Commensal gut bacterium critically regulates alveolar bone homeostasis

A gut-oral microbiome–driven axis controls oropharyngeal candidiasis through retinoic acid

“…Therefore, as expected, Abx treatment reduced SFB levels in fecal pellets from SPF mice ( Figure 2B ), correlating with OPC susceptibility. However, SFB is not detectable within the oral mucosa ( 28 , 50 ) ( Supplemental Figure 1A ; supplemental material available online with this article; https://doi.org/10.1172/jci.insight.160348DS1 ). Accordingly, to determine if SFB that is selectively gut resident can influence immune events in the oral mucosa, WT-GF mice were given SFB (or PBS control) by gavage.…”

“…Moreover, SFB in the gut amplifies IL-17 production in a manner dependent on IL-17R signaling within the gut epithelium (37). In contrast, the influence of SFB on oral mucosal immunity is not well described, though a recent study demonstrated that SFB modulates alveolar bone homeostasis in a model of periodontal bone loss (50,82).…”

“…Numerous studies have shown convincingly that SFB is not found in the mouth ( 28 , 32 , 50 ). Rather, intestine-resident SFB appears to establish a gut-oral axis that limits oral candidiasis.…”

C3a-C3aR signaling is a novel modulator of skeletal homeostasis

“…Confluent cultures were then treated with osteogenic media (α-MEM media, 10 % FBS (Hyclone), 1 % PSG, 50 mg/mL ascorbic acid, and 10 mM β-glycerophosphate) for 11 days. Cultures were stained by the von Kossa method to detect mineralization, as previously reported ( Hathaway-Schrader et al, 2020 , Hathaway-Schrader et al, 2022 ). Differentiation potential quantitative real-time PCR (qRT-PCR) assay: BMSCs were plated at 2.0 × 10 4 cells/cm 2 in 12-well plates and cultured in α-MEM media, 10 % FBS, 1 % PSG, to assess alterations in multipotent differentiation potential in unstimulated cultures.…”

Microbiome, alveolar bone, and metabolites: Connecting the dots

“…Studies in mice suggest that ingested OM bacteria can reach the gut and induce an inflammatory immune response (72), and immune cells exposed to OM can reach the gut to interact with OM-derived gut microbes (73). Gut colonization with specific bacterial species can also influence T cell development in alveolar bone marrow and increase alveolar bone osteoclast activity, further illustrating the potential bidirectional mechanisms whereby microbial populations in both gut and oral cavity can help disrupt or maintain bone homeostasis (74).…”