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Title: The potential role of Osteopontin in the maintenance of commensal bacteria homeostasis in the intestine
Authors: Ito, Koyu
Nakajima, Akira
Fukushima, Yuji  kyouindb  KAKEN_id
Suzuki, Keiichiro
Sakamoto, Keiko
Hamazaki, Yoko  kyouindb  KAKEN_id
Ogasawara, Kouetsu
Minato, Nagahiro
Hattori, Masakazu  kyouindb  KAKEN_id
Author's alias: 濵﨑, 洋子
湊, 長博
服部, 雅一
Issue Date: 15-Mar-2017
Publisher: Public Library of Science (PLoS)
Journal title: PloS one
Volume: 12
Issue: 3
Thesis number: e0173629
Abstract: Osteopontin (Opn), a multifunctional extracellular matrix protein, is implicated in the pathogenesis of various inflammatory disorders. Under physiologic conditions, its expression is restricted to certain tissues including bone and kidney tubule. However, cellular activation during disease development induces Opn expression in various immune cells. In this study, using Opn-EGFP knock-in (KI) mice we found that CD8α⁺ T cells in the intestinal tissues, including Peyer’s patch, lamina propria and epithelium, express Opn under steady state conditions. Therefore, we examined the role of Opn-expressing CD8α⁺ T cells in intestinal homeostasis. Interestingly, Opn knockout (KO) mice had altered fecal microflora concordant with a reduction of TCRγδ⁺ intraepithelial lymphocytes (IELs). Consistent with this result, both treatment with anti-Opn blocking antibody and deficiency of Opn resulted in decreased survival of TCRγδ⁺ and TCRαβ⁺ IELs. This data suggests that a possibility that Opn may function as a survival factor for IELs in the intestinal tissue. Collectively, these data suggest the possibility that Opn might regulate the homeostasis of intestinal microflora through maintenance of TCRγδ⁺ IELs, possibly by support of IEL survival.
Rights: © 2017 Ito et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
URI: http://hdl.handle.net/2433/232505
DOI(Published Version): 10.1371/journal.pone.0173629
PubMed ID: 28296922
Appears in Collections:Journal Articles

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