Alaa Alhazmi1,2. 1. Department of Biology, Lakehead University, 955 Oliver Road, Thunder Bay, ON, P7B 5E1, Canada. aalhazmi@lakeheadu.ca. 2. Department of Medical Laboratory Technology, Jazan University, Jazan, Kingdom of Saudi Arabia. aalhazmi@lakeheadu.ca.
Abstract
INTRODUCTION: Molecular mechanisms underlying the interactions between Pseudomonas aeruginosa, the common opportunistic pathogen in cystic fibrosis individuals, and host induce a number of marked inflammatory responses and associate with complex therapeutic problems due to bacterial resistance to antibiotics in chronic stage of infection. METHODS: Pseudomonas aeruginosa is recognized by number of pattern recognition receptors (PRRs); NOD-like receptors (NLRs) are a class of PRRs, which can recognize a variety of endogenous and exogenous ligands, thereby playing a critical role in innate immunity. RESULTS: NLR activation initiates forming of a multi-protein complex called inflammasome that induces activation of caspase-1 and resulted in cleavage of pro-inflammatory cytokines interleukin (IL)-1β and IL-18. When the IL-1β is secreted excessively, this causes tissue damage and extensive inflammatory responses that are potentially hazardous for the host. CONCLUSIONS: Recent evidence has laid out inflammasome-forming NLR far beyond inflammation. This review summarizes current knowledge regarding the various roles played by different NLRs and associated down-signals, either in recognition of P. aeruginosa or may be associated with such bacterial pathogen infection, which may relate to for the complexity of lung diseases caused by P. aeruginosa.
INTRODUCTION: Molecular mechanisms underlying the interactions between Pseudomonas aeruginosa, the common opportunistic pathogen in cystic fibrosis individuals, and host induce a number of marked inflammatory responses and associate with complex therapeutic problems due to bacterial resistance to antibiotics in chronic stage of infection. METHODS:Pseudomonas aeruginosa is recognized by number of pattern recognition receptors (PRRs); NOD-like receptors (NLRs) are a class of PRRs, which can recognize a variety of endogenous and exogenous ligands, thereby playing a critical role in innate immunity. RESULTS: NLR activation initiates forming of a multi-protein complex called inflammasome that induces activation of caspase-1 and resulted in cleavage of pro-inflammatory cytokines interleukin (IL)-1β and IL-18. When the IL-1β is secreted excessively, this causes tissue damage and extensive inflammatory responses that are potentially hazardous for the host. CONCLUSIONS: Recent evidence has laid out inflammasome-forming NLR far beyond inflammation. This review summarizes current knowledge regarding the various roles played by different NLRs and associated down-signals, either in recognition of P. aeruginosa or may be associated with such bacterial pathogen infection, which may relate to for the complexity of lung diseases caused by P. aeruginosa.
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