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Innate lymphoid cell type 3-derived interleukin-22 boosts lipocalin-2 production in intestinal epithelial cells via synergy between STAT3 and NF-B
Karolinska Inst, Sweden.
Karolinska Inst, Sweden.
Karolinska Inst, Sweden.
Karolinska Inst, Sweden.
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2019 (English)In: Journal of Biological Chemistry, ISSN 0021-9258, E-ISSN 1083-351X, Vol. 294, no 15, p. 6027-6041Article in journal (Refereed) Published
Abstract [en]

Escherichia coli and Klebsiella pneumoniae are opportunistic pathogens that are commonly associated with infections at mucosal surfaces, such as the lung or the gut. The host response against these types of infections includes the release of epithelial-derived antimicrobial factors such as lipocalin-2 (LCN-2), a protein that specifically inhibits the iron acquisition of Enterobacteriaceae by binding and neutralizing the bacterial iron-scavenging molecule enterobactin. Regulation of epithelial antimicrobial responses, including the release of LCN-2, has previously been shown to depend on IL-22, a cytokine produced by innate lymphoid cells type 3 (ILC3) during Enterobacteriaceae infections. However, much remains unknown about the extent to which antimicrobial responses are regulated by IL-22 and how IL-22 regulates the expression and production of LCN-2 in intestinal epithelial cells (IECs). Our study demonstrates how IL-22-induced activation of STAT3 synergizes with NF-B-activating cytokines to enhance LCN-2 expression in human IECs and elucidates how ILC3 are involved in LCN-2-mediated host defense against Enterobacteriaceae. Together, these results provide new insight into the role of ILC3 in regulating LCN-2 expression in human IECs and could prove useful in future studies aimed at understanding the host response against Enterobacteriaceae as well as for the development of antimicrobial therapies against Enterobacteriaceae-related infections.

Place, publisher, year, edition, pages
American Society for Biochemistry and Molecular Biology, 2019. Vol. 294, no 15, p. 6027-6041
Keywords [en]
innate immunity; antimicrobial peptide (AMP); microbiology; mucosal immunology; signal transduction; interleukin-22; STAT3
National Category
Immunology
Identifiers
URN: urn:nbn:se:liu:diva-157216DOI: 10.1074/jbc.RA118.007290ISI: 000465077500033PubMedID: 30782844Scopus ID: 2-s2.0-85064338073OAI: oai:DiVA.org:liu-157216DiVA, id: diva2:1324390
Note

Funding Agencies|Swedish Research Council (Vetenskapsradet); Scandinavian Society for Antimicrobial Chemotherapy (SSAC); Groschinsky Foundation; Karolinska Institutet; German Research Foundation (Deutsche Forschungsgemeinschaft) [RA 2986/1-1]

Available from: 2019-06-13 Created: 2019-06-13 Last updated: 2019-06-18Bibliographically approved

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Lindforss, Ulrik
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Department of Clinical and Experimental MedicineFaculty of Medicine and Health Sciences
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