pylori interactions within a cellular biology context will undoubtedly be rewarding. Infection with H. pylori is known to lead to the release of many chemo- and cytokines; however, more comprehensive characterization of their individual roles is still required. Wong et al. [22] recent characterization of macrophage migration inhibitory factor (MIF) expression in mice infected

with H. pylori revealed that a negligible inflammatory response in H. pylori-infected MIF-deficient mice correlated with a substantially reduced inflammatory T-cell response, characterized by lower IFN-γ and TNF-α production. Inflammation in response to H. pylori infection may not only be induced by recruitment of leukocytes, selleck inhibitor but, alternatively, the induction of IL-1β by H. pylori neutrophil-activating protein (HP-NAP) may increase survival of inflammatory monocytes, and in turn neutrophils extending the local life time of these cells, as shown by Cappon

et al. [23]. Several studies have shed more light to the many facets of IL-1β in this infection, such as the loosening of tight junctions by disrupting claudin-4 [24], and the involvement of sonic hedge hog signaling in IL-1-dependent reduction in gastric acid output [25]. Thus, step-by-step, we are gaining an increased understanding of why the genetic background of IL-1/IL-1R impacts the course of H. pylori-triggered disease [26]. In recent years, the study of a novel selleckchem class of regulators, small RNAs, has gained momentum [27]. Small or micro RNAs (miR) are noncoding RNAs mostly transcribed by RNA polymerase II. They are processed by ribonucleases in the nucleus and further in the cytoplasm by the machinery that also generates small interfering RNAs and by other enzymes. The mature miRs (classified using a nomenclature of the kind medchemexpress miR followed by a number, e.g. miR-155) preferentially bind to complementary sequences in the 3′ UTRs of target mRNAs leading

to degradation or inhibition of translation. Depending on the target gene, this can affect multiple host cell processes, including cell development, differentiation, and even malignant transformation, possibly also gastric cancer [28]. Over 700 miR species are predicted from the human genome, and for a number of them a role in regulating expression of genes in cells of the immune system has been demonstrated (for recent review see [27]). Specific microarrays have been produced to detect miR sequences in samples of small RNAs to allow parallel assessment of miR expression. Matsushima et al. [29] used this technology to investigate signatures of 470 miRs in biopsies from Japanese H. pylori infected patients in comparison with non-infected controls. From a total of 242 miRs detected, 55 miRs showed differential abundance in these samples. Validation with another patient cohort revealed that the levels of 30 miRs were consistently decreased in infected patients.