Literature DB >> 3264266

Endogenous corticosteroids mediate seasonal cyclic changes in immunity of lizards.

A H Saad1, R el Ridi.   

Abstract

Endogenous corticosteroid (CS) blood levels were radioimmunoassayed in fresh, field-collected lizards Chalcides ocellatus at two week-intervals throughout the four consecutive seasons. These animals were used in parallel to investigate the splenic T and B lymphocyte level, lymphoproliferative responsiveness to concanavalin A and primary antibody production in vitro against rat erythrocytes (RRBC). The recorded data indicated that fully developed splenic lymphoid tissue and powerful immune responsiveness are coincident with a continuously low CS level, and characterize the period from spring through early autumn. On the other hand, the dramatic lymphocytic destruction and impairment of immune reactivity observed in autumn and winter are associated with not only a high, but above all sustained, rise in endogenous CS levels. Apparently, exposure of lizard lymphocytes to comparatively high, yet physiologic, levels of endogenous CS for prolonged periods of time lead to impairment of their immune functions. In support, long-term administration of exogenous hydrocortisone acetate (HC) to "summer" lizards resulted in a high and lasting elevation in blood CS levels that was associated with a considerable depletion of lymphoid elements and abrogation of immune reactivity, exactly as in normal lizards collected from the field in autumn through winter. In addition, pharmacologic inhibition of CS synthesis by administration of metyrapone at the beginning of autumn greatly modulated the lizard lymphocyte response to the autumn-related immunodepression. The study thus strongly suggests that the autumn/winter-dependent immunosuppression in lizards is essentially due to a high and lasting rise in levels of endogenous CS. The results are discussed from the perspective of the role played by CS in mediating the seasonal rhythms that affect reptilian immunity.

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Year:  1988        PMID: 3264266     DOI: 10.1016/S0171-2985(88)80007-X

Source DB:  PubMed          Journal:  Immunobiology        ISSN: 0171-2985            Impact factor:   3.144


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