BACKGROUND: Lactobacilli are one of the probiotics and there is strong evidence for the efficacy of lactobacilli administration as a nonspecific immunostimulant in increasing host defense mechanisms. The present study tested the hypothesis that heat-killed Lactobacillus casei (LC9018) has a protective activity against fecal peritonitis. METHODS: Cecal ligation and tip resection (CLTR) induced fecal peritonitis was developed as a novel mouse model of abdominal sepsis, and the effects of LC9018 pretreatment on survival after CLTR, of the peritoneal exudate cells before or after CLTR and of bacterial growth in the peritoneal cavity after CLTR were investigated. RESULTS: Mortality after CLTR varied directly with the length of the opened bowel. To obtain a sublethal experimental group, the length of the opened bowel was fixed at 4 mm, where mortality was 87%, for further experiments. Survival of mice after CLTR was augmented in mice that had been pretreated intraperitoneally (ip) with LC9018 24 h previously. Viable bacterial growth in the peritoneal cavity was markedly inhibited in LC9018-pretreated mice. Peritoneal exudate cell accumulation observed 24 h after ip injection of LC9018 was significantly enhanced, suggesting that augmentation of the resistance of mice to CLTR was caused especially by the induction of polymorphonuclear cells. CONCLUSIONS: CLTR may provide a reproducible and simple murine model of bacterial sepsis and pretreatment with LC9018 developed a protective activity against CLTR surgery.
BACKGROUND: Lactobacilli are one of the probiotics and there is strong evidence for the efficacy of lactobacilli administration as a nonspecific immunostimulant in increasing host defense mechanisms. The present study tested the hypothesis that heat-killed Lactobacillus casei (LC9018) has a protective activity against fecal peritonitis. METHODS: Cecal ligation and tip resection (CLTR) induced fecal peritonitis was developed as a novel mouse model of abdominal sepsis, and the effects of LC9018 pretreatment on survival after CLTR, of the peritoneal exudate cells before or after CLTR and of bacterial growth in the peritoneal cavity after CLTR were investigated. RESULTS: Mortality after CLTR varied directly with the length of the opened bowel. To obtain a sublethal experimental group, the length of the opened bowel was fixed at 4 mm, where mortality was 87%, for further experiments. Survival of mice after CLTR was augmented in mice that had been pretreated intraperitoneally (ip) with LC9018 24 h previously. Viable bacterial growth in the peritoneal cavity was markedly inhibited in LC9018-pretreated mice. Peritoneal exudate cell accumulation observed 24 h after ip injection of LC9018 was significantly enhanced, suggesting that augmentation of the resistance of mice to CLTR was caused especially by the induction of polymorphonuclear cells. CONCLUSIONS: CLTR may provide a reproducible and simple murine model of bacterial sepsis and pretreatment with LC9018 developed a protective activity against CLTR surgery.
Authors: Misha D Luyer; Wim A Buurman; M'hamed Hadfoune; Gea Speelmans; Jan Knol; Jan A Jacobs; Cornelis H C Dejong; Aldwin J M Vriesema; Jan Willem M Greve Journal: Infect Immun Date: 2005-06 Impact factor: 3.441