Absence of direct relationship between intraperitoneal cellular influx and resistance to experimental peritonitis.

Intraperitoneal inflammation is an essential defence mechanism against microbial invasion of the abdominal cavity. We have recently demonstrated that a single contact with heat killed E. Coli or Staphylococcus aureus increased the intraabdominal leukocyte influx in rats later challenged by these microorganisms. The aim of the present study was to investigate some of the mechanisms of this phenomenon and to determine its effect on rats survival in an experimental model of peritonitis. The intraabdominal influx of leukocytes following intraperitoneal injection of E. coli, Pseudomonas aeruginosa or Staphylococcus was stimulated by previous intraperitoneal injection of heat killed microbes. The phenomenon was not specific, pretreatment with E. Coli enhanced the intraperitoneal inflammatory reaction against Pseudomonas and vice versa. On the contrary, pretreating the rats with heat killed microorganisms specifically improved their survival after induction of peritonitis with live bacteria, there was no cross-protection. Heat killed staphylococcus aureus which stimulated a subsequent inflammatory reaction against heat killed E. Coli had no effect on the mortality rates of E. Coli peritonitis. In conclusion, there is no direct relationship between resistance to peritonitis and the amount of leukocytes migrating into the abdominal cavity.