English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

Helicobacter pylori  is a gram-negative, microaerophilic, and spiral-shaped bacterium and causes gastrointestinal diseases in human. IL-1β is a representative cytokine produced in innate immune cells and is considered to be a key factor in the development of gastrointestinal malignancies. However, the mechanism of IL-1β production by neutrophils during  H. pylori  infection is still unknown. We designed this study to identify host and bacterial factors involved in regulation of  H. pylori -induced IL-1β production in neutrophils. We found that  H. pylori -induced IL-1β production is abolished in NLRP3-, ASC-, and caspase-1/11-deficient neutrophils, suggesting essential role for NLRP3 inflammasome in IL-1β response against  H. pylori . Host TLR2, but not TLR4 and Nod2, was also required for transcription of NLRP3 and IL-1β as well as secretion of IL-1β.  H. pylori  lacking  cagL , a key component of the type IV secretion system (T4SS), induced less IL-1β production in neutrophils than did its isogenic WT strain, whereas  vacA  and  ureA  were dispensable. Moreover, T4SS was involved in caspase-1 activation and IL-1β maturation in  H. pylori -infected neutrophils. We also found that FlaA is essential for  H. pylori -mediated IL-1β production in neutrophils, but not dendritic cells. TLR5 and NLRC4 were not required for  H. pylori -induced IL-1β production in neutrophils. Instead, bacterial motility is essential for the production of IL-1β in response to  H. pylori . In conclusion, our study shows that host TLR2 and NLRP3 inflammasome and bacterial T4SS and motility are essential factors for IL-1β production by neutrophils in response to  H. pylori .

frontiers in immunology

Unveiling the Crucial Role of Type IV Secretion System and Motility of Helicobacter pylori in IL-1β Production via NLRP3 Inflammasome Activation in Neutrophils