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Abdominal Distension and Escherichia coli Peritonitis in Mice Lacking Myeloid Differentiation Factor 88
Linda K Johnson1, Antin Yn Widi2, Serrin Rowarth3
1College of Public Health, Medical and Veterinary Science, James Cook University, Townsville, Queensland, Australia. linda.johnson2@jcu.edu.au.
Abstract:
Here we describe the gross and microscopic findings of naturally occurring, β-hemolytic Escherichia coli peritonitis in B6.129-Myd88(tm1Aki) male and female mice. Over approximately 5 mo, 10 homozygous mutant mice deficient in myeloid differentiation factor 88 (C57BL/6 strain; male and female) that had not been used in research protocols developed rapid-onset abdominal swelling associated with copious viscous ascites. Each mouse developed an anterior peritonitis, primarily involving the parietal peritoneum and the visceral surface of the spleen, liver, diaphragm, and stomach. Inflammation was confined to the organ surfaces, with no indication of septicemia or grossly apparent gastrointestinal perforation or other tissue compromise that would initiate peritonitis. Peritonitis was likely attributable to compromised antibacterial innate immunity; cohoused, similarly immunodeficient littermates did not develop similar clinical signs. An unusual finding in all cases was mesothelial cell hyperplasia and hypertrophy. Although the underlying innate immune deficiency accounts for much of the observed pathology, the remarkable mesothelial cell morphology and the episodic nature of the peritonitis in some littermates and not others remain unexplained.
Insights
Mice lacking myeloid differentiation factor 88 (Myd88) developed Escherichia coli peritonitis due to compromised immunity. Unusual mesothelial cell changes were observed, but the exact cause remains unclear.
Area of Science:
- Immunology
- Microbiology
- Pathology
Background:
- Myeloid differentiation factor 88 (Myd88) is crucial for innate immune responses to bacterial infections.
- Deficiencies in Myd88 signaling can lead to increased susceptibility to pathogens.
- Peritonitis is inflammation of the peritoneum, often caused by bacterial infection.
Purpose of the Study:
- To describe the pathological findings of naturally occurring peritonitis in Myd88-deficient mice.
- To investigate the role of Myd88 in susceptibility to Escherichia coli-induced peritonitis.
- To characterize the gross and microscopic changes associated with this condition.
Main Methods:
- Observation of gross and microscopic findings in B6.129-Myd88(tm1Aki) mice over five months.
- Examination of peritoneal fluid and affected tissues.
- Comparison with cohoused, similarly immunodeficient littermates.
Main Results:
- Homozygous Myd88-deficient mice developed rapid abdominal swelling and ascites.
- Peritonitis primarily affected the parietal peritoneum and visceral surfaces of organs.
- Inflammation was localized, with no signs of septicemia or gastrointestinal perforation.
- Mesothelial cell hyperplasia and hypertrophy were consistently observed.
- Cohoused littermates did not develop similar clinical signs, suggesting a role for Myd88 deficiency.
Conclusions:
- Compromised antibacterial innate immunity due to Myd88 deficiency likely caused peritonitis.
- The observed mesothelial cell changes and episodic nature of the disease in some mice remain unexplained.
- Further research is needed to elucidate the mechanisms behind these findings.
