The resident prokaryotic microbiota of the mammalian intestine is a numerically vast and taxonomically complex symbiotic community that influences diverse homeostatic functions including maintenance of the epithelial barrier, modulation of immune responses, and control over cellular growth/differentiation and restitutive pathways. Specifically, recent advances have implicated the commensal microbiota in regulating epithelial cell cycle and stem cell dynamics in wide variety of organisms, thus indicating a role in normal gut growth and development and suggesting that “dysbiosis” of the bacterial community may influence initiation and progression of Gl cancers. However, there is a gap in the knowledge concerning a mechanistic understanding of how the commensal microbiota influences regulation of cellular growth signaling networks in . health and disease. Insight has come from studies of lower organisms, which have revealed a common I paradigm wherein contact of prokaryotic organisms stimulate the enzymatic generation of reactive oxygen species (ROS) in the host, as an anti-microbial effector, or more significantly, as a cellular signaling intermediate. In mammals, while the induced generation of ROS via stimulation of formyl peptide receptors (FPRs) is a cardinal feature of the cellular response of phagocytes to all bacteria, evidence is accumulating that ROS are also similarly elicfted in other cell types, including intestinal epithelia, also in response to microbial signals and FPRs.
展开▼
