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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.
Development of a PHBV nanoparticle as a peptide vehicle for NOD1 activation
Published in Drug Delivery, 2021
Mauricio Cabaña-Brunod, Pablo A. Herrera, Valeria Márquez-Miranda, Felipe M. Llancalahuen, Yorley Duarte, Danilo González-Nilo, Juan A. Fuentes, Cristián Vilos, Luis Velásquez, Carolina Otero
Pathogen recognition receptors (PRR) are responsible for detecting different microorganisms by recognizing conserved structures, known as pathogen-associated molecular patterns (PAMPs). PAMPs, which initiate an innate immune response during infection (Motta et al., 2015), compromise members of the nucleotide-linked oligomerization domain type receptors (NLR) family. NLR family consists of 22 cytoplasmic pathogen sensors, which are characterized by having a trimeric structure. NOD1 and NOD2 receptors belong to an NLR subfamily, both containing LRR and NOD domains, and differ only in one or two copies of the caspase activation recruitment domains (CARDs). Both NOD1 and NOD2 exert a fundamental role in the defense against bacterial infections and regulate the host inflammatory response (Charlotte et al., 2013). NOD2 agonists are highly pyrogenic; thereby, their use in humans has been restricted (Monie, 2017). Since it is not the case for NOD1 agonists, these represent an attractive focus to obtain a more controlled response.
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.
Bacterial imbalance and gut pathologies: Association and contribution of E. coli in inflammatory bowel disease
Published in Critical Reviews in Clinical Laboratory Sciences, 2019
Shahanavaj Khan, Ahamad Imran, Abdul Malik, Anis Ahmad Chaudhary, Abdur Rub, Arif Tasleem Jan, Jakeera Begum Syed, Christian Rolfo
NOD and NOD-like receptor proteins (Nlrps) are a family of proteins involved in innate immune signaling in humans [67–69]. These proteins identify bacterial molecules and regulate immune reactions [70]. Alterations in Nod1, Nod2, Nlrp3, and Nlrp6 have been shown to affect microbiota homeostasis, which leads to increased disease susceptibility [64,71,72]. Notably, the enhanced susceptibility to colitis detected in Nlrp6-deficient mice can be passed on to other mice that are co-housed. Therefore, it was proposed that a lack in Nlrp6 predisposes mice to a colitogenic microbiota in which the Prevototellaceae family and candidate phylum TM7 were observed [64]. Conversely, a comprehensive report revealed that the diverse microbiota population observed in TLR-deficient mice was due to caging isolation instead of defective innate immunity, and loss of TLR signaling did not affect the microbiota population. Therefore, there is still much debate on the role of TLR in the control and regulation of the microbiota population [73].