Gs, at the same time as in animals with chronic gastritis (10). In humans, this Helicobacter species has been linked with gastritis, gastric and duodenal ulcers, and low-grade mucosa-associated lymphoid tissue (MALT) lymphoma. It has been detected in 8 to 19 of gastric biopsy specimens with histological proof of NHPH infection (102). Living in close speak to with cats and dogs has been iden-Htified as a substantial risk factor for these infections in humans (10). Given that this species has only lately been isolated and cultured in vitro, facts on how H. heilmannii interacts with the human stomach and causes illness nevertheless remains poor. Comparative genomic analyses showed that despite the fact that the H. heilmannii genome includes several genes encoding homologues of known H. Dopamine Receptor Antagonist site pylori virulence components, it lacks a Cag pathogenicity island (CagPAI), too as genes encoding the vacuolating cytotoxin VacA and quite a few outer membrane proteins involved in the binding of H. pylori to the gastric mucosa, for example BabA/-B, SabA, AlpA/-B, OipA, HopZ, HopQ, and HomB (13). As a result, elements that contribute towards the colonization properties of H. heilmannii, specifically adhesion, stay to become identified. A recent infection study inside a Mongolian gerbil model for human Helicobacter-induced pathology showed variations in colonization capacity and virulence among distinct H. heilmannii strains isolated in the gastric mucosa of cats. These findings are most most likely also relevant for infection with this bacterium in humans (14). Unlike H. pylori, which is mostly observed at the surface epithelium and close to MUC1- and MUC5AC-producing cells (1, 3), H. heilmannii is Toll-like Receptor (TLR) Biological Activity mainly discovered within the gastric pits, as has also been described forReceived 2 April 2014 Accepted 12 May well 2014 Published ahead of print 27 May 2014 Editor: S. R. Blanke Address correspondence to Annemieke Smet, [email protected]. C.L. in addition to a.S. share 1st authorship. S.L. and F.H. share senior authorship. Supplemental material for this article could be located at http://dx.doi.org/10.1128 /IAI.01867-14. Copyright 2014, American Society for Microbiology. All Rights Reserved. doi:10.1128/IAI.01867-August 2014 Volume 82 NumberInfection and Immunityp. 3227iai.asm.orgLiu et al.iai.asm.orgInfection and ImmunityMuc13 and SPEM Induced by H. heilmannii Sensu Strictoother NHPH (14, 15). This bacterium could be identified in close association with parietal cells but can also be able to bind to human mucussecreting epithelial cells, too as to mucin samples containing extremely glycosylated MUC5AC and MUC6 (unpublished data). No matter whether an H. heilmannii infection has an effect around the distribution and expression in the gastric MUC1, MUC5AC, and MUC6 mucins is currently unknown. Specific-pathogen-free (SPF) inbred C57BL/6 and BALB/c mice happen to be shown to be helpful models for the study of Helicobacter-related human gastric illness (15). C57BL/6 mice have been described genetically as predominant Th1 responders, although BALB/c mice are primarily Th2 responders (15). It has been shown that infection with H. suis induces a predominant Th17/Th2 immune response in BALB/c mice and also in C57BL/6 mice inside the absence of a Th1 response, but with a far more pronounced inflammation in BALB/c mice (16). Extra not too long ago, it has been recommended that infection with H. heilmannii also elicits a Th2 immune response (14). These benefits are in contrast to the predominant Th17/Th1 response mainly seen for the duration of H. pylori infection in mice (16). Hence, within the presen.
