Dietary abscisic acid ameliorates influenza-virus-associated disease and pulmonary immunopathology through a PPARγ-dependent mechanism.
Dietary abscisic acid ameliorates influenza-virus-associated disease and pulmonary immunopathology through a PPARγ-dependent mechanism.
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膳食脱落酸通过 PPARγ 依赖性机制改善流感病毒相关疾病和肺部免疫病理学。
DOI：
10.1016/j.jnutbio.2012.07.010
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发表时间：
2013-06
期刊：
影响因子：
--
通讯作者：
Bassaganya-Riera J
中科院分区：
文献类型：
--
作者：
Hontecillas R;Roberts PC;Carbo A;Vives C;Horne WT;Genis S;Velayudhan B;Bassaganya-Riera J
抗炎植物激素脱落酸（阿坝）调节结肠炎和肥胖小鼠模型的免疫和炎症反应。阿坝是羊毛硫氨酸合成酶C-like 2的配体，是过氧化物酶体增殖物激活受体γ（PPAR γ）通路上游的一个新的治疗靶点。本研究的目的是探讨阿坝对流感相关肺部炎症的抗炎作用的免疫调节机制。经口给予或不给予阿坝（100 mg/kg饮食）治疗的肺上皮细胞和造血细胞（cKO）中有缺陷的PPAR γ表达的野生型（WT）和条件性敲除小鼠，用甲型流感/Udorn（H3 N2）进行攻击，以评估阿坝对疾病、肺部病变和基因表达的影响。饮食阿坝改善疾病活动，肺部炎症病理，加速恢复和增加WT小鼠的存活率。阿坝通过PPAR γ抑制WT小鼠的白细胞浸润和MCP-1 mRNA表达，因为这种作用在cKO小鼠中被消除。当在感染的同一天对WT而不是骨髓细胞中缺乏PPAR γ的小鼠进行治疗性给药时，阿坝改善了疾病。我们还表明，阿坝的更大的影响是在7和10天之间的挑战后，当它调节参与决议，如5-脂氧合酶和其他成员的5-脂氧合酶途径的基因的表达。此外，阿坝显着增加WT小鼠的免疫调节细胞因子IL-10的表达。我们的研究结果表明，预防性或治疗性给予阿坝，通过激活肺免疫细胞中的PPAR γ，抑制初始促炎反应并促进消退来改善流感病毒诱导的病理学。
The anti-inflammatory phytohormone abscisic acid (ABA) modulates immune and inflammatory responses in mouse models of colitis and obesity. ABA has been identified as a ligand of lanthionine synthetase C-like 2, a novel therapeutic target upstream of the peroxisome proliferator-activated receptor γ (PPAR γ) pathway. The goal of this study was to investigate the immune modulatory mechanisms underlying the anti-inflammatory efficacy of ABA against influenza-associated pulmonary inflammation. Wild type (WT) and conditional knockout mice with defective PPAR γ expression in lung epithelial and hematopoietic cells (cKO) treated orally with or without ABA (100 mg/kg diet) were challenged with Influenza A/Udorn (H3N2) to assess ABA’s impact in disease, lung lesions and gene expression. Dietary ABA ameliorated disease activity, lung inflammatory pathology, accelerated recovery and increased survival in WT mice. ABA suppressed leukocyte infiltration and MCP-1 mRNA expression in WT mice through PPAR γ, since this effect was abrogated in cKO mice. ABA ameliorated disease when administered therapeutically on the same day of the infection to WT but not mice lacking PPAR γ in myeloid cells. We also show that ABA’s greater impact is between days 7 and 10 post-challenge when it regulates the expression of genes involved in resolution, like 5 lipoxygenase and other members of the 5-lipoxygenase pathway. Furthermore, ABA significantly increased the expression of the immunoregulatory cytokine IL-10 in WT mice. Our results show that ABA, given preventively or therapeutically, ameliorates influenza virus-induced pathology by activating PPAR γ in pulmonary immune cells, suppressing initial proinflammatory responses and promoting resolution.
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Toll样受体（TLR）3对病毒诱导的急性肺炎的有害贡献。
影响因子：
6.7
作者：
Le Goffic, Ronan;Balloy, Viviane;Lagranderie, Micheline;Alexopoulou, Lena;Escriou, Nicolas;Flavell, Richard;Chignard, Michel;Si-Tahar, Mustapha
通讯作者：
Si-Tahar, Mustapha
影响因子：
6.3
作者：
Guri, Amir J.;Hontecillas, Raquel;Bassaganya-Riera, Josep
通讯作者：
Bassaganya-Riera, Josep
影响因子：
64.8
作者：
Kash, John C.;Tumpey, Terrence M.;Katze, Michael G.
通讯作者：
Katze, Michael G.
DOI：
10.1016/j.clnu.2010.02.009
发表时间：
2010-12
期刊：
Clinical nutrition (Edinburgh, Scotland)
影响因子：
--
作者：
Guri AJ;Hontecillas R;Bassaganya-Riera J
通讯作者：
Bassaganya-Riera J
DOI：
10.1016/s1473-3099(08)70070-7
发表时间：
2008-09
期刊：
The Lancet. Infectious diseases
影响因子：
--
作者：
Fedson DS
通讯作者：
Fedson DS