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      Thymus involution in alloxan diabetes: analysis of mast cells

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          Abstract

          We previously reported that alloxan-induced diabetes results in reduction in the number and reactivity of mast cells at different body sites. In this study, the influence of diabetes on thymic mast cells was investigated. Thymuses from diabetic rats showed marked alterations including shrinkage, thymocyte depletion, and increase in the extracellular matrix network, as compared to those profiles seen in normal animals. Nevertheless, we noted that the number and reactivity of mast cells remained unchanged. These findings indicate that although diabetes leads to critical alterations in the thymus, the local mast cell population is refractory to its effect. This suggests that thymic mast cells are under a different regulation as compared to those located in other tissues.

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          Mast cells as sentinels of innate immunity.

          Stephen J. Galli, Marcus Maurer, Chris S. Lantz (1999)
          Mast cells are widely regarded as important effector cells in immune responses associated with Th2 cells and IgE. Recent work shows that they can also contribute significantly to the expression of innate immunity; furthermore, survival in a model of acute bacterial infection that is dependent on complement and mast cells can be greatly enhanced by long-term treatment of mice with the kit ligand (stem cell factor) at least in part because of the effects of such treatment on mast cell numbers and/or function. These findings not only indicate that mast cells can represent a critical component of host defense in natural immunity but also suggest that mast cell function in this setting can be manipulated for therapeutic ends.
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            Association between atopic dermatitis and insulin-dependent diabetes mellitus: a case-control study.

            Jens K Pedersen, S Juul, N Birkebaek … (2001)
            Up to two-thirds of children with atopic dermatitis have IgE-mediated allergic reactions and a Th2 immune reactivity pattern with low production of interferon gamma and high production of interleukin 4 after allergen stimulation of T lymphocytes. Insulin-dependent diabetes mellitus (IDDM) seems to be associated with a Th1 immune reactivity pattern. We therefore postulated that these diseases may be inversely associated. We designed a case-control study including 920 children with IDDM, registered in the Danish Registry for Childhood Diabetes, and a sample of 9732 non-diabetic children registered in the Danish Medical Birth Registry. The children were aged 3-15 years. Information on atopic dermatitis was obtained by questionnaires. The cumulative incidence of atopic dermatitis up to age 15 years was 13.1% among children with IDDM and 19.8% in non-diabetic children (p<0.0001). Among children who developed IDDM, the incidence of atopic dermatitis was significantly lower than in the controls before onset of IDDM (73 cases in 5314 person-months vs 1375 in 57432 person-months; odds ratio 0.49 [0.39-0.63]). After onset of IDDM, diabetic and non-diabetic groups did not differ in incidence of atopic dermatitis (1.36 [0.89-2.07]). Our findings may be explained by different acquired or inherited reactivity patterns associated with atopic dermatitis (Th2) and IDDM (Th1). The results do not allow us to find out whether early development of atopic dermatitis reduces the risk of IDDM, or a propensity for IDDM reduces the risk of early-onset atopic dermatitis.
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              Alloxan diabetes reduces pleural mast cell numbers and the subsequent eosinophil influx induced by allergen in sensitized rats.

              João C. F. Corrêa, Isabelle Cordeiro, Francisca Serra … (1996)
              Alloxan damages insulin-producing cells and has been used as an inducer of experimental diabetes in several animal species. In this study, administration of alloxan (40 mg/kg, i.v.) to rats was followed by a selective and time-dependent reduction in the number of pleural mast cells (50 +/- 2.2%, p < 0.01; mean +/- SEM), while mononuclear cell and eosinophil counts were not altered. As compared to naive rats, the reduction in mast cell numbers was first noted 48 h following alloxan administration and remained unaltered for at least 60 days. It is noteworthy, that the depletion in the mast cell population was not accompanied by alterations in the total amount of histamine stored per cell. Sensitized rats turned diabetic by alloxan treatment performed 72 h before challenge showed a less pronounced antigen-induced mast cell degranulation compared to nondiabetic rats. Moreover, rats injected with alloxan 72 and 48 but not 24 h before challenge, reacted to allergenic challenge with 50% reduction in the number of eosinophils recruited to the pleural cavity within 24 h. We found that the less pronounced eosinophil accumulation did not relate to an intrinsic cell locomotor abnormality since eosinophils from diabetic rats presented similar chemotactic responses to LTB4 and PAF in vitro as compared to matching controls. Insulin (3 IU/rat) restored basal levels of mast cells and reversed the subsequent inhibition of allergen-induced pleural eosinophilia, suggesting a causative relationship between these phenomena. Treatment with insulin also significantly increased the number of mast cells in the pleural cavity of naive rats (from 637 +/- 57 to 978 +/- 79 x 10(3) cells/cavity, p < 0.001). Consistently, previous depletion of mast cells by means of local treatment with compound 48/80 significantly reduced the antigen-induced eosinophil recruitment in sensitized animals. We conclude that the reduction in the pleural mast cell population noted in alloxan-treated rats could be directly implicated in the diminished pleural eosinophil influx following allergen challenge. This hyporesponsiveness is independent of an intrinsic abnormality of cell chemotaxis, but can be imitated by local mast cell depletion.
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                Author and article information

                Journal
                Journal ID (publisher-id): mioc
                Title: Memórias do Instituto Oswaldo Cruz
                Abbreviated Title: Mem. Inst. Oswaldo Cruz
                Publisher: Instituto Oswaldo Cruz, Ministério da Saúde (Rio de Janeiro, RJ, Brazil )
                ISSN (Print): 0074-0276
                ISSN (Electronic): 1678-8060
                Publication date (Print and electronic): March 2005
                Volume: 100
                Issue: suppl 1
                Pages: 127-130
                Affiliations
                [02] Rio de Janeiro RJ orgnameFiocruz orgdiv1Instituto Oswaldo Cruz orgdiv2Departamento de Imunologia Brasil
                [01] Rio de Janeiro RJ orgnameFiocruz orgdiv1Instituto Oswaldo Cruz orgdiv2Departamento de Fisiologia e Farmacodinâmica Brasil
                Article
                Publisher ID: S0074-02762005000900022 Publisher ID: S0074-0276(05)10000022
                DOI: /S0074-02762005000900022
                PubMed ID: 15962111
                SO-VID: 1e8af8d7-3808-4b10-a83b-b02c153cf291
                License:

                This work is licensed under a Creative Commons Attribution 4.0 International License.

                History
                Date received : 08 November 2004
                Date accepted : 30 December 2004
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 16, Pages: 4
                Product

                SciELO Brazil


                Keywords: mast cells,thymus,extracellular matrix,diabetes
                Data availability:
                Keywords: mast cells, thymus, extracellular matrix, diabetes

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