Peptic Ulcer Research Today is a free monthly online journal that collates and summarizes the latest research about Peptic Ulcer, including details on helicobacter pylori, diet, symptoms, treatment.

Lactobacillus rhamnosus GG exacerbates intestinal ulceration in a model of indomethacin-induced enteropathy.

Kamil R, Geier MS, Butler RN, Howarth GS

entre for Paediatric and Adolescent Gastroenterology, Children, Youth and Women's Health Service, 72 King William Road, North Adelaide, South Australia, Australia.

Lactobacillus rhamnosus GG (LGG) and Bifidobacterium lactis Bb12 (Bb12) were assessed for their potential to prevent indomethacin-induced ulceration in the small intestine of Sprague-Dawley rats. Rats were gavaged skim milk, LGG, or Bb12 twice daily for 14 days. Between days 7-14, rats were gavaged indomethacin (Indo; 6 mg/kg). At sacrifice, small intestine was scored for ulceration and sampled for histologic, immunohistochemical, and myeloperoxidase (MPO) analyses. Indo+LGG-treated rats exhibited a 2.3-fold increase in MPO activity and a 9.8-fold increase in ulceration area compared to Indo-treated controls; these parameters did not differ significantly between Indo+Bb12 and Indo-treated controls. Crypt cell apoptosis decreased by 82% in Indo+Bb12-treated and 55% in Indo+LGG-treated rats compared to Indo-treated controls. Proliferation increased by 209% in Indo+LGG-treated animals compared to Indo-treated controls. Bb12 did not reduce indomethacin-induced intestinal ulceration, whereas LGG actually increased some indicators of injury. LGG and Bb12, at the doses tested, cannot alleviate indomethacin-induced intestinal injury.

Published 18 April 2007 in Dig Dis Sci, 52(5): 1247-52.
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