PubMed · 2978216
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R G Elmslie. 1988. Closed abdominal surgery.. https://doi.org/10.1111/j.1445-2197.1988.tb01051.x
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Intraperitoneal administration of the cytokine interleukin-1beta (IL-1beta) induces brain-mediated sickness symptoms that can be blocked by subdiaphragmatic vagotomy. Intraperitoneal IL-1beta also induces expression of the activation marker c-fos in vagal primary afferent neurons, suggesting that IL-1beta is a key component of vagally mediated immune-to-brain communication. The cellular sources of IL-1beta activating the vagus are unknown, but may reside in either blood or in the vagus nerve itself. We assayed IL-1beta protein after intraperitoneal endotoxin [lipopolysaccharide (LPS)] injection in abdominal vagus nerve, using both an ELISA and immunohistochemistry, and in blood plasma using ELISA. IL-1beta levels in abdominal vagus nerve increased by 45 min after LPS administration and were robust by 60 min. Plasma IL-1beta levels increased by 60 min, whereas little IL-1beta was detected in cervical vagus or sciatic nerve. IL-1beta-immunoreactivity (IR) was expressed in dendritic cells and macrophages within connective tissues associated with the abdominal vagus by 45 min after intraperitoneal LPS injection. By 60 min, some immune cells located within the nerve and vagal paraganglia also expressed IL-1beta-IR. Thus, intraperitoneal LPS induced IL-1beta protein within the vagus in a time-frame consistent with signaling of immune activation. These results suggest a novel mechanism by which IL-1beta may serve as a molecular link between the immune system and vagus nerve, and thus the CNS.
A previously healthy male aged 32 years with noticeably long extremities went into shock whilst straining to defaecate. He did not lose consciousness and reported pain high in the back and in the abdomen. Transoesophageal echocardiography revealed no abnormalities. Ultrasonography of the abdomen showed blood in the abdominal cavity, following which laparotomy was performed. An aneurysm of the splenic artery was found to have ruptured. The aneurysm and the spleen were removed. Morbid-anatomical examination showed no vascular abnormalities. The postoperative course was uneventful.
To explore the mechanism of immunosuppression associated with sepsis, we developed a murine model of sepsis-induced Pseudomonas aeruginosa pneumonia. CD-1 mice underwent either cecal ligation and 26-gauge needle puncture (CLP) or sham surgery, followed by the intratracheal (i.t.) administration of P. aeruginosa or saline. Survival in mice undergoing CLP followed 24 h later by the i.t. administration of saline or P. aeruginosa was 58% and 10%, respectively, whereas 95% of animals undergoing sham surgery followed by P. aeruginosa administration survived. Increased mortality in the CLP/P. aeruginosa group was attributable to markedly impaired lung bacterial clearance and the early development of P. aeruginosa bacteremia. The i.t. administration of bacteria to CLP-, but not sham-, operated mice resulted in an impressive intrapulmonary accumulation of neutrophils. Furthermore, P. aeruginosa challenge in septic mice resulted in a relative shift toward enhanced lung IL-10 production concomitant with a trend toward decreased IL-12. The i.p., but not i.t., administration of IL-10 Abs given just before P. aeruginosa challenge in septic mice significantly improved both survival and clearance of bacteria from the lungs of septic animals administered P. aeruginosa. Finally, alveolar macrophages isolated from animals undergoing CLP displayed a marked impairment in the ability to ingest and kill P. aeruginosa ex vivo, and this defect was partially reversed by the in vivo neutralization of IL-10. Collectively, these observations indicate that the septic response substantially impairs lung innate immunity to P. aeruginosa, and this effect is mediated primarily by endogenously produced IL-10.