Erythromycin and roxithromycin potentiate human neutrophil locomotion in vitro by inhibition of leukoattractant-activated superoxide generation and autooxidation.

doi:10.1093/INFDIS/159.5.966

Paper

Erythromycin and roxithromycin potentiate human neutrophil locomotion in vitro by inhibition of leukoattractant-activated superoxide generation and autooxidation.

Published May 1, 1989 · R. Anderson

The Journal of infectious diseases

Q1 SJR score

151

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3

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Abstract

Erythromycin and especially roxithromycin (1.25-20 micrograms/mL) stimulated neutrophil migration in vitro. Both antibiotics selectively inhibited superoxide generation by neutrophils activated with the N-formylated leukotactic tripeptide FMLP, the calcium ionophore A23187 and the pharmacologic agent benoxaprofen, while the responses initiated by the tumor promotor PMA and opsonized zymosan were unaffected. Neutrophil autooxidation during exposure to FMLP was also decreased by both antibiotics. The antimicrobial agents did not scavenge superoxide. Likewise, the interactions of [3H]FMLP with specific receptors on neutrophils, FMLP-activated degranulation and intracellular calcium fluxes, the activity of cytosolic protein kinase C and the release of [3H]arachidonate from calcium ionophore-stimulated neutrophils were all unaffected by the antibiotics. Erythromycin and roxithromycin in particular appear to enhance neutrophil migration by an antioxidant mechanism that is not due to inhibition of transductional events involved in the activation of NADPH-oxidase or to oxidant scavenging properties.

In Vitro Study

Highly Cited

Study Snapshot

Erythromycin and roxithromycin enhance neutrophil migration in vitro by inhibiting superoxide generation and autooxidation, without affecting NADPH-oxidase activation or oxidant scavenging properties.

PopulationOlder adults (50-71 years)

Sample size24

MethodsObservational

OutcomesBody Mass Index projections

ResultsSocial networks mitigate obesity in older groups.

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Paper

Erythromycin and roxithromycin potentiate human neutrophil locomotion in vitro by inhibition of leukoattractant-activated superoxide generation and autooxidation.

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References

Apparent involvement of phospholipase A2, but not protein kinase C, in the pro-oxidative interactions of clofazimine with human phagocytes.

Clofazimine's pro-oxidative interactions with human phagocytes may contribute to its intraphagocytic antimycobacterial activity, but its effect on protein kinase C remains unclear.

Promotion of DNA strand breaks in cocultured mononuclear leukocytes by protein kinase C-dependent prooxidative interactions of benoxaprofen, human polymorphonuclear leukocytes, and ultraviolet radiation.

Benoxaprofen can promote carcinogenic prooxidative interactions between phagocytes, UV radiation, and certain pharmacological agents, potentially causing DNA damage undetectable by conventional mutagenicity tests.

Benoxaprofen activates membrane‐associated oxidative metabolism in human polymorphonuclear leucocytes by apparent modulation of protein kinase C

Benoxaprofen activates membrane-associated oxidative metabolism in human polymorphonuclear leucocytes by activating protein kinase C.

Erythromycin-induced suppression of pulmonary antibacterial defenses. A potential mechanism of superinfection in the lung.

Erythromycin can suppress pulmonary antibacterial defenses, potentially leading to superinfections in respiratory patients.

Charge-dependent regulation of NADPH oxidase activity in guinea-pig polymorphonuclear leukocytes.

NADPH oxidase activation in guinea-pig polymorphonuclear leukocytes is regulated by membrane charges, suggesting a reaction(s) involved in respiratory burst initiation.

Citations