Campylobacter jejuni induces differentiation of human neutrophils to the CD16hi/CD62Llo subtype. Issue 6 (22nd July 2022)

• Record Type: Journal Article
• Authors: Dolislager, Carolina G.; Callahan, Sean M.; Donohoe, Dallas R.; Johnson, Jeremiah G.
• Is Part Of: Journal of leukocyte biology. Volume 112:Issue 6(2022)
• Page Start: 1457
• Page End: 1470
• Publication Date: 2022-07-22
• Subjects: NF‐κB -- Campylobacter -- colonocyte -- hypoxia‐inducible factor -- neutrophil -- T cell; Leucocytes -- Periodicals; Reticulo-endothelial system -- Periodicals; 571.96
• DOI: 10.1002/JLB.4A0322-155RR
• Languages: English
• ISSNs: 0741-5400

Abstract

Abstract: The discovery of neutrophil subtypes has expanded what is known about neutrophil functions, yet there is still much to learn about the role of these subtypes during bacterial infection. We investigated whether Campylobacter jejuni induced differentiation of human neutrophils into the hypersegmented, CD16 hi /CD62L lo subtype. In addition, we investigated whether C. jejuni ‐dependent differentiation of this neutrophil subtype induced cancer‐promoting activities of human T cells and colonocytes, which were observed in other studies of hypersegmented, CD16 hi /CD62L lo neutrophils. We found that C. jejuni causes a significant shift in human neutrophil populations to the hypersegmented, CD16 hi /CD62L lo subtype and that those populations exhibit delayed apoptosis, elevated arginase‐1 expression, and increased reactive oxygen species production. Furthermore, incubation of C. jejuni ‐infected neutrophils with human T cells resulted in decreased expression of the ζ‐chain of the TCR, which was restored upon supplementation with exogenous l ‐arginine. In addition, incubation of C. jejuni‐ infected neutrophils with human colonocytes resulted in increased HIF‐1α stabilization and NF‐κB activation in those colonocytes, which may result in the up‐regulation of protumorigenic genes. Graphical Abstract: Campylobacter jejuni infection of neutrophils results in differentiation of a subtype which activates HIF‐1 and NF‐κB in colonocytes and decreases TCRζ in T cells.