期刊
FRONTIERS IN IMMUNOLOGY
卷 12, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2021.677722
关键词
serglycin proteoglycan; knockout mouse; infection; Giardia intestinalis; innate intestinal immunity
类别
资金
- Vetenskapsradet VR-M [201203364, 2011-03533]
- Vinnova [2011-03533] Funding Source: Vinnova
- Swedish Research Council [2011-03533] Funding Source: Swedish Research Council
The proteoglycan serglycin plays a regulatory role in intestinal immune responses by influencing the expression levels of chemokines and cytokines, leading to delayed weight gain in young SG(-/-) mice infected with Giardia intestinalis.
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 (asymptotic to 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-alpha and CXCL2, and increased IFN-gamma, 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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