Interplay between NOD1 and TLR4 Receptors in Macrophages: Nonsynergistic Activation of Signaling Pathways Results in Synergistic Induction of Proinflammatory Gene Expression.

Interactions between pattern-recognition receptors shape innate immune responses to pathogens. NOD1 and TLR4 are synergistically interacting receptors playing a pivotal role in the recognition of Gram-negative bacteria. However, mechanisms of their cooperation are poorly understood.

Glycolytic reprogramming of macrophages activated by NOD1 and TLR4 agonists: No association with proinflammatory cytokine production in normoxia.

Upon activation with pathogen-associated molecular patterns, metabolism of macrophages and dendritic cells is shifted from oxidative phosphorylation to aerobic glycolysis, which is considered important for proinflammatory cytokine production. Fragments of bacterial peptidoglycan (muramyl peptides) activate innate immune cells through nucleotide-binding oligomerization domain (NOD) 1 and/or NOD2 receptors. Here, we show that NOD1 and NOD2 agonists induce early glycolytic reprogramming of human monocyte-derived macrophages (MDM), which is similar to that induced by the Toll-like receptor 4 (TLR4) agonist lipopolysaccharide.

Synergistic interactions between NOD receptors and TLRs: Mechanisms and clinical implications.

Interactions between pattern recognition receptors (PRRs) shape innate immune responses to particular classes of pathogens. Here, we review interactions between TLRs and nucleotide-binding oligomerization domain 1 and 2 (NOD1 and NOD2) receptors, two major groups of PRRs involved in innate recognition of bacteria. Most of experimental data both in vitro and in vivo suggest that NODs and TLRs synergize with each other at inducing the production of cytokines and antimicrobial peptides.

[The dependence of Toll-receptor expression on pathomorphological features of nasal polyps in patients with polypous rhinosinusitis].

This work was designed to study expression of Toll 1-10 receptors on the surface of cells present in inflammatory infiltrate from nasal polyps and peripheral blood of the patients with polypous rhinosinusitis. It was shown that the intensity of expression depended on the pathomorphological characteristics of nasal polyps. Tissues removed from the patients with polyps of the oedematous type contained more Toll-10 positive cells and showed enhanced expression of Toll-5 receptors on monocytes and lymphocytes, Toll-3 receptors on monocytes, granulocytes, and lymphocytes, and Toll-9 receptors on granulocytes.