Splenectomy changes the pattern of cytokine production in beta-thalassemic patients.

Ghollam-Reza Moshtaghi-Kashanian, Ahmad Gholamhoseinian, Afrooz Hoseinimoghadam, Saeeid Rajabalian

Journal: Cytokine 2007;35(5-6):253-7

PMID: 17081768

Abstract

A major cause of morbidity and mortality in beta-thalassemic patients is infections, assumed to be the result of immunological changes. To determine the possible defect, we investigated the cytokine productions by blood cells of beta-thalassemic patients using in-vivo and in-vitro methods. Heparinized blood samples collected aseptically from 22 beta-thalassemic children aged 10-12yrs (half of them were splenectomized). Samples from 10 healthy children served as control group. Part of samples was used for evaluation of plasma IL-2, IL-10 and TGF-beta1. Other part were stimulated with a mixture of LPS and PHA (1 and 10 microg/ml final concentration), for different time period (4, 24, 48 and 72h). Results showed circulating TGF-beta1 of splenectomized patients was significantly higher (p<0.01) than the control group. In-vitro results showed IL-2 production of patients' groups were significantly (p<0.01) lower than corresponding value obtained for the control group. In addition, IL-10 production by splenectomized group were less than other two group (p<0.01), while their TGF-beta1 were higher (p<0.001) at all time points treated. In conclusion, multi-transfusions could be responsible for a change in the subset of circulating lymphocytes that could contribute to a state of partial immune deficiency in beta-thalassemic patients, which is more prominence among the splenectomized patient.

Address: Physiology Research center of Kerman University of Medical Sciences, Kerman, Iran.
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