Importance of the vagus nerve for fever and neutrophil migration induced by intraperitoneal LPS injection.
Level 5 - mechanism / opinion, no new human data
Animal research (preclinical rodent model)
PubMed 12861394 · doi:10.1007/s00011-003-1174-8
What was done
Naïve, sham-operated, or subdiaphragmatically vagotomized male Wistar rats received lipopolysaccharide (LPS, 0.02–200 µg/kg, intraperitoneally or intrapleurally) or pre-formed pyrogenic factor (PFPF, intravenously, intracerebroventricularly, or intraperitoneally). Researchers measured core temperature via rectal probe and quantified neutrophil counts in blood, peritoneal fluid, and pleural fluid, while also assessing PFPF production and fever response.
What was found
In naïve rats, intraperitoneal LPS produced dose-dependent fever and neutrophilia, alongside a bell-shaped peritoneal neutrophil migration response. Subdiaphragmatic vagotomy reduced the peritoneal resident cell population by 56%, LPS-induced fever by 71%, and peritoneal neutrophil migration by 43%. Vagotomy did not alter systemic neutrophilia, pleural neutrophil migration, PFPF production, or PFPF-induced fever.
Why it matters
The findings demonstrate that subdiaphragmatic vagal innervation modulates both systemic febrile responses and local peritoneal leukocyte recruitment after abdominal endotoxin exposure, partly by regulating local resident cell populations.
Limits
The study was conducted exclusively in male Wistar rats, limiting direct translation to human inflammatory pathology. The abstract omits specific sample sizes per group, dispersion statistics (error bars/confidence intervals), and exact time courses.
Cited by
- supports Experimental injection of lipopolysaccharide (LPS) into the gut induces a fever response that is abolished if the vagus nerve is transected.