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Induction of neutrophil extracellular traps by Campylobacter jejuni.
Authors Callahan S, Doster RS, Jackson JW, Kelley BR, Gaddy JA, Johnson JG
Submitted By Submitted Externally on 5/28/2020
Status Published
Journal Cellular microbiology, REFERENCES
Year 2020
Date Published 4/1/2020
Volume : Pages Not Specified : e13210
PubMed Reference 32329205
Abstract Campylobacter jejuni is the leading cause of bacterial-derived gastroenteritis
worldwide and can lead to several post-infectious inflammatory disorders.
Despite the prevalence and health impacts of the bacterium, interactions between
the host innate immune system and C. jejuni remain poorly understood. To expand
on earlier work demonstrating that neutrophils traffic to the site of infection
in an animal model of campylobacteriosis, we identified significant increases in
several predominantly neutrophil-derived proteins in the faeces of C.
jejuni-infected patients, including lipocalin-2, myeloperoxidase and neutrophil
elastase. In addition to demonstrating that these proteins significantly
inhibited C. jejuni growth, we determined they are released during formation of
C. jejuni-induced neutrophil extracellular traps (NETs). Using quantitative and
qualitative methods, we found that purified human neutrophils are activated by
C. jejuni and exhibit signatures of NET generation, including presence of
protein arginine deiminase-4, histone citrullination, myeloperoxidase,
neutrophil elastase release and DNA extrusion. Production of NETs correlated
with C. jejuni phagocytosis/endocytosis and invasion of neutrophils suggesting
that host- and bacterial-mediated activities are responsible for NET induction.
Further, NET-like structures were observed within intestinal tissue of C.
jejuni-infected ferrets. Finally, induction of NETs significantly increased
human colonocyte cytotoxicity, indicating that NET formation during C. jejuni
infection may contribute to observed tissue pathology. These findings provide
further understanding of C. jejuni-neutrophil interactions and inflammatory
responses during campylobacteriosis.


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