Bacterial surface (S-) layer glycosylation orchestrates oral microbial communities by tuning the host immunity (MUC4P.841)

Abstract

Abstract Human mucosal surfaces begin to get colonized after birth with microbial communities, which co-exist in the host by modulating the host immune responses. In this process, some microbes decorate with unique sugars to mold the host immunity conducive to their survival. Recently we have shown that oral pathogen Tannerella forsythia (Tf) exploits a similar strategy to facilitate its survival in the oral cavity, and subsequently cause the alveolar bone destruction by dampening Th17-dependent neutrophil infiltration. The present study was aimed to assess the role of Tf surface O-glycans in the manipulation of host immunity and test if this might impact the colonization and persistence of other co-habitants, such as Porphyromonas gingivalis (Pg). Periodontitis mouse model was utilized to compare the ability of Tf or its O-glycan deficient mutant ED1 in impacting Pg colonization and induced alveolar bone loss. In comparison to the ED1: Pg infected group, higher alveolar bone loss was observed in the Tf: Pg group. This paralleled with osteoclastic numbers. Elevated numbers of neutrophils observed in the ED1: Pg group over Tf: Pg group, associated with bacterial colonization levels. Our study suggests that Tf tunes host immunity to promote its colonization and of its co-habiting partner P. gingivalis, leading to increased alveolar bone loss and this scenario parallels with clinical settings where the increased periodontitis severity has been observed in patients harboring Pg and Tf.