Role of leukotoxin in the phagocytosis and killing of actinobacillus actinomycetemcomitans by localized aggressive periodontitis neutraphils
Date
2001
DOI
Authors
Dagher, Maroun F.
Version
OA Version
Citation
Abstract
Localized Aggressive Periodontitis (LAP), previously called Localized Juvenile Periodontitis (LJP), is a unique form of periodontal disease with circumpubertal onset characterized by bone loss localized to first molars and incisors. In LAP, neutrophils exhibit a number of functional abnormalities such as depressed chemotaxis. Actinobacillus actinomycetemcomitans (A. a.) is a gram-negative capnophilic coccobacillus implicated in the pathogenesis of LAP. A. a. produces an 115KDa heat-labile leukotoxin, which lyses human neutrophils. However, infected patients rapidly produce neutralizing antibody to the leukotoxin (Kalmar et al., 1987), so its role beyond initial colonization is questionable. Previous reports by Kalmar et al., suggested that although neutrophils from LAP patients phagocytose A. a., they do not kill the ingested A. a. normally. The purpose of the study was to investigate the role of leukotoxin in the phagocytosis and killing of A. actinomycetemcomitans. In this study, chemotaxis, phagocytosis and killing were assessed in LAP. Two different strains of A. actinomycetemcomitans were used; a low producer of leukotoxin (Y4), and a high producer of leukotoxin (JP2). Bacteria were either not opsonized or opsonized with control serum, or immune (LAP) serum. The results revealed that overall, chemotaxis of neutrophils among LAP patients was less than 70% of chemotaxis of neutrophils among matched controls. The phagocytosis and killing assay demonstrated that in the presence of serum (Control, or LAP), the percentage of phagocytosing neutrophils was increased, and both sera (Control and LAP) increased killing of A. a by neutrophils. More specifically, in the presence of LAP serum, the percentage of phagocytosing neutrophils, and the number of phagocytosed bacteria were increased for both control neutrophils and LAP neutrophils. The JP2 strain (high leulotoxin) was not phagocytosed as well as strain Y4 (low leukotoxin), suggesting a role for leukotoxin in inhibition of phagocytosis, However, killing of A. a. by neutrophils (Control or LAP) increased with time, regardless of which strain was used.
In summary, all LAP patients exhibited neutrophil chemotaxis abnormalities. Both control and LAP neutrophils phagocytosis of JP2 was reduced compared to Y4, but no abnormality of killing of either strain by LAP neutrophils was demonstrable.
Description
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Thesis (M.Sc.D)--Boston University, Henry M. Goldman School of Dental Medicine, 2001 (Periodontology and Oral Biology).
Includes bibliographical references (leaves 47-55).
Thesis (M.Sc.D)--Boston University, Henry M. Goldman School of Dental Medicine, 2001 (Periodontology and Oral Biology).
Includes bibliographical references (leaves 47-55).
License
This work is protected by copyright. Downloading is restricted to the BU community. If you are the author of this work and would like to make it publicly available, please contact open-help@bu.edu.