Abstract
A neural reflex mediated by the splanchnic sympathetic nerves regulates systemic inflammation in negative feedback fashion, but its consequences for host responses to live infection are unknown. To test this, conscious instrumented sheep were infected intravenously with live E. coli bacteria and followed for 48 h. A month previously, animals had undergone either bilateral splanchnic nerve section or a sham operation. As established for rodents, sheep with cut splanchnic nerves mounted a stronger systemic inflammatory response: higher blood levels of tumor necrosis factor alpha and interleukin-6 but lower levels of the anti-inflammatory cytokine interleukin-10, compared with sham-operated animals. Sequential blood cultures revealed that most sham-operated sheep maintained high circulating levels of live E. coli throughout the 48-h study period, while all sheep without splanchnic nerves rapidly cleared their bacteraemia and recovered clinically. The sympathetic inflammatory reflex evidently has a profound influence on the clearance of systemic bacterial infection.
Highlights
A neural reflex mediated by the splanchnic sympathetic nerves regulates systemic inflammation in negative feedback fashion, but its consequences for host responses to live infection are unknown
What has not yet been established, is how the anti-inflammatory action of this reflex affects the body’s ability to combat a bacterial infection. To this end we compared the effect of prior splanchnic nerve section on the disease course of a well characterized large animal model of septicaemia: the conscious sheep infused with a bolus of live Escherichia coli (E. coli) bacteria
We report that reflex neural influences, mediated by the splanchnic sympathetic nerves, have a profound effect on the resolution of sublethal E. coli bacteraemia
Summary
A neural reflex mediated by the splanchnic sympathetic nerves regulates systemic inflammation in negative feedback fashion, but its consequences for host responses to live infection are unknown. Systemic inflammation is most commonly evoked experimentally by intravenous administration of lipopolysaccharide to cause an acute, sterile endotoxaemia In such a model in rats, the inhibitory influence of autonomic neural pathways is revealed by loss of function when the splanchnic sympathetic nerves are cut: the circulating levels of pro-inflammatory cytokines, including tumor necrosis factor alpha (TNF-α), interleukin (IL)-6 and interferon gamma (IFN-γ), are strongly enhanced, while those of the antiinflammatory cytokine IL-10 are d ecreased[4,5]. What has not yet been established, is how the anti-inflammatory action of this reflex affects the body’s ability to combat a bacterial infection To this end we compared the effect of prior splanchnic nerve section (or a sham operation) on the disease course of a well characterized large animal model of septicaemia: the conscious sheep infused with a bolus of live Escherichia coli (E. coli) bacteria
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