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. 1988 Jan;56(1):267–269. doi: 10.1128/iai.56.1.267-269.1988

Stimulation of superoxide and lactoferrin release from polymorphonuclear leukocytes by the type 2 fimbrial lectin of Actinomyces viscosus T14V.

A L Sandberg 1, L L Mudrick 1, J O Cisar 1, J A Metcalf 1, H L Malech 1
PMCID: PMC259267  PMID: 2891619

Abstract

Polymorphonuclear leukocyte (PMN)-dependent destruction of Actinomyces viscosus T14V is initiated by the recognition of galactose-containing receptors on sialidase-treated PMNs by the lectin associated with the type 2 fimbriae of these bacteria. A. viscosus T14V also stimulates the respiratory burst in PMNs as well as the release of contents of the secondary granules, as determined by the presence of lactoferrin in the culture supernatants. Under the experimental conditions employed, these bacteria do not induce the release of beta-glucuronidase, a constituent of primary granules. None of the three PMN responses studied occurs in cultures containing a mutant of A. viscosus T14V that lacks fimbriae. Activation of the PMNs is mediated by the lectin associated with the type 2 fimbriae, as demonstrated by the finding that beta-linked galactosides inhibit stimulation of the respiratory burst. Thus, the interaction of the Actinomyces fimbrial lectin with its complementary receptors on PMNs results not only in killing of these bacteria but also in the release of reactive oxygen intermediates and enzymes that may be detrimental to surrounding host tissues.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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