PLA2-II, which is abundant in intestinal crypts, may be important in inflammatory processes. PLA2-II is upregulated by cytokines, LPS and PAF, an endogenous mediator for endotoxin shock and gut injury. Here we examined the role of bacterial products (e.g., LPS) in PAF-induced PLA2-II activation by using germ free rats and antibiotic treated rats (mixture of neomycin, polymyxin B and metronidazole in drinking water for 7 days) to reduce gut flora. This protocol has been shown to protect against PAF-induced injury. Adult S.D. rats were injected with PAF (1.5 μg/kg, iv) which only caused transient hypotension and no gross bowel injury, and the small bowel was removed for PLA2-II assay at 30 min. We found that, compared with conventional rats, germ-free rats have lower baseline PLA2-II activity and did not show any increase of PLA2-II activity after PAF stimulation. However, antibiotics did not lower the basal PLA2-II activity and a similar increase of PLA2-II activity was seen in both conventional and antibiotic groups after PAF. Their B.P. and Hct responses were also similar. Thus, bacterial products may play a role in PLA2-II activation. Partially depleting gut flora, although alleviationg PAF-induced injury, had no effect on PLA2-II activation in the small intestine.
|Original language||English (US)|
|State||Published - Dec 1 1997|
ASJC Scopus subject areas
- Molecular Biology