Abstract
Early sensing of pathogenic bacteria by the host immune system is important to develop effective mechanisms to kill the invader. Microbial recognition, activation of signaling pathways, and effector mechanisms are sequential events that must be highly controlled to successfully eliminate the pathogen. Host recognizes pathogens through pattern-recognition receptors (PRRs) that sense pathogen-associated molecular patterns (PAMPs). Some of these PRRs include Toll-like receptors (TLRs), nucleotide-binding oligomerization domain-like receptors (NLRs), retinoic acid-inducible gene-I- (RIG-I-) like receptors (RLRs), and C-type lectin receptors (CLRs). TLRs and NLRs are PRRs that play a key role in recognition of extracellular and intracellular bacteria and control the inflammatory response. The activation of TLRs and NLRs by their respective ligands activates downstream signaling pathways that converge on activation of transcription factors, such as nuclear factor-kappaB (NF-κB), activator protein-1 (AP-1) or interferon regulatory factors (IRFs), leading to expression of inflammatory cytokines and antimicrobial molecules. The goal of this review is to discuss how the TLRs and NRLs signaling pathways collaborate in a cooperative or synergistic manner to counteract the infectious agents. A deep knowledge of the biochemical events initiated by each of these receptors will undoubtedly have a high impact in the design of more effective strategies to control inflammation.
Highlights
All living organisms are constantly challenged by microorganisms and a variety of particles that represent a health threat
Since some pathogenic bacteria possess pathogen-associated molecular patterns (PAMPs) that can be simultaneously recognized by several pattern-recognition receptors (PRRs) and this leads to the activation of common transcription factors, it is likely that a collaborative response among different signaling molecules may exert regulatory functions after recognition of Mediators of Inflammation
Among the most important PAMPs are lipoteichoic acid (LTA) and peptidoglycan (PGN) from Gram-positive bacteria, lipopolysaccharide (LPS) from Gram-negative bacteria, lipoarabinomannan (LAM), lipopeptides, lipoglycans and lipomannans from mycobacteria, glycosylphosphatidylinositol (GPI), anchored lipids from Trypanosoma cruzi, zymosan isolated from yeast, profilin from Toxoplasma gondii, and DNA from bacteria and mycobacteria [5,6,7,8]
Summary
All living organisms are constantly challenged by microorganisms and a variety of particles (from air pollution and cellular stresses) that represent a health threat To counteract this burden, the innate immune system needs to react promptly and adequately to eliminate them, while at the same time to preserve tissue normal function. The different subcellular localization of PRRs and the broad array of PAMPs that can be recognized by them, allows the host to sense a large number of pathogen bacteria and develop an adequate immune response. Since some pathogenic bacteria possess PAMPs that can be simultaneously recognized by several PRRs and this leads to the activation of common transcription factors, it is likely that a collaborative response among different signaling molecules may exert regulatory functions after recognition of Mediators of Inflammation. The aim of this review is to discuss recent findings on the collaborative activity of TLRs and NLRs in the modulation of the inflammatory response induced by virulence factors of pathogenic bacteria
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