Chronic peroral immunization of conventional laboratory rats with mutans streptococci leads to stable acquired suppression of salivary antibodies

Riviere, George R.; Wagoner, Murriel A.; Freeman, I. L.

doi:10.1111/j.1399-302x.1992.tb00526.x

Cited by 6 publications

(9 citation statements)

References 9 publications

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“…In the present study, whole bacterial cells were used as antigens, and consequently the ELISA readings may have been the result of antibody reactions with many different antigens. It is possi-Age-related saliva antibodies 61 ble that antibodies to irrelevant antigens may dominate those reacting with antigens involved in colonization and pathogenesis and salivary antibody responses to whole cells may have differed from those when measured against extracted antigens (23). On the other hand, the use of purified antigens may not represent relevant pathogenic mechanisms (5).…”

Section: Discussionmentioning

confidence: 99%

Age‐related changes in salivary antibodies to commensal oral and gut biota

Percival

Marsh

Challacombe

1997

Oral Microbiology and Immunology

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The prevalence of mucosally derived infections appears to increase with age, suggesting dysfunction at the mucosal surfaces. The present investigation was undertaken to examine any age-related changes in secretion rates and concentrations of secretory antibodies in whole and parotid saliva in a healthy adult population. A total of 116 subjects were subdivided into the following age groups: 20-39 years, 40-59 years, 60-79 years and 80 years and over. Specific immunoglobulin A (IgA), IgG and IgM antibodies in whole and parotid saliva to Streptococcus mutans (serotype c), Actinomyces viscosus NCTC 10951, and Escherichia coli NCTC 10418 were quantified by enzyme-linked immunosorbent assay. IgA antibodies to all three organisms examined increased with age in both whole and parotid saliva, whereas IgG antibody levels to S. mutans in whole saliva were significantly decreased with age. IgG antibodies to E. coli in parotid saliva were reduced in older age groups. IgM antibody levels to S. mutans were reduced with age in both secretions, whereas IgM antibodies to A. viscosus were greatest in the oldest age groups. No significant changes with age were observed in salivary IgM antibody levels to E. coli. No significant reduction in the secretion rates of IgA antibodies were observed in parotid or whole saliva, whereas IgG and IgM antibody secretion rates to all three microorganisms were reduced in most age groups in both whole and parotid saliva. The results of this investigation have demonstrated age-related changes with salivary antibodies, but, whereas salivary IgG and IgM antibodies showed decreases, salivary IgA levels generally increased with age. This suggests that the ability to form IgA antibody responses is not impaired with increased age, and that secretion rates and functional properties of antibodies may be as important as concentrations in protection against mucosal infective diseases.

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Section: Discussionmentioning

confidence: 99%

Age‐related changes in salivary antibodies to commensal oral and gut biota

Percival

Marsh

Challacombe

1997

Oral Microbiology and Immunology

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“…As stated earlier, there is evidence that the host is more tolerant to autochthonous than allochthonous bacteria (115,281). The chronic exposure of the host immune system to resident bacteria may result in the suppression of the antibody response (391,392,433). Riviere et al (391,392) demonstrated that primary oral immunization with S. mutans may induce SIgA antibodies in rats but that continued exposure to S. mutans whole cells led to progressive suppression of the SIgA response and the level of salivary IgA antibodies returned to baseline (391,392).…”

Section: Active Immunization Against Oral Diseasesmentioning

confidence: 92%

“…Most studies on inducing salivary IgA against mutans streptococci to confer protection against dental caries have been performed in rodents ( Table 7). Different antigen preparations were used for immunization and include whole cells (245,321,331,333,341,392,479), cell walls (331,332), glucosyltransferase (448-450, 480, 482), surface proteins (100,214,382,409,516,534), ribosomal preparations (172), synthetic peptides In general, immunization with whole cells gives rise only to salivary IgA antibodies while immunization with soluble antigens and adjuvant, which render the antigens particulate, may also lead to an increase in the level of antibodies in serum. (260), and anti-idiotypic antibodies (207).…”

Section: Active Immunization Against Oral Diseasesmentioning

confidence: 99%

“…Only Hajishengallis et al (184,185) were able to induce a SIgA response that persisted for at least 11 months by oral immunization of mice with a chimeric protein in which the toxic A1 subunit of cholera toxin had been genetically replaced by a 42-kDa segment representing the saliva-binding region of antigen I/II. In most of the studies, a second immunization procedure resulted in a faster but generally not in a greater or longer response than did the primary immunization (78,129,185,262,272,391,392,409,443,534). Only a few studies demonstrated an anamnestic SIgA response against mutans streptococcal antigens in rodents (516) and humans (170,325).…”

Section: Active Immunization Against Oral Diseasesmentioning

confidence: 99%

“…Experiments with animal models showed that salivary IgA induced against Streptococcus mutans leads to a reduction in the colonization of this bacterium and to the prevention of caries (328). More recent studies indicate that the immunity is not maintained (392). IgA-deficient humans were found to be more or less susceptible to caries and periodontal diseases (90,393,394).…”

Section: Introductionmentioning

confidence: 99%

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Oral Microbial Ecology and the Role of Salivary Immunoglobulin A

Marcotte¹,

Lavoie

1998

Microbiol Mol Biol Rev

439

294

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SUMMARY In the oral cavity, indigenous bacteria are often associated with two major oral diseases, caries and periodontal diseases. These diseases seem to appear following an inbalance in the oral resident microbiota, leading to the emergence of potentially pathogenic bacteria. To define the process involved in caries and periodontal diseases, it is necessary to understand the ecology of the oral cavity and to identify the factors responsible for the transition of the oral microbiota from a commensal to a pathogenic relationship with the host. The regulatory forces influencing the oral ecosystem can be divided into three major categories: host related, microbe related, and external factors. Among host factors, secretory immunoglobulin A (SIgA) constitutes the main specific immune defense mechanism in saliva and may play an important role in the homeostasis of the oral microbiota. Naturally occurring SIgA antibodies that are reactive against a variety of indigenous bacteria are detectable in saliva. These antibodies may control the oral microbiota by reducing the adherence of bacteria to the oral mucosa and teeth. It is thought that protection against bacterial etiologic agents of caries and periodontal diseases could be conferred by the induction of SIgA antibodies via the stimulation of the mucosal immune system. However, elucidation of the role of the SIgA immune system in controlling the oral indigenous microbiota is a prerequisite for the development of effective vaccines against these diseases. The role of SIgA antibodies in the acquisition and the regulation of the indigenous microbiota is still controversial. Our review discusses the importance of SIgA among the multiple factors that control the oral microbiota. It describes the oral ecosystems, the principal factors that may control the oral microbiota, a basic knowledge of the secretory immune system, the biological functions of SIgA, and, finally, experiments related to the role of SIgA in oral microbial ecology.

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Salivary IgA subclasses and bacteria‐reactive IgA in patients with aggressive periodontitis

Hägewald¹,

Bernimoulin²,

Köttgen

et al. 2002

J of Periodontal Research

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The local salivary immunoglobulin A (IgA) response in patients with aggressive periodontitis to oral microorganisms and its role for the pathogenesis has not been determined. This study investigated the hypothesis that aggressive periodontitis patients have impaired oral secretory immunity. Our test group was made-up of 19 aggressive periodontitis patients and 19 age- and gender-matched periodontally healthy controls. Total IgA, IgA subclass 1, IgA subclass 2 and IgA reactive to Actinobacillus actinomycetemcomitans Y4, Treponema denticola ATCC 35404 and Candida albicans DSM 3454 were determined by enzyme-linked immunosorbent assay in whole unstimulated and stimulated saliva. A statistically significantly lower concentration and secretion rate of total salivary IgA (P < 0.01) and IgA1 (P < 0.001) was found in the aggressive periodontitis group in resting and stimulated saliva. A decrease of IgA2 (P < 0.05) was seen in resting saliva. Although only minor differences were detected in the concentration and secretion of bacteria-reactive IgA in both groups, the proportion of bacteria-reactive IgA from the total IgA was significantly higher (P < 0.01) in the aggressive periodontitis group in all three microorganisms tested. Our results indicate an inhibition of total secretory IgA. In particular an IgA subclass 1-specific decrease in aggressive periodontitis was noted, while the bacteria-reactive humoral immune system in saliva was activated. The role of the decrease of IgA1 immunoglobulins in aggressive periodontitis with respect to susceptibility for periodontal diseases has to be elucidated.

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Chronic peroral immunization of conventional laboratory rats with mutans streptococci leads to stable acquired suppression of salivary antibodies

Cited by 6 publications

References 9 publications

Age‐related changes in salivary antibodies to commensal oral and gut biota

Age‐related changes in salivary antibodies to commensal oral and gut biota

Oral Microbial Ecology and the Role of Salivary Immunoglobulin A

Salivary IgA subclasses and bacteria‐reactive IgA in patients with aggressive periodontitis

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