M along the lesser curvature (Fig. 7G) and, to a lesser extent, mGluR6 web inside the antrum (Fig. 7E) and fundus (Fig. 7F) of the stomach of Helicobacter-infected mice. Quantification of blue-stained metaplastic cells in 5 randomly selected high-power fields within the forestomach/stomach transition zone also highlighted the presence of mucous metaplasia inside the stomach of animals infected for 52 weeks with ASB1.four and SS1 but not in the noninfected controls (Fig. 7H).DISCUSSIONIn BALB/c mice infected with H. heilmannii ASB1.four and H. pylori SS1 for 52 weeks, MALT lymphoma-like lesions have been observed inside a narrow zone inside the fundus close to the forestomach/stomach transition zone. These pathological lesions may eventually cause gastric MALT lymphoma (12). The risk of building MALT lymphoma has been recommended to be higher in humans struggling with an NHPH gastritis than in those infected with H. pylori (15). Gastric MALT lymphoma is characterized by a powerful proliferation of B-lymphocytes, which may be dependent on Th2-type cytokines (15, 16). Experimental NHPH infections have certainly been shown to evoke a Th2-polarized response (14, 16), suggesting that Th2prone BALB/c mice (27) infected with NHPH is usually noticed as a important model for the development of MALT lymphoma induced by NHPH. It has been demonstrated that H. pylori strains mostly stimulate Th1 responses both in humans and in mouse models (28). Having said that, as an exception, the H. pylori strain SS1 doesn’t cause a substantial upregulation of gamma interferon (IFN-), a signature Th1 marker, in either BALB/c or C57BL/6 mice. Nevertheless, in frequent with other NHPH, it elicits a Th2 response in mice (17, 29). This may possibly clarify the development of MALT lymphoma-like lesions in the stomach noticed within this and also other research (29). Common for H. pylori strains inducing MALT lymphoma is that they lack genes encoding major virulence elements, for example a functional CagPAI, Bab, and Sab adhesins (30). H. pylori SS1 certainly lacks a functional CagPAI (17). This strain also doesn’t bind to the glycan structures Leb and sLex that are expressed by human gastric mucins (1, 3; also unpublished data). Binding to Leb and sLex has been shown to be mediated by the H. pylori BabA and SabA adhesins, respectively (1, three), suggesting that SS1 does not express these adhesins. These virulence factors, also as a functional CagPAI, are also absent in H. heilmannii and also other NHPH (314). Within this study, H. heilmannii ASB1.4 and H. pylori SS1 colonized both the antrum and fundus of the stomach but using a greater colonization Thrombopoietin Receptor web density in the antrum. This can be equivalent to what has been described in human patients. Certainly, in humans infected with NHPH, colonization primarily occurs in the antrum from the stomach but these bacteria could be found in the fundus at the same time, which has also been described for H. pylori (ten). Within the present study, H. heilmannii-infected BALB/c mice showed greater colo-nization prices within the antrum and fundus with the stomach than H. pylori-infected mice. This indicates that the capacity of ASB1.4 to persist inside the stomach of BALB/c mice is higher than that of SS1, which showed a reduction in colonization throughout the later stages of infection. The latter discovering has also been reported by Schmitz et al. (20). DNA from H. heilmannii ASB1.4 and H. pylori SS1 was also found within the duodenum. Because each species happen to be linked to duodenal ulcer illness (ten), it remains to become elucidated irrespective of whether they are able to colonize the duodenum or no matter whether the q.
