Commensal bacteria promote migration of mast cells into the intestine
Commensal bacteria promote migration of mast cells into the intestine
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DOI：
10.1016/j.imbio.2010.10.007
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发表时间：
2011-06-01
期刊：
影响因子：
2.8
通讯作者：
Kaminogawa, Shuichi
中科院分区：
文献类型：
--
作者：
Kunii, Junichi;Takahashi, Kyoko;Kaminogawa, Shuichi
肥大细胞从骨髓中的造血干细胞分化，并通过循环迁移到外周组织，在那里它们在诱导先天性和适应性免疫应答中起关键作用。在这项研究中，肠道寄生菌对肥大细胞迁移到肠道的影响进行了研究。组织化学分析表明，无菌（GF）小鼠小肠肥大细胞密度低于正常小鼠。流式细胞仪检测结果显示，GF小鼠小肠固有层白细胞中肥大细胞比例较正常小鼠低，血液中肥大细胞比例较高。这些结果表明，肥大细胞从血液到肠道的迁移是由肠道寄生菌促进的。此外，MyD 88（-/-）小鼠的肠道肥大细胞密度低于CV小鼠，表明阿司匹林的促进作用至少部分依赖于TLR。CXC趋化因子受体2（CXCR 2）的配体在正常小鼠的肠组织和肠上皮细胞（IEC）中的表达高于GF或MyD 88（-/-）小鼠。总的来说，这表明，唾液酸通过诱导CXCR 2配体以TLR依赖性方式从IEC促进肥大细胞迁移到肠道中。(C)2010年Elsevier GmbH。All rights reserved.
Mast cells differentiate from hematopoietic stem cells in the bone marrow and migrate via the circulation to peripheral tissues, where they play a pivotal role in induction of both innate and adaptive immune responses. In this study, the effect of intestinal commensal bacteria on the migration of mast cells into the intestine was investigated. Histochemical analyses showed that germ-free (GF) mice had lower mast cell densities in the small intestine than normal mice. It was also shown that GF mice had lower mast cell proportion out of lamina propria leukocytes in the small intestine and higher mast cell percentages in the blood than normal mice by flow cytometry. These results indicate that migration of mast cells from the blood to the intestine is promoted by intestinal commensal bacteria. In addition, MyD88(-/-) mice had lower densities of intestinal mast cells than CV mice, suggesting that the promotive effect of commensals is, at least in part, TLR-dependent. The ligands of CXC chemokine receptor 2 (CXCR2), which is critical for homing of mast cells to the intestine, were expressed higher in intestinal tissues and in intestinal epithelial cells (IECs) of normal mice than in those of GF or MyD88(-/-) mice. Collectively, it is suggested that commensals promote migration of mast cells into the intestine through the induction of CXCR2 ligands from IECs in a TLR-dependent manner. (C) 2010 Elsevier GmbH. All rights reserved.