TLR2 Signaling and Th2 Responses Drive Tannerella forsythia -Induced Periodontal Bone Loss
Myneni Venkatasatya, Srinivas Rao
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Periodontal disease (PD) is a multifactorial chronic inflammatory disease that is triggered by the colonization and invasion of periodontopathic bacteria, particularly by a select group of Gram-negative anaerobes. Foremost among them are the so-called 'red complex' bacteria, namely Porphyromonas. gingivalis, Treponema denticola and Tannerella forsythia. These bacteria are frequently found together and are strongly associated with diseased sites in the mouth. While P. gingivalis has been a well-studied periodontal pathogen, T. forsythia, has remained relatively less understood. Although bacteria are required for the disease initiation, the ensuing destruction of the tooth-supporting soft tissue and alveolar (jaw) bone seen in PD results mainly from the effects of the immune responses. Previous studies from our laboratory revealed that T. forsythi a induces periodontal bone loss in mice and that this bone loss depends on the expression of a bacterial virulence factor, BspA protein. Extending these findings, we now show that T. forsythia activates TLR2 via BspA and T. forsythia infection in mice causes Th cell polarization towards the Th2 subset. Furthermore, deficiencies in TLR2 or Th2 result in resistance to T. forsythia-induced alveolar bone loss. Our results demonstrate that TLR2 signaling and Th2 cells play pathogenic roles in T. forsythia -induced alveolar bone destruction.