Decreased vitamin A levels in common variable immunodeficiency: vitamin A supplementation in vivo enhances immunoglobulin production and downregulates inflammatory responses

Citation
P. Aukrust et al., Decreased vitamin A levels in common variable immunodeficiency: vitamin A supplementation in vivo enhances immunoglobulin production and downregulates inflammatory responses, EUR J CL IN, 30(3), 2000, pp. 252-259
Citations number
39
Categorie Soggetti
General & Internal Medicine","Medical Research General Topics
Journal title
EUROPEAN JOURNAL OF CLINICAL INVESTIGATION
ISSN journal
00142972 → ACNP
Volume
30
Issue
3
Year of publication
2000
Pages
252 - 259
Database
ISI
SICI code
0014-2972(200003)30:3<252:DVALIC>2.0.ZU;2-Z
Abstract
Background Vitamin A has a broad range of immunological effects, and vitami n A deficiency is associated with recurrent: infections. Common variable im munodeficiency (CVI) is a group of B-cell deficiency syndromes with impaire d antibody production and recurrent bacterial infections as the major manif estations, but the immunological dysfunctions may also include T cells and macrophages. In the present study pre 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 clin ical, immunological and metabolic parameters in CVI. In the six CVI patient s with the lowest vitamin A levels we also studied the effect of vitamin A supplementation in vivo an several immunological functions in these patient s. Results (i) The majority of CVI patients had decreased vitamin A levels com pared with healthy controls, as found in both cross-sectional and longitudi nal 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 obse rved, (iii) Vitamin A supplementation in patients with lour vitamin A level s resulted in increased interleukin-10 (IL-10) and decreased tumour necrosi s factar-alpha (TNF alpha) levels, as found in both plasma and monocyte sup ernatants, 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 characteri zed by low vitamin A levels. Our findings support a possible role for vitam in A supplementation in CVI, perhaps resulting in enhanced immunoglobulin s ynthesis and downregulated inflammatory responses.