Apoptosis is implicated in the generation and resolution of inflammation in
response to bacterial pathogens. All bacterial pathogens produce lipoprote
ins (BLPs), which trigger the innate immune response. BLPs were found to in
duce apoptosis in THP-1 monocytic cells through human Toll-like receptor-2
(hTLR2). BLPs also initiated apoptosis in an epithelial cell line transfect
ed with hTLR2. In addition, BLPs stimulated nuclear factor-kappa B, a trans
criptional activator of multiple host defense genes, and activated the resp
iratory burst through hTLR2. Thus, hTLR2 is a molecular link between microb
ial products, apoptosis, and host defense mechanisms.