractPathogen recognition and triggering pattern of host innate immune system is critical to understanding pathogen-host interaction. It is generally accepted that the microbial infection can be recognized by host via pattern-triggered immunity (PTI) or effector-triggered immunity (ETI) responses. Recently, non-PRR-mediated cellular surveillance systems have been reported as an important supplement strategy to PTI and ETI responses. However, the mechanism of how surveillance systems sense pathogens and trigger innate immune responses is largely unknown. In the present study, using Bacillus thuringiensis-Caenorhabditis elegans as a model, we found a new approach for surveillance systems to sense the pathogens through no-PPRs patterns. We reported C. elegans can monitor intracellular energy status through the mitochondrial surveillance system to triggered innate immune responses against pathogenic attack via AMP-activated protein kinase (AMPK). Consider that the mitochondria surveillance systems and AMPK are conserved components from worms to mammals, our study suggests that disrupting mitochondrial homeostasis to activate the immune system through AMPK-dependent pathways may widely existing in animals.

Role of the innate immune system in the development of chronic colitis

2002 ◽  
Vol 37 (S14) ◽  
pp. 38-42 ◽  
Author(s):  
Takanori Kanai ◽  
Ryoichi Iiyama ◽  
Takahiro Ishikura ◽  
Koji Uraushihara ◽  
Teruji Totsuka ◽  
...  
Keyword(s):  
Immune System ◽  
Innate Immune System ◽  
Innate Immune ◽  
Chronic Colitis

scholarly journals Toll-like receptor-mediated innate immunity against herpesviridae infection: a current perspective on viral infection signaling pathways

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Wenjin Zheng ◽  
Qing Xu ◽  
Yiyuan Zhang ◽  
Xiaofei E ◽  
Wei Gao ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Immune System ◽  
Signaling Pathways ◽  
Critical Role ◽  
Innate Immune ◽  
Host Cells ◽  
Main Body ◽  
Current Perspective ◽  
Viral Components

Abstract Background In the past decades, researchers have demonstrated the critical role of Toll-like receptors (TLRs) in the innate immune system. They recognize viral components and trigger immune signal cascades to subsequently promote the activation of the immune system. Main body Herpesviridae family members trigger TLRs to elicit cytokines in the process of infection to activate antiviral innate immune responses in host cells. This review aims to clarify the role of TLRs in the innate immunity defense against herpesviridae, and systematically describes the processes of TLR actions and herpesviridae recognition as well as the signal transduction pathways involved. Conclusions Future studies of the interactions between TLRs and herpesviridae infections, especially the subsequent signaling pathways, will not only contribute to the planning of effective antiviral therapies but also provide new molecular targets for the development of antiviral drugs.

Sign in / Sign up

Export Citation Format

Share Document