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Neutrophil modulation by Actinobacillus actinomycetemcomitans I. Chemotaxis, surface receptor expression and F‐actin polymerization
Author(s) -
Ashkenazi Malka,
White Robert R.,
Dennison David K.
Publication year - 1992
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/j.1600-0765.1992.tb01677.x
Subject(s) - chemotaxis , actinobacillus , cd18 , zymosan , chemotaxis assay , microbiology and biotechnology , biology , n formylmethionine leucyl phenylalanine , chemistry , receptor , integrin alpha m , flow cytometry , biochemistry , in vitro , bacteria , genetics
Localized juvenile periodontitis is an early onset periodontitis, usually localized to molars and incisors. Patients usually present with decreased chemotaxis of systemic neutrophils (PMNs) and infection with Actinobacillus actinomycetemcomitans . The pathogenic mechanisms involved have not been clarified. The purpose of this study was to determine if an extract of A. actinomycetemcomitans could induce changes in PMN chemotaxis similar to those reported in LJP patients. It was demonstrated that the bacterial extract was chemotactic for neutrophils. When neutrophils were pre‐incubated with the bacterial extract, chemotaxis toward zymosan‐activated serum, FMLP and the bacterial extract was inhibited in two different chemotaxis assays (Boyden chamber and under‐agarose). Bacterial extract had no effect on random migration in either assay. Pre‐incubation with the extract induced increased expression of CD11b/CD18 (Mac‐l), Gp110, and FMLP receptors and increased F‐actin polymerization following FMLP or PMA stimulation compared to cells not treated with the extract. Treatment of the bacterial extract with proteinase K or phenol extraction reversed the PMN chemotaxis inhibition activity, but increased significantly the random migration of PMNs. Heating the bacterial extract to 56°C had no effect on its activity. The component(s) in the bacterial extract that inhibits chemotaxis is therefore a protein(s), not sensitive to 56 C, and is not endotoxin. This study suggests that A. actinomycetemcomitans may contribute to the pathogenesis of localized juvenile periodontitis by inhibiting chemotaxis. Interference with chemotaxis by A. actinomycetemcomitans , however, occurs through a mechanism other than inhibition of actin assembly, reduction of CD1 lb/CD18 or Gp110 expression, or blockage/downregulation of FMLP receptors.