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Official websites use. Share sensitive information only on official, secure websites. This article was submitted to Infectious Diseases, a section of the journal Frontiers in Microbiology. The use, distribution or reproduction in other forums is permitted, provided the original author s and the copyright owner s are credited and that the original publication in this journal is cited, in accordance with accepted academic practice.
No use, distribution or reproduction is permitted which does not comply with these terms. Bacterial host tropism is a primary determinant of the range of host organisms they can infect.
Salmonella serotypes are differentiated into host-restricted and host-adapted specialists, and host-unrestricted generalists. In order to elucidate the underlying molecular mechanisms of host specificity in Salmonella infection, we investigated the role of the intestinal host cell receptor zymogen granule membrane glycoprotein 2 GP2 , which is recognized by FimH adhesin of type 1 fimbriae found in Enterobacteriaceae.
We compared four human and two porcine GP2 isoforms. FimH genes of Salmonella isolates were sequenced and the 10 identified FimH variants were compared regarding adhesion static adhesion assay and infection cell line assay using an isogenic model. By comparing all isoforms in the static adhesion assay, FimH variants were assigned to high, low or no-binding phenotypes.
However, cell line infection assays revealed fundamental differences: using HEp-2 cells, infection was also FimH variant-specific but mainly independent of human GP2. Salmonella specialists as well as generalists demonstrated similar binding to GP2. Future studies should focus on spatial distribution of GP2 isoforms in the human and porcine intestine, especially comparing health and disease. Zymogen granule membrane glycoprotein 2 GP2 , a microbiota-sensing and immune modulating molecule, contains an N-terminal signal peptide, an EGF-like domain, a zona pellucida domain, and a C-terminal glycosylphosphatidylinositol GPI -anchor Jovine et al.