Cell Activation and Apoptosis by Bacterial Lipoproteins Through Toll-like Receptor-2

TLDR

Apoptosis contributes to inflammation initiated by bacterial pathogens, whose lipoproteins activate innate immunity. BLPs trigger apoptosis and stimulate NF‑κB and respiratory burst in hTLR2‑expressing cells, linking microbial products, apoptosis, and host defense.

Abstract

Apoptosis is implicated in the generation and resolution of inflammation in response to bacterial pathogens. All bacterial pathogens produce lipoproteins (BLPs), which trigger the innate immune response. BLPs were found to induce apoptosis in THP-1 monocytic cells through human Toll-like receptor–2 (hTLR2). BLPs also initiated apoptosis in an epithelial cell line transfected with hTLR2. In addition, BLPs stimulated nuclear factor–κB, a transcriptional activator of multiple host defense genes, and activated the respiratory burst through hTLR2. Thus, hTLR2 is a molecular link between microbial products, apoptosis, and host defense mechanisms.