Microbiology Select

Symbiotic, parasitic, and commensal relationships have precise definitions in biology, but often the nature of the relationship between two organisms is not clear-cut and fluctuates over time. This Microbiology Select highlights recent studies that demonstrate how communication between the host and its microbial inhabitants largely determines whether their interaction is beneficial, hurtful, or harmless. Although the nonpathogenic bacteria in our guts are traditionally thought of as commensal—that is, they derive nutrients from our meals without directly disturbing our overall health—accumulating evidence indicates that these microscopic residents contribute significantly to the development of metabolic disorders, such as diabetes and obesity. What transforms these friendly inhabitants into harmful foes? Wang et al. (2010) now tackle this question in their new study. They show that Toll-like receptor 5 (TLR5), which is expressed on the surface of intestinal cells in mammals, promotes metabolic health partially by regulating the composition of the gut microflora. TLR5 is a critical component of the innate immune system in mammals and specifically recognizes molecular components of bacterial flagella. The authors find that engineering mice to lack TLR5 induced symptoms that are similar to metabolic syndrome in humans, including overeating, obesity, and insulin resistance. Remarkably, antibiotic treatments that decimated 90% of the gut bacteria in these mice almost completely resolved their metabolic problems. Meanwhile, transplanting the gut microflora of the TLR5-deficient mice into germ-free wild-type mice disrupted the metabolic health of the transplanted animals, producing symptoms similar to those exhibited by the TLR5-deficient mice. Thus, the composition of the bacterial species that initially colonizes our guts at birth may have a significant impact on our metabolic health later in life. Further, metabolic disorders stemming from the current obesity epidemic may be due, in part, to the breakdown in communication between the gut microflora and components of our innate immune system. Communication between the human immune system and the gut bacterium Helico-bacter pylori also greatly affects the outcome of infection. Colonization of the intestinal wall by H. pylori always triggers an inflammatory response by the human immune system; however, depending on the severity of this response, H. pylori can be a benign inhabitant associated with no symptoms, a mild pathogen associated with peptic ulcers, or a major pathogen associated with stomach cancer. It has been difficult to pinpoint the key factors that regulate the degree of pathogenicity by H. pylori because very little is known about the regulation of gene expression …