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Decreased vitamin A levels in common variable immunodeficiency: vitamin A supplementation in vivo enhances immunoglobulin production and downregulates inflammatory responses
Author(s) -
Pål Aukrust,
Fredrik Müller,
Thor Ueland,
Asbjørn Svardal,
Rolf K. Berge,
Stig S. Frøland
Publication year - 2000
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1046/j.1365-2362.2000.00619.x
Subject(s) - neopterin , phytohaemagglutinin , common variable immunodeficiency , medicine , vitamin , immunology , endocrinology , monocyte , vitamin d and neurology , peripheral blood mononuclear cell , in vivo , cytokine , vitamin d deficiency , antibody , immune system , biology , in vitro , biochemistry , microbiology and biotechnology
Background Vitamin A has a broad range of immunological effects, and vitamin A deficiency is associated with recurrent infections. Common variable immunodeficiency (CVI) is a group of B‐cell deficiency syndromes with impaired antibody production and recurrent bacterial infections as the major manifestations, but the immunological dysfunctions may also include T cells and macrophages. In the present study we examined the possible role of vitamin A deficiency in CVI. Patients and methods We analysed plasma vitamin A levels in 20 CVI patients and 16 controls, and examined the relationships between vitamin A and clinical, immunological and metabolic parameters in CVI. In the six CVI patients with the lowest vitamin A levels we also studied the effect of vitamin A supplementation in vivo on several immunological functions in these patients. Results (i) The majority of CVI patients had decreased vitamin A levels compared with healthy controls, as found in both cross‐sectional and longitudinal testing. (ii) Low vitamin A levels were associated with the occurrence of chronic bacterial infections and splenomegaly as well as high neopterin levels. Decreased levels of carrier protein and malabsorption were not observed. (iii) Vitamin A supplementation in patients with low vitamin A levels resulted in increased interleukin‐10 (IL‐10) and decreased tumour necrosis factor‐α (TNFα) levels, as found in both plasma and monocyte supernatants, possibly favouring anti‐inflammatory net effects. (iv) Vitamin A supplementation in vivo also enhanced anti‐CD40‐stimulated IgG production, serum IgA levels and phytohaemagglutinin (PHA)‐stimulated peripheral blood mononuclear cell (PBMC) proliferation. Conclusion A considerable subgroup of CVI patients appears to be characterized by low vitamin A levels. Our findings support a possible role for vitamin A supplementation in CVI, perhaps resulting in enhanced immunoglobulin synthesis and downregulated inflammatory responses.