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May 17th:Jan Pieter Konsman, Fixing bugs along the gut-brain axis
17 May 2018 @ 13 h 30 min - 14 h 30 min UTC+1
Jan Pieter Konsman is a researcher in neuroscience (neuroimmunology, neuroinflammation), CNRS UMR 5287 Institute for Cognitive and Integrative Neuroscience (INCIA) in Bordeaux. He also has a background in philosophy of science.
Gut bacteria are an important source of sepsis, which has long been defined as the systemic inflammatory response syndrome to infection. Work on animals indicates that moderate fevers as well as reduced activity and food intake during a systemic inflammatory response to bacterial infection can be considered adaptive strategies to promote host survival (Hart, Neurosci. Biobehav. Rev. 1988).
Given that body temperature, behavior and energy intake are regulated by the brain, we have tried to unravel the pathways between the innate immune system and the nervous system underlying reduced activity and food intake in an animal model consisting of intraperitoneal injections of bacterial lipopolysaccharides (LPS). We have shown that the vagus nerve and brainstem glutamate action (Konsman et al., Eur. J. Neurosci., 2000; Chaskiel et al., J. Neuropharmacol., 2016) as well as production of the pro-inflammatory cytokine interleukin-1 at the blood-brain interface and its action on forebrain cells expressing the interleukin-1 receptor are involved in the reduction of food intake and activity after detection of bacterial LPS (Konsman et al., Eur. J. Neurosci., 2008; Chaskiel et al., unpublished observations). Our findings thus indicate the existence of both nervous and humoral gut-brain axes mediating changes in behavior in response to the presence of bacteria in the peritoneal cavity.
Most recently, we have developed animal models of infection-induced reactivation of colitis and cancer chemotherapy, to study long(er)-term behavioral changes related to in relation to more chronic challenges to the gut-brain axis. After their initial behavioral characterization, we are now exploring activation of brainstem circuits and brain production of cytokines in these models.
Overall, our findings suggest that, although the innate neuroimmune interactions underlying increased body temperature, decreased activity and food intake may be considered adaptive in response to acute bacterial infection, they may also contribute to long-term sensitization of visceroception and cognitive sequela in inflammatory bowel disease and cancer.
Invited by Thomas Pradeu.