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Microglia-released leukotriene B4 promotes neutrophil infiltration and microglial activation following intracerebral hemorrhage.

Abstract：

:Intracerebral hemorrhage (ICH) from blood vessel rupture results in parenchymal hematoma formation and neuroinflammation, ultimately leading to neurodegeneration. Several lines of evidence suggest that the severity of ICH-induced neural damage is exacerbated by infiltration of T-cells, monocytes, and especially neutrophils into the hematoma. Neutrophil migration is regulated by chemokines, formyl peptides, and leukotriene B4 (LTB4), a metabolite of arachidonic acid. In this study, we demonstrate that LTB4 is a key signaling factor promoting microglial activity and leukocyte infiltration into hematoma and thus a potentially critical determinant of ICH pathogenesis and clinical outcome. Lipidomic analysis revealed markedly increased LTB4 concentration in the hematoma-containing brain tissues 6-24 h after experimental ICH in mice. Expression of 5-lipoxygenase, a rate-limiting enzyme for LTB4 production, was upregulated in activated microglia and neutrophils within the hematoma following ICH. Treatment of cultured BV-2 microglia with thrombin, which is abundant in hematoma, promoted activation, proinflammatory cytokine expression, and LTB4 secretion. Further, conditioned medium from thrombin-stimulated BV-2 cells potentiated the transwell migration of neutrophil-like cells, a response blocked by a LTB4 receptor antagonist. These results suggest that arachidonic acid conversion to LTB4 following ICH contributes to neuroinflammation and ensuing neural tissue damage by inducing microglial activation and neutrophil recruitment.

journal_name

Int Immunopharmacol

journal_title

International immunopharmacology

authors

Hijioka M,Futokoro R,Ohto-Nakanishi T,Nakanishi H,Katsuki H,Kitamura Y

doi

10.1016/j.intimp.2020.106678

subject

Has Abstract

pub_date

2020-08-01 00:00:00

pages

106678

eissn

1567-5769

issn

1878-1705

pii

S1567-5769(20)30284-8

journal_volume

85

pub_type

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