Gut dysbiosis promotes M2 macrophage polarization and allergic airway inflammation via fungi-induced PGE₂.
Gut dysbiosis promotes M2 macrophage polarization and allergic airway inflammation via fungi-induced PGE₂.
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DOI：
10.1016/j.chom.2013.12.010
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发表时间：
2014-01-15
影响因子：
30.3
通讯作者：
Shibuya A
中科院分区：
文献类型：
--
作者：
Kim YG;Udayanga KG;Totsuka N;Weinberg JB;Núñez G;Shibuya A
尽管肠道菌群组成失衡或“生态失调”与许多疾病有关，但肠道生态失调对宿主全身生理的影响尚未得到很好的表征。我们报道抗生素（Abx）治疗诱导的肠道生态失调通过将肺巨噬细胞极化向交替激活的M2表型转移来促进过敏性气道炎症。来自abx处理小鼠的肺泡巨噬细胞的过继性转移足以增加过敏性气道炎症。abx处理导致肠道中共生真菌念珠菌过度生长，前列腺素E2 （PGE2）血浆浓度升高，从而诱导肺中M2巨噬细胞极化。环加氧酶抑制剂阿司匹林和塞来昔布对PGE2合成的抑制抑制了abx处理小鼠M2巨噬细胞极化，减少了过敏性气道炎症细胞浸润。因此，abx处理可引起肠道中特定真菌物种的过度生长，促进远处M2巨噬细胞的激活，从而影响包括过敏性炎症在内的全身反应。
Although imbalances in gut microbiota composition, or “dysbiosis”, are associated with many diseases, the effects of gut dysbiosis on host systemic physiology are less well characterized. We report that gut dysbiosis induced by antibiotic (Abx)-treatment promotes allergic airway inflammation by shifting macrophage polarization in the lung toward the alternatively activated M2 phenotype. Adoptive transfer of alveolar macrophages derived from Abx-treated mice was sufficient to increase allergic airway inflammation. Abx-treatment resulted in the overgrowth of a commensal fungal Candida species in the gut and increased plasma concentrations of prostaglandin E2 (PGE2), which induced M2 macrophage polarization in the lung. Suppression of PGE2 synthesis by the cyclooxygenase inhibitors aspirin and celecoxib suppressed M2 macrophage polarization and decreased allergic airway inflammatory cell infiltration in Abx-treated mice. Thus, Abx-treatment can cause overgrowth of particular fungal species in the gut and promote M2 macrophage activation at distant sites to influence systemic responses including allergic inflammation.
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DOI：
10.4049/jimmunol.1101873
发表时间：
2012-04-15
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Church RJ;Jania LA;Koller BH
通讯作者：
Koller BH
影响因子：
64.8
作者：
Arumugam, Manimozhiyan;Raes, Jeroen;Pelletier, Eric;Le Paslier, Denis;Yamada, Takuji;Mende, Daniel R.;Fernandes, Gabriel R.;Tap, Julien;Bruls, Thomas;Batto, Jean-Michel;Bertalan, Marcelo;Borruel, Natalia;Casellas, Francesc;Fernandez, Leyden;Gautier, Laurent;Hansen, Torben;Hattori, Masahira;Hayashi, Tetsuya;Kleerebezem, Michiel;Kurokawa, Ken;Leclerc, Marion;Levenez, Florence;Manichanh, Chaysavanh;Nielsen, H. Bjorn;Nielsen, Trine;Pons, Nicolas;Poulain, Julie;Qin, Junjie;Sicheritz-Ponten, Thomas;Tims, Sebastian;Torrents, David;Ugarte, Edgardo;Zoetendal, Erwin G.;Wang, Jun;Guarner, Francisco;Pedersen, Oluf;de Vos, Willem M.;Brunak, Soren;Dore, Joel;Weissenbach, Jean;Ehrlich, S. Dusko;Bork, Peer
通讯作者：
Bork, Peer
影响因子：
158.5
作者：
COHEN, R;ROTH, FJ;KALSER, MH
通讯作者：
KALSER, MH
影响因子：
4.4
作者：
Claveau, D;Sirinyan, M;Mancini, JA
通讯作者：
Mancini, JA
影响因子：
4.9
作者：
Lee, Herng-Sheng;Lee, Chung-Shinn;Salter, Donald M.
通讯作者：
Salter, Donald M.