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      Immunological Characteristics of Hyperreactive Malarial Splenomegaly Syndrome in Sudanese Patients

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          Abstract

          Hyperreactive Malarial Splenomegaly (HMS) is defined as a massive enlargement of the spleen resulting from abnormal immune responses after repeated exposure to the malaria parasites. This study was carried out in Khartoum, Sudan. Sudan is considered to be one of the countries where HMS is quite prevalent. The objective of the study was to determine the incidence of HMS in patients who reported to the Omdurman Tropical Diseases Hospital (OMTDH) in Sudan and to investigate the basic laboratory and immunological characteristics of this condition in these patients. A cross-sectional study was carried out in OMTDH, and all patients with enlarged spleens were included in the study. Thirty-one out of 335 (9.3%) patients were diagnosed as having the HMS condition using international criteria for HMS diagnosis. The mean serum immunoglobulin M (IgM) levels in HMS patient groups were 14.3 ± 5 g/L, and this was significantly higher compared with geographically matched controls ( P < 0.001). Immunoglobulin G (IgG) C anticircumsporozoite (CSP) antibody levels were higher in the HMS patients although the difference was not statistically significant, when compared with a group of patients with mild malaria. In comparison with naïve European controls, both the HMS and the mild malaria groups had significantly higher antimalarial antibody levels P < 0.001 and P < 0.01, respectively. Plasma levels of interleukin 10 (IL10) and interferon gamma (IFN γ ) were significantly increased in the HMS patients compared with the healthy control donors ( P < 0.05 and P < 0.01) for IL10 and IFN γ , respectively. The findings of this study suggest that HMS is one of the significant causes of tropical splenomegaly in Sudan. HMS is associated with significant elevations of circulating IgM and antimalarial IgG antibodies as well as IL10 and IFN γ .

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          Most cited references28

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          High sensitivity of detection of human malaria parasites by the use of nested polymerase chain reaction.

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            Pathology of Plasmodium chabaudi chabaudi infection and mortality in interleukin-10-deficient mice are ameliorated by anti-tumor necrosis factor alpha and exacerbated by anti-transforming growth factor beta antibodies.

            Interleukin-10 (IL-10)-deficient (IL-10(-/-)) mice infected with Plasmodium chabaudi (AS) suffer a more severe disease and exhibit a higher rate of mortality than control C57BL/6 mice. Here, we show that a drop in body temperature to below 28 degrees C and pronounced hypoglycemia of below 3 mM are reliable indicators of a lethal infection. Elevated inflammatory responses have been shown to accompany pathology in infected IL-10(-/-) mice. We show that neutralization of tumor necrosis factor alpha (TNF-alpha) in IL-10(-/-) mice abolishes mortality and ameliorates the hypothermia, weight loss, and anemia but does not affect the degree of hypoglycemia. These data suggest that TNF-alpha is involved in some of the pathology associated with a P. chabaudi infection in IL-10(-/-) mice but other factors play a role. IL-10(-/-) mice that survive a primary infection have been shown to control gamma interferon (IFN-gamma) and TNF-alpha production, indicating that other cytokines or mechanisms may be involved in their down-regulation. Significantly higher levels of transforming growth factor beta (TGF-beta), a cytokine with such properties, are present in the plasma of infected IL-10(-/-) mice at a time that coincides with the disappearance of IFN-gamma and TNF-alpha from the blood. Neutralization of TGF-beta in IL-10(-/-) mice resulted in higher circulating amounts of TNF-alpha and IFN-gamma, and all treated IL-10(-/-) mice died within 12 days with increased pathology but with no obvious increase in parasitemia. Our data suggest that a tight regulation of the balance between regulatory cytokines such as IL-10 and TGF-beta and inflammatory cytokines such as IFN-gamma and TNF-alpha is critical for survival in a mouse malaria infection.
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              Interleukin-10.

              Despite the short history of interleukin-10, accumulated evidence indicates that this interleukin plays a major role in suppressing immune and inflammatory responses. Yet interleukin-10 also maintains cell viability and acts as a cofactor to promote the growth of lymphoid and myeloid cells in vitro. Here we review the present knowledge on the structure and function of interleukin-10.
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                Author and article information

                Journal
                J Trop Med
                J Trop Med
                JTM
                Journal of Tropical Medicine
                Hindawi Publishing Corporation
                1687-9686
                1687-9694
                2013
                5 March 2013
                : 2013
                : 961051
                Affiliations
                1Institute of Endemic Diseases, University of Khartoum, Sudan
                2Faculty of Medicine, University of Khartoum, Sudan
                3Faculty of Medicine, Jazan University, P.O. Box 114, Jazan, Saudi Arabia
                4Department of Immunology, The Wenner-Gren Institute, Stockholm University, Sweden
                Author notes
                *Ibrahim M. Elhassan: ibrahimelhassan@ 123456iend.org

                Academic Editor: Aditya Prasad Dash

                Article
                10.1155/2013/961051
                3603278
                23533445
                472ea2ae-e369-4471-b531-ee40a0dc2288
                Copyright © 2013 Tayseer Alkadarou et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 2 December 2012
                : 8 February 2013
                Categories
                Clinical Study

                Infectious disease & Microbiology
                Infectious disease & Microbiology

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