Serglycin-Deficiency Causes Reduced Weight Gain and Changed Intestinal Cytokine Responses in Mice Infected With Giardia intestinalis.
Serglycin-Deficiency Causes Reduced Weight Gain and Changed Intestinal Cytokine Responses in Mice Infected With Giardia intestinalis.
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DOI：
10.3389/fimmu.2021.677722
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发表时间：
2021
影响因子：
7.3
通讯作者：
Åbrink M
中科院分区：
文献类型：
--
作者：
Li Z;Peirasmaki D;Svärd S;Åbrink M
蛋白聚糖丝甘肽（SG）由不同的先天性和适应性免疫细胞表达，例如肥大细胞、巨噬细胞、嗜中性粒细胞和细胞毒性T淋巴细胞，其中SG有助于炎症介质的正确颗粒储存和细胞外活性。在此，使用丝氨酸蛋白酶缺陷（SG-/-）小鼠品系研究SG在感染非侵入性原生动物寄生虫贾第鞭毛虫期间对肠道免疫反应的影响。与感染的SG+/+同窝小鼠和PBS激发的SG −/−和SG+/+同窝小鼠相比，经口灌胃感染的年轻（约11周龄）同系SG −/−小鼠显示体重增加减少。感染未引起小肠的重大形态学变化。然而，观察到SG非依赖性杯状细胞和粒细胞计数增加，这与髓过氧化物酶或中性粒细胞弹性蛋白酶活性增加无关。此外，感染的小鼠显示血清IL-6水平增加，感染的SG缺陷小鼠的血清IL-6水平显著降低，感染的SG缺陷小鼠的肠IL-6表达水平降低。在感染小鼠中，警报素、趋化因子、细胞因子和一氧化氮合酶（NOS）的qPCR分析显示，与SG感受态小鼠相比，SG缺乏导致TNF-α和CXCL 2的肠表达水平降低，IFN-γ、CXCL 1和NOS 1水平升高。这项研究表明，SG在肠道免疫反应中起着调节作用，这反映在感染G的年轻SG−/−小鼠中趋化因子和细胞因子表达水平的变化以及体重增加延迟。好吧
The proteoglycan serglycin (SG) is expressed by different innate and adaptive immune cells, e.g. mast cells, macrophages, neutrophils, and cytotoxic T lymphocytes, where SG contributes to correct granule storage and extracellular activity of inflammatory mediators. Here the serglycin-deficient (SG−/−) mouse strain was used to investigate the impact of SG on intestinal immune responses during infection with the non-invasive protozoan parasite Giardia intestinalis. Young (≈11 weeks old) oral gavage-infected congenic SG−/− mice showed reduced weight gain as compared with the infected SG+/+ littermate mice and the PBS-challenged SG−/− and SG+/+ littermate mice. The infection caused no major morphological changes in the small intestine. However, a SG-independent increased goblet cell and granulocyte cell count was observed, which did not correlate with an increased myeloperoxidase or neutrophil elastase activity. Furthermore, infected mice showed increased serum IL-6 levels, with significantly reduced serum IL-6 levels in infected SG-deficient mice and decreased intestinal expression levels of IL-6 in the infected SG-deficient mice. In infected mice the qPCR analysis of alarmins, chemokines, cytokines, and nitric oxide synthases (NOS), showed that the SG-deficiency caused reduced intestinal expression levels of TNF-α and CXCL2, and increased IFN-γ, CXCL1, and NOS1 levels as compared with SG-competent mice. This study shows that SG plays a regulatory role in intestinal immune responses, reflected by changes in chemokine and cytokine expression levels and a delayed weight gain in young SG−/− mice infected with G. intestinalis.
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影响因子：
15.9
作者：
Bartelt, Luther A.;Roche, James;Guerrant, Richard
通讯作者：
Guerrant, Richard
影响因子：
4.3
作者：
Hafte, T. T.;Fagereng, G. L.;Tveit, H.
通讯作者：
Tveit, H.
DOI：
10.1016/0035-9203(88)90153-8
发表时间：
1988-05-01
影响因子：
2.2
作者：
HALLIDAY, CEW;CLARK, C;FARTHING, MJG
通讯作者：
FARTHING, MJG
DOI：
10.1093/cid/ciw391
发表时间：
2016-09-15
期刊：
Clinical infectious diseases : an official publication of the Infectious Diseases Society of America
影响因子：
--
作者：
Donowitz JR;Alam M;Kabir M;Ma JZ;Nazib F;Platts-Mills JA;Bartelt LA;Haque R;Petri WA Jr
通讯作者：
Petri WA Jr
影响因子：
2
作者：
Jimenez, Juan C.;Fontaine, Josette;Dei-Cas, Eduardo
通讯作者：
Dei-Cas, Eduardo