Neutrophil infiltration does not contribute to the ulcerogenic effects of indomethacin in the rat gastric antrum.
We have previously suggested (Trevethick et al., Gut 34, 156-160) that indomethacin-induced ulceration of the rat gastric antrum may be a neutrophil-dependent process. Accordingly, in this study we have used an anti-neutrophil serum (ANS) to investigate the effects of neutrophil depletion on this pathology. In animals pretreated with the ANS to induce a nearly total neutropaenia, indomethacin-induced increases in blood neutrophilia and cell infiltration into the gastric antrum (assessed as LTB4 release ex vivo) were eliminated. In marked contrast, however, ANS pretreatment affected neither the area of mucosa damaged nor the microscopic characteristics or distribution of the lesions. These results suggest that, in contrast to the published reports examining indomethacin-induced ulceration of the gastric fundus, neutrophil infiltration is not involved in the pathogenesis of indomethacin-induced ulceration of the rat gastric antrum.
Trevethick
M A
MA
Biology Division, Glaxo Research and Development Ltd. Pharmacology, Ware, Herts, UK.
Bahl
A K
AK
Clayton
N M
NM
Strong
P
P
Sanjar
S
S
Harman
I W
IW
D000818:Animals; D005260:Female; D007213:Indomethacin / Q000633:toxicity*; D009504:Neutrophils / Q000187:drug effects / Q000502:physiology*; D011706:Pyloric Antrum / Q000187:drug effects* / Q000473:pathology; D011863:Radioimmunoassay; D051381:Rats; D017207:Rats, Sprague-Dawley; D013276:Stomach Ulcer / Q000139:chemically induced* / Q000473:pathology / Q000503:physiopathology
D007213:Indomethacin