We found a match
Your institution may have rights to this item. Sign in to continue.
- Title
Lack of Small Intestinal Dysbiosis Following Long-Term Selective Inhibition of Cyclooxygenase-2 by Rofecoxib in the Rat.
- Authors
Lázár, Bernadette; Brenner, Gábor B.; Makkos, András; Balogh, Mihály; László, Szilvia B.; Al-Khrasani, Mahmoud; Hutka, Barbara; Bató, Emese; Ostorházi, Eszter; Juhász, János; Kemény, Ágnes; László, Terézia; Tiszlavicz, László; Bihari, Zoltán; Giricz, Zoltán; Szabó, Dóra; Helyes, Zsuzsanna; Ferdinandy, Péter; Gyires, Klára; Zádori, Zoltán S.
- Abstract
Intestinal dysbiosis is linked to numerous gastrointestinal disorders, including inflammatory bowel diseases. It is a question of debate if coxibs, selective inhibitors of cyclooxygenase (COX)-2, cause dysbiosis. Therefore, in the present study, we aimed to determine the effect of long-term (four weeks) selective inhibition of COX-2 on the small intestinal microbiota in the rat. In order to avoid mucosal damage due to topical effects and inflammation-driven microbial alterations, rofecoxib, a nonacidic compound, was used. The direct inhibitory effect of rofecoxib on the growth of bacteria was ruled out in vitro. The mucosa-sparing effect of rofecoxib was confirmed by macroscopic and histological analysis, as well as by measuring the intestinal levels of cytokines and tight junction proteins. Deep sequencing of bacterial 16S rRNA revealed that chronic rofecoxib treatment had no significant influence on the composition and diversity of jejunal microbiota. In conclusion, this is the first demonstration that long-term selective inhibition of COX-2 by rofecoxib does not cause small intestinal dysbiosis in rats. Moreover, inhibition of COX-2 activity is not likely to be responsible per se for microbial alterations caused by some coxibs, but other drug-specific properties may contribute to it.
- Subjects
ROFECOXIB; INFLAMMATORY bowel diseases; CYCLOOXYGENASE inhibitors; BACTERIAL growth; TIGHT junctions; RATS
- Publication
Cells (2073-4409), 2019, Vol 8, Issue 3, p251
- ISSN
2073-4409
- Publication type
Article
- DOI
10.3390/cells8030251