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Mycobacterial granulomatous inflammation in the ulcerated caecum of indomethacin-treated rats
A Anthony1, A P Dhillon, H Fidler
1University Department of Histopathology, Royal Free Hospital School of Medicine, London, UK.
Abstract:
We report mycobacterial granulomatous inflammation in the ulcerated caecum of rats that received indomethacin. Two groups of male rats were treated with dietary indomethacin 3 mg/kg/day or untreated diet for 3 weeks. Six out of 8 indomethacin treated rats showed both ulceration and inflammation of the caecal mucosa. Two of the rats showing caecal ulceration also showed distinct granulomatous inflammation of the caecal mucosa and acid-fast bacilli were identified within granulomata. None of the other indomethacin treated or control rats contained acid-fast bacilli within caecal tissue sections but they were present, in the same sections, within the lumen of most rats in both groups. Polymerase chain reaction analysis identified the mycobacterial 65 kDa GroEL gene within control and granulomatous caecal tissue. In a repeat of indomethacin administration to a third group of rats, culture of both non-granulomatous caecal tissue (containing histologically identified luminal acid-fast bacilli) and faecal samples for mycobacteria was negative.
Insights
Indomethacin treatment induced caecal ulceration and inflammation in rats. Mycobacterial granulomatous inflammation was observed in some ulcerated tissues, with acid-fast bacilli identified within granulomata.
Area of Science:
- Gastroenterology
- Microbiology
- Pathology
Background:
- Non-steroidal anti-inflammatory drugs (NSAIDs) like indomethacin are known to cause gastrointestinal damage.
- The role of the gut microbiome, including mycobacteria, in NSAID-induced enteropathy is not fully understood.
Purpose of the Study:
- To investigate the pathological changes in the caecum of rats treated with indomethacin.
- To determine the presence and role of mycobacteria in indomethacin-induced caecal inflammation and ulceration.
Main Methods:
- Rats were administered dietary indomethacin (3 mg/kg/day) or an untreated diet for 3 weeks.
- Caecal tissues were examined histopathologically for ulceration and inflammation.
- Acid-fast bacilli were identified using staining techniques.
- Polymerase chain reaction (PCR) was used to detect the mycobacterial 65 kDa GroEL gene.
- Bacterial cultures were performed on caecal tissue and fecal samples.
Main Results:
- Six out of eight indomethacin-treated rats exhibited caecal ulceration and inflammation.
- Two rats with caecal ulceration also displayed granulomatous inflammation, with acid-fast bacilli identified within the granulomata.
- Acid-fast bacilli were present in the lumen of the caecum in both treated and control rats, but not within the tissue of non-granulomatous samples.
- The mycobacterial 65 kDa GroEL gene was detected by PCR in both control and granulomatous caecal tissues.
- Bacterial cultures for mycobacteria from non-granulomatous tissue and fecal samples were negative.
Conclusions:
- Indomethacin administration can lead to caecal ulceration and inflammation in rats.
- Mycobacterial presence within granulomatous inflammation in the caecum of indomethacin-treated rats suggests a potential role for these bacteria in the inflammatory process.
- Further research is needed to elucidate the specific mechanisms by which mycobacteria interact with NSAID-induced intestinal injury.