Mycobacterial Phenolic Glycolipids Selectively Disable TRIF-Dependent TLR4 Signaling in Macrophages

Mycobacterial Phenolic Glycolipids Selectively Disable TRIF-Dependent TLR4 Signaling in Macrophages

Phenolic glycolipids (PGLs) are cell wall components of a subset of pathogenic mycobacteria, with immunomodulatory properties. Here, we show that in addition, PGLs exert antibactericidal activity by limiting the production of nitric oxide synthase (iNOS) in mycobacteria-infected macrophages. PGL-mediated downregulation of iNOS was complement receptor 3-dependent and comparably induced by bacter...

MyD88-dependent TLR4 signaling is selectively impaired in alveolar macrophages from asymptomatic HIV+ persons.

Alveolar macrophages (AMs) are the predominant effector cell in the lungs and contribute to a critical first line of defense against bacterial pathogens through recognition by pattern recognition receptors such as Toll-like receptor 4 (TLR4). TLR4-mediated tumor necrosis factor alpha (TNFalpha) release is significantly impaired in HIV(+) macrophages, but whether HIV impairs myeloid differentiat...

TLR4 Signaling via MyD88 and TRIF

Dancing with the Stars: Phenolic Glycolipids Partners with Macrophages.

How Mycobacterium leprae infection causes demyelination to mediate leprosy pathogenesis has been a long-standing question. In a recent Cell paper, Madigan et al. (2017) use a zebrafish model of M. leprae infection to show that infected macrophages patrol axons to trigger mitochondrial damage and induce demyelination of nerve cells.

PHAGOCYTES, GRANULOCYTES, AND MYELOPOIESIS MyD88-dependent TLR4 signaling is selectively impaired in alveolar macrophages from asymptomatic HIV persons

Alveolar macrophages (AMs) are the predominant effector cell in the lungs and contribute to a critical first line of defense against bacterial pathogens through recognition by pattern recognition receptors such as Toll-like receptor 4 (TLR4). TLR4mediated tumor necrosis factor (TNF ) release is significantly impaired in HIV macrophages, but whether HIV impairs myeloid differentiation factor 88 ...