It has also been shown that spermine can reduce the inflammatory

It has also been shown that spermine can reduce the inflammatory response by post-transcriptional inhibition of the production of pro-inflammatory cytokines, including TNFα, IL6, MIP-1α, and MIP-1β [19], and even though IL-8 was not included in this study, it is possible that it is regulated by spermine as well. Thus, in the interaction of wild type H. pylori with AGS cells, spermine levels may be elevated in the AGS cells, leading to a dampening of the chemokine/cytokine pro-inflammatory response. These possibilities await selleck screening library further in depth analyses. We performed pair-wise comparison of transcriptome on

the human adenocarcinoma CA4P manufacturer gastric cell line AGS after infection with 26695 wild type, its isogenic rocF- knockout mutant, and a rocF- complemented (rocF+) H. pylori strain, with uninfected AGS cells as a control. The first observation with the microarray analysis was an overall increase in the number of genes that participate in several signaling pathways previously investigated with H. pylori infection, notably with NFKB and AP-1 activation and mitogen-activated protein

kinase (especially ERKs, JNKs, SAPKs) [20], along with JUN-mediated signaling. From this activation cascade, the induction of IL-8 marked the greatest difference between the rocF- mutant H. pylori versus either the WT or the rocF + complemented strain. Our results show

a significant increase of mRNA and protein levels of IL-8 in AGS cells infected with the rocF- mutant strain, suggesting that WT bacteria may be able to control the inflammatory infiltration of immune cells by controlling the production of IL-8, which is a potent chemotactic factor for inflammatory cells, especially neutrophils [21–24]. While many H. pylori factors have been suggested to stimulate IL-8 expression, including peptidoglycan, LPS, CagA, VacA, PicB, IceA, urease (and even ammonia) [25–28], less is known about bacterial factors involved in suppression of cytokine production, especially in epithelial cells. Mechanisms for immune 17-DMAG (Alvespimycin) HCl evasion by H. pylori have been demonstrated, including the presence of a less potent LPS and cholesterol glycosylation [29]; however, fewer studies dealt with reduced host cytokine production as an immune suppressive mechanism, including effects on IL-12 [30–32]. While an increased amount of cytokines can result in histologically more intense gastritis [33], the limitation of this cytokine induction could be an advantage to the bacteria so that it can stay under the radar of the immune system. However, due to the complexity of the H.

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