Identification of a signaling cascade for interleukin-8 production by Helicobacter pylori in human gastric epithelial cells

The cytokine response in THP-1 (monocyte) and HL-60 (neutrophil-differentiated) cells infected with different genotypes of Helicobacter pylori strains

“…IL-8 plays a major role in gastric mucosal damage induced by H. pylori with its activator and chemotactic effects (24,25). IL-8 production starts when the cagPAI positive H. pylori strains interact with the gastric epithelium (26,27). IL-8 was secreted from the gastric epithelial cells infected with H. pylori and causes the recruitment of neutrophils to the gastric mucosa and subsequently pro-inflammatory cytokine production like IL-1β.…”

Rescue of Helicobacter pylori–Induced Cytotoxicity by Red Ginseng

“…Since stimulation of NF-κB does not require protein synthesis and it is utilized particularly rapidly in immune, inflammatory, and acute phase responses, where rapid activation of defense genes following exposure to pathogens can be critical for the survival of an organism (24,25,35), the involvement of NF-κB, one of the critical transcription factors involved in redox-and inflammation-associated changes, was measured by EMSA. Accumulating evidence indicates that H. pylori infection induces activation of the NF-κB transcription factor followed by increased IL-8 messenger RNA and protein levels (23,24,38), which can also regulate cellular growth responses, including apoptosis in AGS or MKN28. Moreover, Nozawa et al have recently demonstrated that stimulation of ERK pathways by H. pylori was directly responsible for activation of the NF-κB transcription factors and subsequent synthesis of IL-8 (38).…”

“…Accumulating evidence indicates that H. pylori infection induces activation of the NF-κB transcription factor followed by increased IL-8 messenger RNA and protein levels (23,24,38), which can also regulate cellular growth responses, including apoptosis in AGS or MKN28. Moreover, Nozawa et al have recently demonstrated that stimulation of ERK pathways by H. pylori was directly responsible for activation of the NF-κB transcription factors and subsequent synthesis of IL-8 (38). In the current experiment, we obtained important data showing that either the ERK signaling pathway or the transcriptional regulation of NF-κB was regulated by RGE pretreatment (Figure 3C), by which either the attenuation of IL-8 gene expression or the enhancement of gastric mucosal cell viability was achieved.…”

The importance of Helicobacter pylori in the development of gastric MALT lymphoma — induction of proliferation and immune suppression

“…The unphosphorylated CagA protein induces Erk1/2 kinase through an alternative Ras-Raf signalling pathway [2,16]. Both processes contribute to activating the NF-kB transcription factor and increased IL-8 expression [17]. Moreover, peptydoglycan fragments delivered through T4SS to host cells also activate NF-kB and increase IL-8 secretion by inducing Nod1 proteins (nucleotide-binding oligomerization domain 1) [18].…”

“…The transcription factor NF-kB controls B and T cells maturation and survival, exerting an anti-apoptotic effect on these cells [29]. Through CagA and peptidoglycan fragment translocation, H. pylori increases NF-kB activity which results in the host immune response being modulated, hyperproliferation of lymphocytes and the potential induction of GML [2,17,18]. Thereby, chronic or recurrent activation of the immune system by H. pylori can lead to lymphoid tissue growth.…”