Fosfomycin inhibits neutrophil function via a protein kinase C-dependent signaling pathway.

Abstract:

:We investigated effects of fosfomycin (FOM) on neutrophil function, specifically the oxidative burst and adhesion molecule expression (CD11b/CD18, or MAC-1) using flow cytometry assay. Preincubation of polymorphonuclear leukocytes (PMNL) with FOM from 1 to 100 microg/ml prior to stimulation by phorbol 12-myristate 13-acetate (PMA, 2 ng/ml) significantly suppressed the oxidative burst in a concentration-dependent manner. However, FOM did not affect the oxidative burst of PMNL stimulated by a chemotactic peptide, N-formyl-methionyl-leucyl-phenylalanine (FMLP). Stimulation with PMA (2 ng/ml) caused a rapid up-regulation of CD11b surface expression on PMNL, followed by time-dependent loss of this receptor. FOM also suppressed loss of CD11b in PMNL stimulated by PMA. FOM then inhibits the PMA-induced oxidative burst and CD11b epitope loss in PMNL. The suppressive effect appears to be mediated by the protein kinase C-dependent signaling pathway.

journal_name

Int Immunopharmacol

authors

Hamada M,Honda J,Yoshimuta T,Fumimori T,Okamoto M,Aizawa H

doi

10.1016/s1567-5769(01)00194-1

keywords:

subject

Has Abstract

pub_date

2002-03-01 00:00:00

pages

511-8

issue

4

eissn

1567-5769

issn

1878-1705

pii

S1567-5769(01)00194-1

journal_volume

2

pub_type

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