The possibility of inducing peritoneal inflammation in three murine species (gerbils, rats and mice) via the oral administration of indomethacin was investigated with the overall aim of developing an experimental animal model for human peritonitis. Gerbils given high doses of indomethacin at a rate of 30 mg and 40 mg/kg body weight showed swelling of the abdomen, depression and dyspnea within 4 days after the treatment. The severity of the clinical symptoms increased with time. The animals were confirmed as having developed peritonitis based on the pathological features including inflammation of the peritoneum, and fibrinous adhesion of the abdominal organs in the abdominal cavity. The severity of peritonitis increased with increasing dose of indomethacin, and was not related to the gender of the animal. On the other hand, peritoneal inflammation did not develop in the rats and mice even at high doses. Therefore, the administration of 30 mg/kg body weight of indomethacin is an effective and simple method of inducing peritonitis in 5-week-old Mongolian gerbils. The animal peritonitis model used in this study can be used as an effective tool for examining potential therapeutic compounds for preventing peritoneal damage during peritonitis, and provide insight into the pathophysiology of peritonitis.
Administration, Oral ; Animals ; Dose-Response Relationship, Drug ; Female ; *Gerbillinae ; Indomethacin/*administration&dosage/*toxicity ; Inflammation/chemically induced/pathology ; Male ; Mice ; Mice, Inbred ICR ; Peritonitis/*chemically induced/pathology ; Rats ; Rats, Sprague-Dawley ; Specific Pathogen-Free Organisms

Tuberculous liver abscesses are rare. Paradoxical response in tuberculosis is common and occurred between 2 weeks and 12 weeks after anti-tuberculous medication. We report here a case of tuberculous liver abscess that developed in a paradoxical response during chemotherapy for tuberculous peritonitis in a 23-year-old male. He was hospitalized, complaining of ascites, epigastric pain. He was diagnosed tuberculous peritonitis by expiratory laparoscopic biopsy and took medication for tuberculosis. After 2 months, a hepatic lesion was detected with CT scan incidentally. Chronic granulomatous inflammation was seen in ultrasound-guided liver biopsy, and tuberculous liver abscess was diasnosed. It was considered as paradoxical response, rather than treatment failure or other else because clinical symptoms of peritoneal tuberculosis and CT scan improved. After continuing initial anti-tuberculous medication, he was successfully treated. Herein, we report a case of tuberculous liver abscess as paradoxical response while treating peritoneal tuberculosis without changing anti-tuberculous treatment regimen.
Antitubercular Agents/*adverse effects/*therapeutic use ; DNA, Bacterial/analysis ; Humans ; Laparoscopy ; Liver/pathology/ultrasonography ; Liver Abscess/*chemically induced/*diagnosis/microbiology ; Male ; Mycobacterium tuberculosis/genetics/isolation & purification ; Necrosis/pathology ; Peritoneum/pathology ; Peritonitis, Tuberculous/*drug therapy ; Tomography, X-Ray Computed ; Tuberculosis/*diagnosis/microbiology ; Young Adult

Pannexin-1 (Panx1) forms nonselective large channel in cell plasma membrane and has been shown to be associated with NLRP3 inflammasome activation, ATP release and phagocytes recruitment. In the current study, by manipulation of Panx1 expression in human myeloid cells and application of Panx1 deficient mice, we failed to find a correlation between Panx1 and NLRP3 inflammasome activation, although an interaction between these two proteins was evident. However, in thioglycollate induced peritonitis, Panx1 deficient mice showed much more phagocytes infiltration. Further analyses showed that mice deficient for Panx1 exhibited enlarged F4/80(low)Gr1(-)Ly6C(-)cell population in the peritonea. Our study thus reveals an important role for Panx1 in regulation of peritoneal cell population and peritonitis development.
Animals ; Carrier Proteins ; metabolism ; Cell Line ; Connexins ; antagonists & inhibitors ; deficiency ; genetics ; metabolism ; HEK293 Cells ; Humans ; Inflammasomes ; metabolism ; Macrophages ; cytology ; metabolism ; Mice ; Mice, Inbred C57BL ; NLR Family, Pyrin Domain-Containing 3 Protein ; Nerve Tissue Proteins ; antagonists & inhibitors ; deficiency ; genetics ; metabolism ; Peritoneal Cavity ; cytology ; Peritonitis ; chemically induced ; metabolism ; pathology ; RNA Interference ; RNA, Small Interfering ; metabolism ; Thioglycolates ; toxicity