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UNDERSTANDING THE MECHANISMS CONTROLLING LEISHMANIA AMAZONENSIS INFECTION IN VITRO: THE ROLE OF LTB4 DERIVED FROM HUMAN NEUTROPHILS.
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Abstract
Neutrophils are rapidly recruited to the site of Leishmania infection and play an active role in capturing and
killing parasites. They are the main source of leukotriene B4 (LTB4), a potent proinflammatory lipid mediator.
However, the role of LTB4 in neutrophil infection by Leishmania amazonensis is not clear. In this study, we show
that L. amazonensis or its lipophosphoglycan can induce neutrophil activation, degranulation, and LTB4 production.
Using pharmacological inhibitors of leukotriene synthesis, our findings reveal an LTB4-driven autocrine/
paracrine regulatory effect. In particular, neutrophil-derived LTB4 controls L. amazonensis killing,
degranulation, and reactive oxygen species production. In addition, L. amazonensis infection induces an
early increase in Toll-like receptor 2 expression, which facilitates parasite internalization. Nuclear factor
kappa B (NFkB) pathway activation represents a required upstream event for L. amazonensis–induced LTB4
synthesis. These leishmanicidal mechanisms mediated by neutrophil-derived LTB4 act through activation of
its receptor, B leukotriene receptor 1 (BLT1)
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