T cell PPARγ is required for the anti-inflammatory efficacy of abscisic acid against experimental IBD.

T cell PPARγ is required for the anti-inflammatory efficacy of abscisic acid against experimental IBD.
复制标题

DOI:
10.1016/j.jnutbio.2010.06.011
复制
发表时间:
2011-09
影响因子:
5.6
通讯作者:
Bassaganya-Riera, Josep
Bassaganya-Riera, Josep
中科院分区:
医学2区
文献类型:
--
作者:
Guri, Amir J.;Evans, Nicholas P.;Hontecillas, Raquel;Bassaganya-Riera, Josep

文献摘要

参考文献

被引文献

相似文献

植物激素脱落酸(阿坝)已被证明在改善慢性和急性炎症中有效。本研究的目的是研究阿坝在肠道中的抗炎功效是否依赖于T细胞中的过氧化物酶体增殖物激活受体γ(PPAR γ)。在用2.5%葡聚糖硫酸钠(DSS)攻击之前,向表达PPAR γ和T细胞特异性PPAR γ缺失小鼠喂食含有或不含阿坝(100 mg/kg)的饮食35天。每天评估临床疾病的严重程度,并在DSS攻击的第7天对小鼠实施安乐死。通过炎症病变的肉眼和组织病理学检查以及基于实时定量RT-PCR的炎症基因定量来评估结肠炎症。使用流式细胞术对血液和肠系膜淋巴结(MLN)中的白细胞群体进行表型表征。结肠切片进行化学染色以确定阿坝对结肠调节性T(Treg)细胞的影响。阿坝对疾病活动的有益作用在T细胞特异性PPAR γ敲除小鼠中完全消失。此外,阿坝改善了结肠组织病理学,减少了血液中F4/80+ CD 11b+单核细胞,增加了血液中表达抑制性分子细胞毒性T淋巴细胞抗原4(CTLA 4)的CD 4 + T细胞的百分比,并增加了表达PPAR γ但不表达T细胞特异性PPAR γ的小鼠MLN和结肠中Treg细胞的数量。我们的结论是,饮食阿坝改善实验性IBD通过增加Treg积累在结肠固有层通过过氧化物酶体增殖物激活受体γ依赖性机制。
The phytohormone abscisic acid (ABA) has been shown to be effective in ameliorating chronic and acute inflammation. The objective of this study was to investigate whether ABA’s anti-inflammatory efficacy in the gut is dependent on peroxisome proliferator activated receptor γ (PPAR γ) in T cells. PPAR γ-expressing and T cell-specific PPAR γ null mice were fed diets with or without ABA (100 mg/kg) for 35 days prior to challenge with 2.5% dextran sodium sulfate (DSS). The severity of clinical disease was assessed daily, and mice were euthanized on day 7 of the DSS challenge. Colonic inflammation was assessed through macroscopic and histopathological examination of inflammatory lesions and real-time quantitative RT-PCR-based quantification of inflammatory genes. Flow cytometry was used to phenotypically characterize leukocyte populations in the blood and mesenteric lymph nodes (MLN). Colonic sections were stained immunohistochemically to determine the effect of ABA on colonic regulatory T (Treg) cells. ABA’s beneficial effects on disease activity were completely abrogated in T cell-specific PPAR γ null mice. Additionally, ABA improved colon histopathology, reduced blood F4/80+CD11b+ monocytes, increased the percentage of CD4+ T cells expressing the inhibitory molecule cytotoxic T lymphocyte antigen 4 (CTLA4) in blood, and enhanced the number of Treg cells in the MLN and colons of PPAR γ expressing but not T cell-specific PPAR γ null mice. We conclude that dietary ABA ameliorates experimental IBD by enhancing Treg accumulation in the colonic lamina propria through a PPAR γ-dependent mechanism.
DOI: 10.4049/jimmunol.178.7.4129
发表时间: 2007-04-01
影响因子: 4.4
作者:
Wohlfert, Elizabeth A.;Nichols, Frank C.;Clark, Robert B.
通讯作者: Clark, Robert B.
DOI: 10.3945/jn.109.115642
发表时间: 2010-03-01
影响因子: 4.2
作者:
Evans, Nicholas P.;Misyak, Sarah A.;Bassaganya-Riera, Josep
通讯作者: Bassaganya-Riera, Josep
DOI: 10.1016/j.clnu.2006.07.008
发表时间: 2007-02-01
期刊: CLINICAL NUTRITION
影响因子: 6.3
作者:
Guri, Amir J.;Hontecillas, Raquel;Bassaganya-Riera, Josep
通讯作者: Bassaganya-Riera, Josep
DOI: 10.1097/01.mib.0000195385.19268.68
发表时间: 2006-01-01
影响因子: 4.9
作者:
Hanauer, SB
通讯作者: Hanauer, SB
DOI: 10.1016/j.cellimm.2009.04.003
发表时间: 2009-01-01
影响因子: 4.3
作者:
Bassaganya-Riera, Josep;Misyak, Sarah;Hontecillas, Raquel
通讯作者: Hontecillas, Raquel