Thus, it is possible that CD4+ T cell depletion from the oral mucosa of HIV infected subjects may also lead to the impairment of epithelial growth and, by extension, host-microbe dysbiosis. In addition, depletion of the Th17 subset of CD4+ T cells has been shown in the gut mucosa impair response to microbial infections [8, 27], in part by dampening expression of epithelial antimicrobial peptides [28]. HIV patients display decreased expression

of histatin-5, a potent antimycotic known to NVP-BSK805 cell line inhibit the growth of Candida albicans[29]. Moreover, in vitro studies suggest that X4-tropic HIV can inhibit expression of human beta defensin-2 (hBD-2) and other innate immune factors in differentiated oral epithelium [30]. Because

hBD-2 functions as buy Torin 1 a chemoattractant for dendritic cells in addition to its antimicrobial activity [31], the loss of hBD-2 during HIV infection could potentiate the colonization of pathogenic species through multiple mechanisms. Thus, it is conceivable that, similar to the gut mucosa, Th17 cells may be depleted from the oral mucosa in SIV/HIV infection, thereby providing a potential mechanism for increased susceptibility to dysbiosis and infection from C. albicans and other non-commensal selleck chemicals llc pathogens. Interestingly, one of the largest and most consistent alterations we detected in the oral microbiome of untreated HIV patients was a shift in the representation of Veillonella species. Although the relative percentage of Veillonella dropped from ~19% of the total lingual bacterial population in healthy controls to just over 10% in untreated HIV infected subjects, that same group displayed a uniform increase in the growth of V. parvula. While V. parvula is a commensal gram negative anaerobic coccus in healthy individuals [32], it is also the only known Veillonella

species associated with oral disease. V. parvula has been implicated in severe early childhood caries [33], primary endodontic infections [34], and other periodontal diseases [35]. Recent studies indicate that V. parvula lipopolysaccharide (LPS) stimulates pro-inflammatory cytokine production and p38 MAPK activation through TLR-4 dependent mechanisms [36]. Thus, it is possible that increased V. parvula colonization (as well as other opportunistic pathogens) could establish O-methylated flavonoid an inflammatory environment in the oral cavity, that in turn, contributes to the chronic inflammation and immune activation that characterizes HIV disease progression. Future studies are warranted to determine whether increased colonization of putative periodontal pathogens on the tongue epithelium reflects similar increased growth in gingival and subgingival tissues, and perhaps a systemic distribution to more distal mucosal compartments. Conclusions In summary, we identify statistically significant increases in the growth of V. parvula P. pallens C. rectus and/or C. concisus, and M.