Polyclonal activation: A form of primitive immunity and its possible role in pathogenesis of inflammatory diseases

Clagett, James; Engel, David

doi:10.1016/s0145-305x(78)80066-4

Cited by 35 publications

(18 citation statements)

References 29 publications

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“…1980. Models for pathogenesis of periodontitis which invoke B-cell function and polyclonal activation of B-cells in particular have been proposed and are consistent with known features of the disease (Seymour et al 1979, Clagett & Engel 1978, Mangan & Lopatin 1981, Ivanyi & Lehner 1974, Ivanyi 1977. It is tempting to speculate that the generally lesser potency of grampositive species in PBA activity, as compared with the gram-negative strains previously tested, is indicative of reasons for compatibility of a gram-positive flora with periodontal health.…”

Section: Discussionmentioning

confidence: 66%

Polyclonal B‐cell activating capacities of gram‐positive bacteria frequently isolated from periodontally diseased sites

Sl¹,

Ph²,

We³

et al. 1982

J of Periodontal Research

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The objective of this study was to determine whether gram‐positive organisms frequently isolated from the periodontium in health and disease contain polyclonal B‐cell activators. Extracts from numerous bacterial strains including Actinomyces viscosus. Actinamyces israelii, Actinomyces NV, Eubacteriun nodatum, Eubacterium brachy, Streptococcus sanguis, Streptococcus anginosus, and Peptostreptococcus micros were tested. All of the organisms contained activity above background, but none of the activators were more potent than pokeweed mitogen, and most were less than half as potent. The aclinomyces appeared to be more active than the eubacteria. streptococci, or peptostreptococci. These PBAs could be significant virulence factors.

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Section: Discussionmentioning

confidence: 66%

Polyclonal B‐cell activating capacities of gram‐positive bacteria frequently isolated from periodontally diseased sites

Sl¹,

Ph²,

We³

et al. 1982

J of Periodontal Research

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“…Mitogenic preparations of mycoplasmal membranes inoculated intranasally in LEW rats produce pathological effects similar to those induced by viable M. pulmonis (32). Hyperresponsiveness to polyclonal activators has been suggested to play a role in other chronic inflammatory diseases, such as lupus and periodontitis (9,16).…”

Section: Discussionmentioning

confidence: 99%

Murine respiratory mycoplasmosis in F344 and LEW rats: evolution of lesions and lung lymphoid cell populations

Davis¹,

Thorp²,

Maddox³

et al. 1982

Infect Immun

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By comparison of two rat strains, LEW and F344, which are known to differ in susceptibility to Mycoplasma pulmonis respiratory disease, it was shown that differences in lesion severity and progression were associated with changes in lung lymphocyte populations. Lung lesions in LEW rats developed earlier after infection, became more severe, and were characterized by continued proliferation of all classes of lymphoid cells, T lymphocytes, B lymphocytes, and plasma cells, throughout the 120-day observation period. In contrast, lymphoid proliferation in F344 rats reached a plateau at 28 days and was restricted to an increase in T lymphocytes, immunoglobulin A (IgA)-bearing B lymphocytes, and IgA and IgG plasma cells. Although approximately 10 times as many IgG B cells and 4 times as many IgG plasma cells were found in infected LEW rats as compared with F344 rats, the specific anti-M. pulmonis IgG response in the two strains was roughly parallel. The same relationships held true, although to a lesser extent, for specific IgA antibody responses and cellular responses. Whereas lung lesions showed a tendency to resolve in F344 rats by 120 days, severe lesions persisted in LEW rats. The disparity between the cellular response and specific antibody response, the seemingly uncontrolled lymphocyte proliferation in LEW rats, and the mitogenic potential of M. pulmonis suggest that differences between LEW and F344 rats in lung lesion severity and progression are related to differences in the degree of nonspecific lymphocyte activation in the two strains, an imbalance in regulation of lymphocyte proliferation in LEW rats, or both.

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“…In any case, once the immunoinhibitory agents are eliminated, a state of immunologic deficiency would then be followed by a vigorous, but delayed immune response to microbial antigens either as a consequence of specific antigenic stimulation or by polyclonal cell activation (Bick et al 1981. Smith et al 1980, Clagett & Engel 1978. If this hypothesis is valid, the immune response so often documented in crosssectional clinical studies of established disease only represents a single moment in the duration of an evolving disease.…”

Section: Immunosuppressjon In the Etiology/ Pathogenesis Of Periodontmentioning

confidence: 99%

Immunologic dysfunction in the pathogenesis of periodontal diseases*

Shenker

1987

J Clinic Periodontology

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Despite significant progress in our understanding of the pathogenesis and etiology of periodontal diseases, the nature and contribution of the immune system to this disorder remains unclear. Several studies provide evidence for either a protective or destructive rôle. These conflicting findings are difficult to reconcile, since most interpretations tend to argue for a static contributory rôle (i.e., either protective or destructive) of the immune system. Current theories on the rôle of the immune response do not address these conflicting findings as well as the contradictory observation of a detectable immune response in the face of persistent infection in these patients. In this article, we present a model, based on available data, for the contribution of the immune system to the pathogenesis of periodontal disease. This model ascribes a dynamic rôle for the immune response. As documented in other infectious diseases, it is entirely possible, for example, that a state of immunologic dysfunction may occur in the earliest stages of periodontal disease progression; this may then be followed by a period of active immune reactivity (humoral and/or cellular) that would represent either a delayed or depressed response. This model is discussed in conjunction with recent findings that several suspected periodontal pathogens are capable of producing immunosuppressive agents. Many of the apparently contradictory clinical observations concerning the host immune response to oral pathogens and its correlation (or lack of) with both the progression and severity of periodontal disease may be accounted for in this model.

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Polyclonal activation: A form of primitive immunity and its possible role in pathogenesis of inflammatory diseases

Cited by 35 publications

References 29 publications

Polyclonal B‐cell activating capacities of gram‐positive bacteria frequently isolated from periodontally diseased sites

Polyclonal B‐cell activating capacities of gram‐positive bacteria frequently isolated from periodontally diseased sites

Murine respiratory mycoplasmosis in F344 and LEW rats: evolution of lesions and lung lymphoid cell populations

Immunologic dysfunction in the pathogenesis of periodontal diseases*

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