Meeting Abstract

S9.6  Tuesday, Jan. 6  Impact of stressor exposure on intestinal microbiota BAILEY, Michael; The Ohio State University bailey.494@osu.edu

The field of PsychoNeuroImmunology (PNI) has clearly demonstrated that exposure to psychological stressors can disrupt immune functioning. For the most part, studies have focused on innate and adaptive immune responses, with few studies focusing on more basic defenses, such as the commensal microbiota. The healthy human is colonized by a vast array of microbes that exceeds cells of the body by a factor of 10:1 (i.e., 10¹⁴ microbes:10¹³ human cells). These microbes have many beneficial effects on the host and comprise a strong natural barrier to invading pathogens; disrupting the microbiota is known to enhance susceptibility to enteric diseases. The factors regulating the types of bacteria that comprise the intestinal microbiota, as well as the levels to which they can grow, are not well defined. But, it is known that certain components of gastrointestinal functioning strongly influence microbial populations. Moreover, these functions are altered during a stress response. Thus, it was hypothesized that stressor exposure would affect the intestinal microbiota. Initial studies in rhesus monkeys (Macaca mulatta) supported this hypothesis by demonstrating that exposure to stressors early in the lifespan significantly reduced levels of commensal lactobacilli that are thought to protect the intestines from infection. In more recent murine studies, exposure to a prolonged stressor (i.e., repeated restraint stress) led to a significant overgrowth of Gram-negative bacteria. Moreover, DNA sequencing, using pyrosequencing methodology, indicated that microbial diversity in the intestines was reduced from 1200 to 900 operational taxonomic units after stressor exposure. While the physiological importance of these alterations is currently being studied, the data indicate that prolonged stressors significantly alter intestinal microbial populations, and implicate an additional mechanism through which stress can affect health.