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BioMed Research International
Volume 2017, Article ID 2014583, 8 pages
https://doi.org/10.1155/2017/2014583
Research Article

Early Production of the Neutrophil-Derived Lipid Mediators LTB4 and LXA4 Is Modulated by Intracellular Infection with Leishmania major

Department of Infectious Diseases and Microbiology, University of Lübeck, Lübeck, Germany

Correspondence should be addressed to Tamás Laskay; ed.hsku@yaksal.samat

Received 24 May 2017; Revised 22 August 2017; Accepted 12 September 2017; Published 18 October 2017

Academic Editor: Remo Lobetti

Copyright © 2017 Michael Plagge and Tamás Laskay. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Recruitment of neutrophil granulocytes to sites of infectious tissue damage is an early event in innate immune responses. Following chemotactic signals neutrophils establish a first line of defense in a swarm-like manner. Intracellular pathogens such as Leishmania major can, however, evade neutrophil-mediated killing and survive inside neutrophils. To achieve this the parasites evolved potent evasion mechanisms. Since neutrophils are a major source of inflammation regulating lipid mediators, we hypothesized that intracellular infection modifies the release of pro- and anti-inflammatory lipid mediators like leukotriene B4 (LTB4) and lipoxin A4 (LXA4), respectively. In the present study, we demonstrated in vitro that L. major-infected primary human neutrophils release an increased amount of LTB4, whereas LXA4 liberation is reduced during the first hours of infection. To investigate whether lipid mediator modulation is a common feature in intracellular infections, we tested the impact of an infection with Anaplasma phagocytophilum. Similarly to L. major, neutrophil infection with A. phagocytophilum led to an enhanced release of LTB4 and decreased LXA4 production. Together, our findings indicate that intracellular infections modulate the lipid mediator profile of neutrophils. This effect is likely to contribute to the survival of the pathogens in neutrophils and to the outcome of the infections.