Sialoadhesin promotes rapid proinflammatory and type I IFN responses to a sialylated pathogen, Campylobacter jejuni.
Sialoadhesin promotes rapid proinflammatory and type I IFN responses to a sialylated pathogen, Campylobacter jejuni.
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DOI：
10.4049/jimmunol.1200776
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发表时间：
2012-09-01
期刊：
影响因子：
--
通讯作者：
Crocker PR
中科院分区：
文献类型：
--
作者：
Klaas M;Oetke C;Lewis LE;Erwig LP;Heikema AP;Easton A;Willison HJ;Crocker PR
唾液酸粘附素（Sialoadhesin，Sn）是一种巨噬细胞（Mφ）限制性受体，识别宿主细胞和病原体上的唾液酸配体。虽然Sn被认为在Mφ与免疫系统细胞的细胞相互作用中是重要的，但Sn对病原体参与的功能后果尚不清楚。作为模型系统，我们研究了Sn在Mφ与表达GD 1a样唾液酸化聚糖的热灭活空肠弯曲杆菌相互作用中的作用。与野生型小鼠的表达Sn的骨髓源性Mφ（BMDM）相比，Sn缺陷或表达非聚糖结合形式Sn的小鼠的BMDM对唾液酸化C的吞噬作用大大降低。空肠。这伴随着TNF-α、IL-6、IL-12和IL-10的MyD 88依赖性分泌的强烈减少。体内研究表明，静脉注射唾液酸化C后，TNF-α和IFN-β的快速应答需要功能性Sn。空肠。静脉注射后几分钟内捕获细菌，并与肝脏和脾脏中的Mφ相关。在脾脏中，IFN-β反应细胞定位于Sn+ Mφ和红髓及边缘区的其它细胞。总之，这些研究表明，Sn在捕获唾液酸化病原体和促进快速促炎细胞因子和I型IFN应答中起关键作用。
Sialoadhesin (Sn) is a macrophage- (Mφ-) restricted receptor that recognizes sialylated ligands on host cells and pathogens. Whilst Sn is thought to be important in cellular interactions of Mφs with cells of the immune system, the functional consequences of pathogen engagement by Sn are unclear. As a model system, we have investigated the role of Sn in Mφ interactions with heat-killed Campylobacter jejuni expressing a GD1a-like, sialylated glycan. Compared to Sn-expressing bone marrow-derived Mφs (BMDM) from wild-type mice, BMDM from mice either deficient in Sn or expressing a non-glycan-binding form of Sn showed greatly reduced phagocytosis of sialylated C. jejuni. This was accompanied by a strong reduction in MyD88-dependent secretion of TNF-α, IL-6, IL-12 and IL-10. In vivo studies demonstrated that functional Sn was required for rapid TNF-α and IFN-β responses to i.v. injected sialylated C. jejuni. Bacteria were captured within minutes following i.v. injection and were associated with Mφs in both liver and spleen. In the spleen, IFN-β-reactive cells were localized to Sn+ Mφs and other cells in the red pulp and marginal zone. Together, these studies demonstrate that Sn plays a key role in capturing sialylated pathogens and promoting rapid pro-inflammatory cytokine and type I IFN responses.
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影响因子：
32.4
作者：
Kontoyiannis, D;Pasparakis, M;Kollias, G
通讯作者：
Kollias, G
影响因子：
32.4
作者：
Kawai, T;Adachi, O;Akira, S
通讯作者：
Akira, S
DOI：
10.1073/pnas.0909541107
发表时间：
2010-01-05
影响因子：
11.1
作者：
Backer, Ronald;Schwandt, Timo;den Haan, Joke M. M.
通讯作者：
den Haan, Joke M. M.
影响因子：
3.6
作者：
Jones, C;Virji, M;Crocker, PR
通讯作者：
Crocker, PR
影响因子：
15.9
作者：
Godschalk, PCR;Heikema, AP;Endtz, HP
通讯作者：
Endtz, HP