CD47 and thrombospondin-1 contribute to immune evasion by .

is a gram-negative anaerobic bacterium linked to periodontal disease. Remarkably, thrives in an inflamed environment rich in activated neutrophils. Toll-like receptor 2 (TLR2) recognition is required for to evade innate immune killing; however, the mechanisms through which uncouples host inflammation from bactericidal activity are only partially known.

-Induced TLR2 Interactome Analysis Reveals Association with PARP9.

is a Gram-negative anaerobic bacterium strongly associated with periodontal disease. Toll-like receptor 2 (TLR2) is indispensable for the host response to , but escapes from immune clearance via TLR2-dependent activation of phosphoinositide-3-kinase (PI3K). To probe the TLR2-dependent escape pathway of , we analyzed the TLR2 interactome induced following infection or activation by a synthetic lipopeptide TLR2/1 agonist on human macrophages overexpressing TLR2.

Porphyromonas gingivalis induction of TLR2 association with Vinculin enables PI3K activation and immune evasion.

Porphyromonas gingivalis is a Gram-negative anaerobic bacterium that thrives in the inflamed environment of the gingival crevice, and is strongly associated with periodontal disease. The host response to P. gingivalis requires TLR2, however P.

Intracellular Promotes the Tumorigenic Behavior of Pancreatic Carcinoma Cells.

is a member of the dysbiotic oral microbiome associated with oral inflammation and periodontal disease. Intriguingly, epidemiological studies link to an increased risk of pancreatic cancer. Given that oral bacteria are detected in human pancreatic cancer, and both mouse and human pancreata harbor microbiota, we explored the involvement of in pancreatic tumorigenesis using cell lines and a xenograft model.