NOD-like receptor(s) and host immune responses with Pseudomonas aeruginosa infection.

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.