Activation in vagal afferents and central autonomic pathways: Early responses to intestinal infection with Campylobacter jejuni

Department of Psychology, University of Virginia, Charlottesville, VA 22904, United States.
Brain Behavior and Immunity (Impact Factor: 5.89). 08/2005; 19(4):334-44. DOI: 10.1016/j.bbi.2004.09.002
Source: PubMed


Abundant evidence now supports the idea that multiple pathways or mechanisms underlie communication from the immune system to the brain. The presence of a variety of mechanisms suggests that they may each contribute something different to immunosensory signaling. For instance, brain mediated immune signal transduction is dependent upon the presence of circulating mediators whereas peripheral sensory nerves are more likely to be important early on in an infection, prior to elevation of circulating cytokines, or in local infections within the terminal fields of these nerves. To test the hypothesis that local infection in the gut activates vagal sensory neurons, we assessed expression of the neuronal activation marker c-Fos in neurons in the vagal sensory ganglia and in the primary sensory relay nucleus for the vagus, the nucleus of the solitary tract (nTS) in mice treated orally either with saline or live Campylobacter jejuni (C. jejuni). Male CF1 mice were inoculated orally with either C. jejuni or saline, and c-Fos expression in the vagal sensory neurons and brain 4-12 h later was assessed via immunohistochemistry. Oral inoculation with C. jejuni led to a significant increase in c-Fos expression in neurons bilaterally in the vagal ganglia, in the absence of elevated levels of circulating pro-inflammatory cytokines. C. jejuni treatment activated neurons in the nTS, as well as in brain regions associated with primary viscerosensory pathways and the central autonomic network. These findings provide evidence that peripheral sensory neurons contribute an early signal to the brain regarding potential pathogens.

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Available from: Lisa E Goehler, Feb 10, 2014
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    • "There is a small but growing literature on visceral interoceptive effects of the NTS on the CeA strongly impacting emotional and higher processes, including those reporting the state of the gut microbiome. Vagally mediated increases in c- Fos expression in NTS and CeA following C. jejuni infection were taken to suggest that this neuronal route may play a key role in the induced anxiety-like behavior driven by gut dysbiosis (Gaykema et al. 2004; Goehler et al. 2005 Goehler et al. , 2008). Dysregulating or altering the vagal afferents via the gut microbiome may interact with this system and promote neuroinflammation. "

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    • "Recent research also suggests that the intestinal microbiome is involved in the development of the brain (for reviews see: Al-Asmakh et al. 2012 ; Douglas-Escobar et al. 2013 ; Collins et al. 2012 ; Sudo 2012 ), including the systems that modulate adaptive responses to stress, the HPA axis (Sudo et al. 2004 ) and the autonomic nervous system (Goehler et al. 2005 "
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    • "As such, the communication of gut microbiota with the brain, through what is referred to as the microbiota-gut-brain axis, represents a new biological axis by which novel diet-based therapies can be designed to influence brain function and behavior. Early studies in animals first demonstrated that the introduction of a single, unique bacterium in the gut resulted in the development of anxiety-like behavior in mice, with concomitant activation of neuronal regions in the brain that were dependent on information received from the gut via the vagus nerve (Goehler et al., 2005). Later studies showed that the transplantation of the fecal microbiome from one mouse strain displaying a phenotypic set of behaviors to another strain resulted in the recipient strain exhibiting the behavioral phenotype of the donor (Bercik et al., 2011a; Collins et al., 2013). "

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