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Cellular and Immunobiology
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
Masood Moghul, Sarah McClelland, Prabhakar Rajan
Initiation of innate immunity begins with pattern recognition receptors:C-type lectin receptors: activated by sugars on yeast, bacterial, and fungal cell walls.Toll-like receptors: results in the activation of NFκβ, causing transcription of immune genes.NOD-like receptors: involved in intracellular pattern recognition (when the pathogen infiltrates host cells).Retinoid acid-inducible gene 1 like receptors: produces cytokine IFN-β.
Inflammatory bowel disease
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Giovanni Monteleone, Markus F. Neurath, Britta Siegmund
DNA sequencing of NOD2/CARD15 in Crohn's disease demonstrated that three main polymorphisms situated in or close to the leucine-rich repeat (LRR) ligand-binding domain of the molecule contribute to 80% of the risk associated with this important genetic risk factor. A gene dosing effect is seen in most studies, such that carriage of one or two copies of the risk allele(s) increases the risk of developing Crohn's disease two- to fourfold or 20- to 40-fold, respectively. Studies from France, Germany, the United Kingdom, and the United States have shown that up to 40% of patients with Crohn's disease (in contrast with 14% of controls) have one or more of these mutations. However, the allelic frequency is much lower in other European regions (e.g., Ireland, Scotland, Scandinavia, and Iceland), and NOD2 mutations are not found in patients with Crohn's disease in Asia, thus highlighting significant ethnic heterogeneity. Moreover, NOD2 mutations are associated with ileal Crohn's disease but not with colonic Crohn's disease or ulcerative colitis. Given that NOD2/CARD15 is an intracellular receptor for muramyl dipeptide (MDP) derived from peptidoglycan of gram-negative and gram-positive bacteria, and is a receptor for the glycolyl MDP of mycobacteria and single-stranded RNA of viruses and a member of the NOD-like pattern recognition receptors (NLR), these studies support a microbial basis for IBD, especially Crohn's disease.
Pathogenesis of Fungal Keratitis
Published in Mahendra Rai, Marcelo Luís Occhiutto, Mycotic Keratitis, 2019
Innate immune system has specific receptors as the first line of defence against infectious invaders that allow the immune system to recognize and initiate a normal inflammatory response to invading microorganisms (Plato et al. 2015). Once hyphae invade corneal tissue, innate immune cells like macrophages, neutrophils, and dendritic cells are recruited to mediate the host defense. The NOD-like (NLR), RIG-I-like (RLR), Toll-like (TLR), and C-type Lectin-like Receptors (CLR) are four receptor families that concur to the recognition of the fungi. Several of these Pattern Recognition Receptors (PRRs) are capable to initiate innate immunity and polarize adaptive responses on the recognition of fungal cell wall components, and other molecular structures including fungal nucleic acids (Plato et al. 2015). These receptors induce effective mechanisms of fungal clearance in normal hosts, but immunosuppression, medical interventions, or genetic predisposition may increase the susceptibility to fungal infections (Plato et al. 2015). The C-type lectin-like receptors, like Dectin-1 and Dectin-2, are the major PRR involved, and mediate secretion of chemokines (CXCL 1 and CXCL2) and proinflammatory cytokines (IL-1b and TNFα) (Plato et al. 2015). Immunopathogenesis of fungal keratitis is summarized in Fig. 9.1.
Role of inflammation in the malignant transformation of pleural mesothelial cells induced by multi-walled carbon nanotubes
Published in Nanotoxicology, 2020
Xiaopei Huang, Yijun Tian, Wenjing Shi, Jikuai Chen, Lang Yan, Lijun Ren, Xiaofang Zhang, Jiangbo Zhu
We observed that low-dose and long-term exposure of MWCNTs can trigger the malignant transformation of Met 5A cells, consistent with the results of Lohcharoenkal et al. (2013), but the specific mechanism requires further study. In order to solve the above problem, we analyzed differentially expressed genes and screened the main molecular pathways that may participate in MWCNT-induced malignant transformation of Met 5A cells via GO and KEGG. The results signified that cytokine–cytokine receptor interaction, several signaling pathways (TNF, NF-κB, PI3K-Akt, and chemokine), and Nod-like and Toll-like receptor pathways played important roles in the transformation of mesothelial cells. NOD-like receptor is a pattern recognition receptor, of which NOD1 and NOD2 can activate NF-κB and mediate an inflammatory response (Cui et al. 2014). MyD88 is a key molecule in the Toll-like receptor signal transduction pathway and may activate NF-κB through a series of pathways (Li, Ogino, and Qian 2014). TNF is a class of cytokines that possess a variety of biological effects. As a member of the TNF family, TNF-α can activate the NF-κB signaling pathway and exert its cytotoxic and immune regulatory functions (Ben-Baruch 2019). In the PI3K-Akt signaling pathway, activated Akt may stimulate NF-κB (Aggarwal et al. 2019). Therefore, the NF-κB signaling pathway may be activated through multiple enriched pathways in cancer development.
Protective effects of ethyl acetate extracts of Rimulus Cinnamon on systemic inflammation and lung injury in endotoxin-poisoned mice
Published in Drug and Chemical Toxicology, 2019
Feng Xu, Wentao Sang, Ling Li, Xinyu He, Feng Wang, Taoqun Wen, Nan Zeng
Further investigations are necessary for understanding the protective effects of EAE in endotoxin-poisoned mice. Toll-like receptors and Nod-like receptors are the two major forms of innate immune sensors, which provide immediate responses against tissue injury or during pathogenic invasion (Fukata et al. 2009). Toll-like receptors and Nod-like receptors act as extracellular and intracellular components that are involved in anti-inflammatory processes and the immune response. NLRP3 belongs to the Nod-like receptor family of proteins. In this study, we observed that EAE could suppress the onset of inflammation by antagonizing the activation of the NLRP3 inflammasome. Toll-like receptors and Nod-like receptors being closely related, the protective effects of EAE might also have been mediated by the negative regulation of Toll-like receptors. The signaling pathways mediated by NF-κB play important roles in various inflammatory processes, and the activation of NF-κB signaling pathways can lead to the activation of the NLRP3 inflammasome (Qiao et al. 2012). EAE could inhibit the activation of the NLRP3 inflammasome. Further evidence is essential for proving that the anti-inflammatory properties of EAE are mediated by the NF-κB/NLRP3 inflammasome pathway. The exact mechanism behind the anti-inflammatory property of EAE needs to be further investigated.
The role of NLRP3 inflammasome in the pathogenesis of rheumatic disease
Published in Autoimmunity, 2022
Ruixue Kong, Lulu Sun, Hua Li, Dashan Wang
The innate immune system is the first line of defense to invading microbes and cellular damage. The innate immune system can sense a wide variety of PAMPs and DAMPs by pattern-recognition receptors (PRRs). PRRs can promptly detect PAMPs and DAMPs and initiate an immune response. The NOD-like receptors (NLRs) are a family of PRRs which can recognise diverse PAMPs and DAMPs [11,12]. NLRs usually contains an N-terminal effector domain including caspase-recruitment domain (CARD), pyrin domain (PYD), acidic transactivating domain, acidic transactivating domain or baculovirus inhibitory-repeat (BIR) domain; a nucleotide-binding oligomerization domain (NACHT); a C-terminal domain that contains leucine-rich repeat domain (LRR) [13–14]. NLRP3 is one important member of NLRs.