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A low-morbidity murine model of peritonitis
Deborah Cooper1, Veronica Yao, Rosalie McCauley
1University Department of Surgery, Royal Perth Hospital and Fremantle Hospital, Western Australia, Australia.
Purpose:
Peritonitis continues to be a major source of mortality and morbidity in patients undergoing abdominal surgery. The aim of this study was to develop a nonfatal model of bacterial peritonitis in mice so that we could study aspects of the pathobiology and treatment of peritonitis in an in vivo model.
Methods:
Mice were inoculated via a midline laparotomy with 0.5 mg of zymosan in 0.1 ml of saline into the subomental space. At 24, 48, and 96 hours after treatment, animals were killed, and analysis was performed to determine the degree of peritoneal inflammation. End points included intraperitoneal cellular influx, tumor necrosis factor-alpha concentrations, and myeloperoxidase activity. In addition, peritoneal lavage fluid was plated onto blood agar for analysis of bacterial colony-forming units. There were 40 mice in each group.
Results:
There were no deaths in either group. Facultative Gram-negative bacteria were cultured from the peritoneal cavities of zymosan-treated animals at 24 and 48 hours after insult (colony-forming unit counts of 92+/-11 vs. 0 in control animals). In the zymosan-treated animals, there were significantly increased numbers of inflammatory cells (especially neutrophils) in the peritoneal cavity at 24 and 48 hours after treatment; these numbers returned to control levels by 96 hours. Myeloperoxidase activity was also elevated both in the peritoneal fluid (2.4 X 10(-4) units/ml compared with 1.6 x 10(-4) units/ml, P < 0.05) and in remote organs (i.e., lung, P < 0.05; liver, P < 0.001; and kidney, P < 0.05) at 24 hours after treatment. There was no significant difference in tumor necrosis factor-alpha levels between zymosan-treated and control mice in either serum or peritoneal fluid at any time point investigated. There was no mortality in either the zymosan-treated or control animals.
Conclusion:
In this model of bacterial peritonitis in mice, we have demonstrated how the peritoneal cavity can resolve a relatively localized inflammatory insult within 96 hours of induction. This response is characterized by a cellular influx of predominantly neutrophils and macrophages and by pronounced oxidative activity. We will use this in vivo model to characterize aspects of the pathobiology and treatment of peritonitis.
Insights
This study developed a nonfatal mouse model for bacterial peritonitis. The model demonstrated that the peritoneal cavity can resolve inflammation within 96 hours, characterized by neutrophil influx and oxidative activity.
Area of Science:
- Surgical pathology
- Immunology
- Infectious disease
Background:
- Peritonitis poses significant mortality and morbidity risks in surgical patients.
- Existing in vivo models often involve high mortality, limiting study of peritonitis pathobiology and treatment.
Purpose of the Study:
- To develop a nonfatal mouse model of bacterial peritonitis.
- To enable in-depth study of peritonitis pathobiology and therapeutic strategies.
Main Methods:
- Mice were inoculated with zymosan into the subomental space via laparotomy.
- Analysis included peritoneal cellularity, cytokine levels, myeloperoxidase activity, and bacterial cultures at 24, 48, and 96 hours.
- Forty mice were used per group.
Main Results:
- No mortality was observed in zymosan-treated or control groups.
- Facultative Gram-negative bacteria were cultured from peritoneal cavities at 24 and 48 hours post-insult.
- Significant neutrophil and macrophage influx into the peritoneal cavity occurred at 24 and 48 hours, resolving by 96 hours.
- Elevated myeloperoxidase activity was noted in peritoneal fluid and remote organs at 24 hours.
- Tumor necrosis factor-alpha levels remained unchanged.
Conclusions:
- A nonfatal mouse model of bacterial peritonitis was successfully established.
- The peritoneal cavity demonstrates resolution of localized inflammation within 96 hours.
- This resolution involves neutrophil/macrophage influx and oxidative activity, suitable for further pathobiological and treatment studies.