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F. Franceschi [1] A.R. Sepulveda [2] A. Gasbarrini [3] G. Gasbarrini [3] D.Y. Graham [1] R.M. Genta [1] [13/05] [*] Cross-Reactivity between anti-CagA Antibodies and Vascular Antigens Objective: Several studies [...]

The variability of the mucosal damage induced by H. pylori may be related to both genetic characteristics of the host and virulence factors expressed by different strains. Aim: To characterize the effect of different H. pylori strains on the gastric mucosal changes induced in Mongolian gerbils (MG). Methods: Ten H. pylori isolates from infected individuals, the strain ATCC-43504 and the CagA and VacA-positive strain C20 isolated from a patient with gastric carcinoma were tested for their ability to infect MG. Two animals were infected with each isolate. H. pylori infection was assessed at 4 weeks after inoculation by histology. Results: Only the C20 strain resulted in consistent infection while another isolate showed mucosal colonization without inflammation. For this reason 40 4-week old male MG were infected with the C20 strain, while 40 controls were used as controls. Groups of 5 infected and 5 non-infected MG were sacrificed 1, 3, 6 and 10 months after inoculation. The stomach of each animal was processed for histology. One month after inoculation, all infected animals showed moderate to severe antral-restricted or -predominant active gastritis with lymphoid aggregates. At 3 months they showed severe chronic active gastritis, involving both antral and oxyntic mucosa. At 6 months they also showed multiple erosions. Three of 5 animals at 10 months showed penetrating ulcers. Intestinal metaplasia was focally present in the antrum of a few animals after 6 months. Neither dysplasia nor carcinomas developed. Conclusions: Successful H. pylori infection of MG results in a progressive disease of the antrum with later extension to the oxyntic mucosa accompanied by mucosal erosion and ulceration. Interestingly, only some H. pylori strains are able to induce an inflammatory response in MG; this finding suggests that the severity of the gastric mucosal lesions may be related to unique H. pylori strain virulence factors. [ABSTRACT FROM AUTHOR]

The impact of H. pylori on the nutritional status of infected subjects is not well understood yet. Intriguingly, H. pylori infection has been epidemiologically related to either obesity or growth retardation. Aim: To assess whether H. pylori infection may affect the weight gain (WG) in Mongolian gerbils (MG). Methods: 40 4-week old male MG were infected with the H. pylori strain C20; 40 control animals were used as controls. All MG were housed in polycarbonate cages and had free access to rodent food and water. Groups of 5 infected and 5 non infected MG were sacrificed l, 3, 6 and 10 months after inoculation. The stomach was processed for histology. The body weight of MG was assessed before inoculation and at the time of sacrifice. Results: The average WG of each group of animals at different times of follow ap were: Hp+ 27,4±4,5 vs Hp- 23,4±4,8 g at 1 month (p=ns); Hp+ 30,8±5,2 vs Hp- 30,2±4,9 g at 3 months (p=ns); Hp+ 28,2±4,3 vs Hp41,8±4,6 g at 6 months (p<0.05); Hp+ 23,8±4,6 vs Hp- 49,0±5,1 g at 10 months (p<0.001). Interestingly, WG of infected animals was inversely related to the severity of the histological damage. In particular, at 1 and 3 months all animals showed severe chronic active gastritis, at 6 months they also showed mucosal erosions and at 10 months 3 of 5 MG showed penetrating ulcers. None of the control animals showed either H. priori infection or inflammation. Conclusions: Infected animals show lower WG compared to the uninfected. This difference becomes statistically significant 6 months after inoculation and correlates with the severity of gastric mucosal damage. Pain and ulcer-related anorexia may explain this phenomenon. An increase of gastric leptin induced by the infection or an enhanced cytokine-related catabolism may possibly also be involved. [ABSTRACT FROM AUTHOR]