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首页> 外文期刊>Infection and immunity >Resistance to infection in murine beta-thalassemia.
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Resistance to infection in murine beta-thalassemia.

机译：对鼠β地中海贫血感染的抵抗力。

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Clinical evidence suggests that individuals with chronic iron overload may be at increased risk of bacterial infection. We studied this question by using a unique model in which mice homozygous for a deletion in the gene encoding for the beta-major globin develop moderate anemia, splenomegaly, and tissue iron overload, a syndrome similar to beta-thalassemia in humans. Mice heterozygous for the gene deletion were phenotypically normal. Homozygous mice were significantly more susceptible to infection with Listeria monocytogenes than were heterozygous mice (P less than 0.01). This increased susceptibility was associated with a greater number of organisms in the liver and spleen than was found in heterozygous mice (P less than 0.05). However, histologic studies demonstrated similar inflammatory responses within these organs in homozygous and heterozygous mice. The increased susceptibility of homozygous mice to infection with L. monocytogenes was not seen when homozygotes were immunized with a low dose of L. monocytogenes. Although the results were not as striking as with L. monocytogenes, homozygous mice were also found to be more susceptible to infection with Salmonella typhimurium than were heterozygous mice (P less than 0.05). Splenic mononuclear cells from homozygous mice demonstrated less responsiveness in vitro to the mitogens concanavalin A and phytohemagglutinin than did those from heterozygotes (P less than 0.05). These data suggest that there is a generalized defect in innate immunity in homozygous mice which makes them more susceptible to infection by L. monocytogenes and S. typhimurium. The site of this immunological defect is not known but is most likely in the mononuclear phagocyte and may be due to tissue iron overload.
机译：临床证据表明，患有慢性铁超负荷的个体可能会增加细菌感染的风险。我们通过使用一个独特的模型研究了这个问题，在该模型中，纯合β-主要球蛋白编码基因的小鼠缺失产生了中度贫血，脾肿大和组织铁超载（一种类似于人类β-地中海贫血的综合征）。基因缺失的杂合小鼠在表型上是正常的。与纯合子小鼠相比，纯合子小鼠更容易感染单核细胞增生性李斯特菌（P小于0.01）。与杂合小鼠相比，这种增加的敏感性与肝脏和脾脏中更多的生物体相关（P小于0.05）。但是，组织学研究表明，在纯合和杂合小鼠中，这些器官内有类似的炎症反应。当用低剂量的单核细胞增生利斯特氏菌免疫纯合子时，未观察到纯合小鼠对单核细胞增生李斯特氏菌感染的易感性增加。尽管结果不如单核细胞增生李斯特菌引人注目，但与纯合子小鼠相比，纯合子小鼠还比鼠伤寒沙门氏菌更易感染（P小于0.05）。与杂合子相比，纯合子小鼠的脾单核细胞在体外对有丝分裂素伴刀豆球蛋白A和植物血凝素的反应性较低（P小于0.05）。这些数据表明在纯合小鼠中先天免疫存在普遍缺陷，这使它们更容易受到单核细胞增生李斯特菌和鼠伤寒沙门氏菌的感染。这种免疫缺陷的部位尚不清楚，但最有可能在单核吞噬细胞中，并且可能是由于组织铁超负荷所致。

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