TY - JOUR
T1 - TLR2-dependent inflammatory response to Porphyromonas gingivalis is MyD88 independent, whereas MyD88 is required to clear infection
AU - Burns, Elia
AU - Eliyahu, Tal
AU - Uematsu, Satoshi
AU - Akira, Shizuo
AU - Nussbaum, Gabriel
PY - 2010/2/1
Y1 - 2010/2/1
N2 - Porphyromonas gingivalis is a Gram-negative anaerobe considered to be a major periodontal pathogen. TLR2 plays a central role in the response to P. gingivalis infection in vivo. In its absence there is a weak inflammatory response; however, bacteria are cleared rapidly compared with wild-type mice. We examined the role of the TLR adaptor proteins MyD88 and TLR/IL-1R - domain-containing adaptor-inducing IFN-β in the inflammatory response to P. gingivalis in vivo and in the ability to clear the bacterial infection. Proinflammatory cytokine production in response to P. gingivalis infection depends on TLR2, but it does not require MyD88 or TLR/IL-1R - domain-containing adaptor-inducing IFN-β. In contrast, the generation of intracellular toxic oxygen species and the ultimate clearance of P. gingivalis infection depend critically on MyD88, independent of TLR2. Thus, robust cytokine production and bacterial clearance are independent events mediated by distinct signaling pathways following infection with P. gingivalis.
AB - Porphyromonas gingivalis is a Gram-negative anaerobe considered to be a major periodontal pathogen. TLR2 plays a central role in the response to P. gingivalis infection in vivo. In its absence there is a weak inflammatory response; however, bacteria are cleared rapidly compared with wild-type mice. We examined the role of the TLR adaptor proteins MyD88 and TLR/IL-1R - domain-containing adaptor-inducing IFN-β in the inflammatory response to P. gingivalis in vivo and in the ability to clear the bacterial infection. Proinflammatory cytokine production in response to P. gingivalis infection depends on TLR2, but it does not require MyD88 or TLR/IL-1R - domain-containing adaptor-inducing IFN-β. In contrast, the generation of intracellular toxic oxygen species and the ultimate clearance of P. gingivalis infection depend critically on MyD88, independent of TLR2. Thus, robust cytokine production and bacterial clearance are independent events mediated by distinct signaling pathways following infection with P. gingivalis.
UR - http://www.scopus.com/inward/record.url?scp=77949316163&partnerID=8YFLogxK
U2 - 10.4049/jimmunol.0900378
DO - 10.4049/jimmunol.0900378
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C2 - 20042569
AN - SCOPUS:77949316163
SN - 0022-1767
VL - 184
SP - 1455
EP - 1462
JO - Journal of Immunology
JF - Journal of Immunology
IS - 3
ER -