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EFFECT OF BACTERIAL ERADICATION AND PROBIOTIC TREATMENT ON H. PYLORI-INDUCED INTESTINAL BARRIER DYSFUNCTION

P Bercik, EF Verdu, J Lu, H Sakai, T Tompkins, E Tsuchida, M Perdue, SM Collins
Intestinal Disease Research Program, McMaster University, Hamilton; Waseda University, Japan; Institute Lallamond, Montreal

BACKGROUND: We have previously shown that chronic H. pylori (Hp) infection in mice leads to long lasting altered gastric physiology, characterized by delayed gastric emptying and altered eating behavior. Here we investigate whether chronic Hp infection alters intestinal permeability and whether this is affected by bacterial eradication and probiotic therapy.
METHODS: Male Balb/c mice infected with Hp for at least 4 months were treated with antibiotics for 2 weeks and then gavaged daily for 2 weeks with Lacidofil (Lactobacillus rhamnosus and L. acidophilus) or placebo. Intestinal permeability was measured 2 months post eradication using an ex vivo jejunal loop. The intestinal segments were perfused arterially with oxygenated hemoglobin vesicles (artificial oxygen carrier) dispensed in a modified Krebs solution to maintain its structural and functional integrity. ⁵¹Cr-EDTA and ¹⁴C-mannitol were perfused luminally. Probe concentration in the venous outflow was measured using scintillation counter and expressed as a percentage of the luminal content. Gastric and jejunal tissue samples were taken and examined for presence of H. pylori, inflammation and mast cell counts.
RESULTS: Hp infection induced chronic gastritis but no overt inflammation was found in the small intestine. Jejunal mast cell counts were similar in uninfected and infected mice. Intestinal permeability for both probes was higher in Hp infected mice compared to uninfected controls. Permeability to ⁵¹Cr-EDTA ameliorated after bacterial eradication and further improved with Lacidofil treatment. Permeability to ¹⁴C-mannitol was not affected by either treatment. Data are presented as means ±SE, *p<0.05 vs uninfected.
                     

	Uninfected n=6	H. pylori  n=7	Eradicated placebo n=6	Eradicated Lacidofil n=7
51 Cr-EDTA	0.27 ± 0.07	0.57 ± 0.08 *	0.55 ± 0.15	0.43 ± 0.14
14 C-mannitol	0.63 ± 0.15	1.10 ± 0.10 *	1.15 ± 0.16 *	1.00 ± 0.10 *

In conclusion, chronic H. pylori infection in mice alters intestinal permeability and this may contribute to the generation of neuromuscular abnormalities by exposing the immune system to increased bacterial and food antigen load. Bacterial eradication and to a larger extent, probiotic treatment improves paracellular permeability to Cr-EDTA but does not affect membrane permeability to mannitol.
Supported by grants from Institute Lallamond and CIHR

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