Temporary upregulation of anti-inflammatory cytokine IL-13 expression in the brains of CD14 deficient mice in the early stage of prion infection

被引：3

作者：

Hasebe, Rie ^{[1
]}

Suzuki, Akio ^{[1
]}

Yamasaki, Takeshi ^{[1
]}

Horiuchi, Motohiro ^{[1
]}

机构：

[1] Hokkaido Univ, Grad Sch Vet Med, Lab Vet Hyg, Kita Ku, Sapporo, Hokkaido 0600818, Japan

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2014年 / 454卷 / 01期

关键词：

Prion disease; CD14; IL-13; Pathogenesis; SIGNAL-TRANSDUCTION; BINDING-PROTEIN; SOLUBLE CD14; LIPOPOLYSACCHARIDE; INTERLEUKIN-13; CELLS; RECEPTOR; DISEASE; ABSENCE;

D O I：

10.1016/j.bbrc.2014.10.043

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

CD14 deficient (CD14(-/-)) mice survived longer than wild-type (WT) C57BL/6J mice when inoculated with prions intracerebrally, accompanied by increased expression of anti-inflammatory cytokine IL-10 by microglia in the early stage of infection. To assess the immune regulatory effects of CD14 in detail, we compared the gene expression of pro- and anti-inflammatory cytokines in the brains of WT and CD14(-/-) mice infected with the Chandler strain. Gene expression of the anti-inflammatory cytokine IL-13 in prion-infected CD14(-/-) mice was temporarily upregulated at 75 dpi, whereas IL-13 gene expression was not upregulated in prion-infected WT mice. Immunofluorescence staining showed that IL-13 was mainly expressed in neurons of the thalamus at 75 dpi. These results suggest that CD14 can suppress IL-13 expression in neurons during the early stage of prion infection. (C) 2014 Elsevier Inc. All rights reserved.

引用

页码：125 / 130

页数：6

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