Host-Microbiome Cross-talk in Oral Mucositis

Abstract

Oral mucositis (OM) is among the most common, painful, and debilitating toxicities of cancer regimen-related treatment, resulting in the formation of ulcers, which are susceptible to increased colonization of microorganisms. Novel discoveries in OM have focused on understanding the host-microbial interactions, because current pathways have shown that major virulence factors from microorganisms have the potential to contribute to the development of OM and may even prolong the existence of already established ulcerations, affecting tissue healing. Additional comprehensive and disciplined clinical investigation is needed to carefully characterize the relationship between the clinical trajectory of OM, the local levels of inflammatory changes (both clinical and molecular), and the ebb and flow of the oral microbiota. Answering such questions will increase our knowledge of the mechanisms engaged by the oral immune system in response to mucositis, facilitating their translation into novel therapeutic approaches. In doing so, directed clinical strategies can be developed that specifically target those times and tissues that are most susceptible to intervention.

Faecal microbiota transplantation protects against radiation‐induced toxicity

“…Compositional and functional changes in commensal microbiota are thought to be involved in the pathogenesis of many diseases (Petrof & Khoruts, 2014;Vanhoecke et al, 2015). Recently, epidemiological and clinical studies on symbiotic microbiota have experienced a renaissance (Vasconcelos et al, 2016). Understanding how the enteric microbiota affects health and disease requires a paradigm shift from focusing on individual pathogens to an ecological approach that considers the community as a whole (Lozupone et al, 2012).…”

CD24 blunts oral squamous cancer development and dampens the functional expansion of myeloid-derived suppressor cells

“…32 Therefore, combining the knowledge that the presence of host CD24 modulates microbial activity in the oral cavity, and that patients with oral cancer have dysbiosis, it is possible that disruption of the CD24-oral microbiome axis alters cancer development. 33,34 Zhang et al 35 demonstrated that probiotic L. salivarius REN treatment significantly damped 4-NQO-induced oral cancer development in rats; however, the significance of the oral microbiome in 4-NQO-induced oral carcinogenesis has never been addressed in mouse models. Further, due to the known role of bacteria-produced sialidase in disrupting the CD24-Siglec-G/10 connection, we investigated if CD24 deficiency alters intra-oral microflora in a manner that may contribute to oral carcinogenesis.…”

Troxerutin Prevents 5-Fluorouracil Induced Morphological Changes in the Intestinal Mucosa: Role of Cyclooxygenase-2 Pathway

“…Nuclear factor kappa B (NF-kB), proinflammatory cytokines, such as interleukin 1 beta (IL-1β), interleukin 6 (IL-6), and tumor necrosis factor alpha (TNF-α), and apoptotic mediators have been known to be associated with this process. The interaction of these factors results in oxidative damage, intense infiltration of inflammatory cells, villous atrophy, crypt hypoplasia, edema, necrosis, and cell death, which ultimately leads to damage and rupture of the intestinal epithelial barrier [4,[9][10][11][12][13][14].…”