Stankovic Marija S, Turuntas Vladimir, De Luka Silvio R, Jankovic Sasa, Stefanovic Srdjan, Puskas Nela, Zaletel Ivan, Milutinović-Smiljanic Sanja, Trbovich Alexander M
Department of Pathophysiology, Faculty of Medicine, University of Belgrade, Dr Subotica 8, 11000, Belgrade, Serbia.
Pediatrics, University hospital Foca, Studentska 5, 73300 Foca, Bosnia and Herzegovina.
Exp Mol Pathol. 2015 Dec;99(3):687-92. doi: 10.1016/j.yexmp.2015.11.016. Epub 2015 Nov 11.
The aim of this study was to examine the role of the IL-33/ST2 pathway in pathogenesis of acute inflammation by investigating its possible role in alteration of iron and hematological parameters in experimental model of acute inflammation.
Wild-type and ST2 knockout BALB/c mice were divided into four groups: wild-type control group, ST2-/- control group, wild-type inflammatory group, and ST2-/- inflammatory group. Acute inflammation was induced by intramuscular injection of turpentine oil, while control groups were injected with saline. After 12h animals were anesthetized, and the treated tissue, blood and spleen were collected. Iron concentration in the treated tissue, hemoglobin blood concentration, mean corpuscular hemoglobin (MCH), hematocrit, erythrocyte, neutrophil and lymphocyte blood count, and erythrocytes percentage in spleen were determined.
Iron concentration in the treated tissue was significantly higher in wild-type inflammatory group (WT-I) when compared to both, the wild-type control group (WT-C) and ST2-/- inflammatory group (KO-I). There was no significant difference in iron concentration between ST2-/- control group (KO-C) and the KO-I. MCH had significantly decreased in WT-I when compared to WT-C, while there was no significant difference between KO-C and KO-I. Hemoglobin blood concentration significantly increased in KO-I in comparison to KO-C, while it did not significantly differ between WT-I and KO-I. Erythrocyte count and hematocrit had significantly increased, while the percentage of erythrocytes in spleen decreased in both inflammatory groups when compared to their controls. Neutrophil count significantly decreased in WT-I, when compared to WT-C. Lymphocyte count decreased in both inflammatory groups when compared to their controls.
Results of this study indicate that the IL-33/ST2 axis could have a role in the alteration of iron in acute inflammation, namely in an increase of iron concentration at the site of acute inflammation and a decrease of blood mean corpuscular hemoglobin.
本研究旨在通过研究白细胞介素-33/ST2通路在急性炎症实验模型中铁和血液学参数改变中的可能作用，来探讨其在急性炎症发病机制中的作用。
将野生型和ST2基因敲除的BALB/c小鼠分为四组：野生型对照组、ST2基因敲除对照组、野生型炎症组和ST2基因敲除炎症组。通过肌肉注射松节油诱导急性炎症，而对照组注射生理盐水。12小时后对动物进行麻醉，并收集处理过的组织、血液和脾脏。测定处理过的组织中的铁浓度、血红蛋白血浓度、平均红细胞血红蛋白含量（MCH）、血细胞比容、红细胞、中性粒细胞和淋巴细胞血细胞计数以及脾脏中红细胞百分比。
与野生型对照组（WT-C）和ST2基因敲除炎症组（KO-I）相比，野生型炎症组（WT-I）处理过的组织中的铁浓度显著更高。ST2基因敲除对照组（KO-C）和KO-I之间的铁浓度没有显著差异。与WT-C相比，WT-I中的MCH显著降低，而KO-C和KO-I之间没有显著差异。与KO-C相比，KO-I中的血红蛋白血浓度显著增加，而WT-I和KO-I之间没有显著差异。与各自的对照组相比，两个炎症组中的红细胞计数和血细胞比容显著增加，而脾脏中红细胞百分比降低。与WT-C相比，WT-I中的中性粒细胞计数显著降低。与各自的对照组相比，两个炎症组中的淋巴细胞计数均降低。
本研究结果表明，白细胞介素-33/ST2轴可能在急性炎症中铁的改变中起作用，即在急性炎症部位铁浓度增加和血液平均红细胞血红蛋白含量降低方面起作用。
