The levels of parotid salivary IgA and serum IgG antibodies from dental caries-resistant (CR) and caries-susceptible (CS) individuals to Streptococcus mutans antigens were determined. In general, the levels of salivary IgA and serum IgG antibodies to S. mutans antigens were significantly higher in CR subjects than in CS individuals. There were significantly higher levels of IgA2, but not IgA1, salivary antibodies to S. mutans whole cells in CR subjects than in CS individuals. These results led us to investigate the functional effects parotid saliva and sera containing these antibodies had on several factors associated with S. mutans virulence. Parotid saliva and sera from CR subjects significantly inhibited S. mutans growth, adherence, acid production, glucosyltransferase and glucose-phosphotransferase activities to a greater extent than saliva and sera from CS individuals. The data suggest that neutralization of S. mutans enzymes and inhibition of S. mutans virulence factors by saliva and serum may be responsible for the lower numbers of carious lesions in CR subjects.
Previous reports have indicated the association of periodontal diseases with elevated levels of serum immunoglobulin G (IgG) antibodies to periodontally relevant bacteria. Recent results from this laboratory suggest that enzymes proteolytic for immunoglobulins are important virulence factors of several periodontal bacteria. Specifically, enzymes from Porphyromonas (Bacteroides) gingivalis culture supernatant fluid (SF) cleaved human IgG (4 subclasses), IgA1 and IgA2, IgM, IgD and IgE. Proteolytic enzymes from Actinobacillus actinomycetemcomitans culture SF cleaved IgG, IgA and IgM. An enriched Ig proteolytic preparation from Capnocytophaga ochracea culture SF was shown to extensively cleave all 4 subclasses of human IgG. Extensive degradation of IgG and IgA in crevicular fluid samples on SDS-PAGE from periodontal disease sites of localized juvenile periodontitis (LJP) patients in comparison to little degradation in healthy sites indicated the potential role the proteolytic enzymes from periodontopathogenic bacteria may play in situ. Treatment of IgG with P. gingivalis, A. actinomycetemcomitans and C. ochracea SF resulted in similar patterns of degradation. LJP patients had significantly higher levels of IgG and IgA proteolytic activity in whole saliva than age-, sex-, and race-matched periodontal disease-free controls. However, not all of the proteolytic activity could be ascribed to bacterial proteases since neutrophils are also present in large numbers at diseased sites. Using similar techniques, lysates of neutrophils from healthy controls cleaved IgG, IgA and IgM. The observation of enhanced Ig cleavage activity in crevicular fluid and saliva in LJP patients suggest a role for Ig proteolytic enzymes in LJP.
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