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 demonstr ated that a single contact with heat killed E. Coli or Staphylococcus aureus increased the intraabdominal leukocyte influx in rats later cha llenged by these microorganisms. The aim of the present study was to i nvestigate some of the mechanisms of this phenomenon and to determine its effect on rats survival in an experimental model of peritonitis. T he intraabdominal influx of leukocytes following intraperitoneal injec tion of E. coli, Pseudomonas aeruginosa or Staphylococcus was stimulat ed by previous intraperitoneal injection of heat killed microbes. The phenomenon was not specific, pretreatment with E. Coli enhanced the in traperitoneal inflammatory reaction against Pseudomonas and vice versa . On the contrary, pretreating the rats with heat killed microorganism s specifically improved their survival after induction of peritonitis with live bacteria, there was no cross-protection. Heat killed staphyl ococcus aureus which stimulated a subsequent inflammatory reaction aga inst heat killed E. Coli had no effect on the mortality rates of E. Co li peritonitis. In conclusion, there is no direct relationship between resistance to peritonitis and the amount of leukocytes migrating into the abdominal cavity.