Expression and characterization of αvβ5 integrin on intestinal macrophages
Autor: | Anika Schridde, Ashok Kumar Kumawat, Silvia C. Finnemann, Elizabeth A. Mann, Chen Yu, Allan McI. Mowat |
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Jazyk: | angličtina |
Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
Angiogenesis Immunology Integrin alpha5 Biology Article 03 medical and health sciences Mice Immune system Phagocytosis Immunology and Allergy Macrophage Animals Homeostasis Humans Receptors Vitronectin Intestinal Mucosa Receptor Tissue homeostasis Cells Cultured Mice Knockout Transplantation Chimera Epidermal Growth Factor Macrophages Colitis Cell biology Intestines Mice Inbred C57BL Haematopoiesis Interleukin 10 030104 developmental biology Gene Expression Regulation Metalloproteases |
Popis: | Macrophages play a crucial role in maintaining homeostasis in the intestine, but the underlying mechanisms have not yet been elucidated fully. Here, we show for the first time that mature intestinal macrophages in mouse intestine express high levels of αvβ5 integrin, which acts as a receptor for the uptake of apoptotic cells and can activate molecules involved in several aspects of tissue homeostasis such as angiogenesis and remodeling of the ECM. αvβ5 is not expressed by other immune cells in the intestine, is already present on intestinal macrophages soon after birth, and its expression is not dependent on the microbiota. In adults, αvβ5 is induced during the differentiation of monocytes in response to the local environment and it confers intestinal macrophages with the ability to promote engulfment of apoptotic cells via engagement of the bridging molecule milk fat globule EGF-like molecule 8. In the absence of αvβ5, there are fewer monocytes in the mucosa and mature intestinal macrophages have decreased expression of metalloproteases and IL 10. Mice lacking αvβ5 on haematopoietic cells show increased susceptibility to chemical colitis and we conclude that αvβ5 contributes to the tissue repair by regulating the homeostatic properties of intestinal macrophages. |
Databáze: | OpenAIRE |
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