Mitochondria: An Organelle of Bacterial Origin Controlling Inflammation.
Mitochondria: An Organelle of Bacterial Origin Controlling Inflammation.
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DOI：
10.3389/fimmu.2018.00536
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发表时间：
2018
影响因子：
7.3
通讯作者：
Geny B
中科院分区：
文献类型：
--
作者：
Meyer A;Laverny G;Bernardi L;Charles AL;Alsaleh G;Pottecher J;Sibilia J;Geny B
炎症是细胞和分子对感染和/或组织损伤的反应。适当的炎症反应在强度和时间上允许杀死病原体，清除坏死组织和愈合损伤；过度的炎症反应驱动各种疾病，其中炎症和组织损伤/应激相互自我维持。微生物在非解决炎症的暗示很差，强调内源性调节炎症的重要性。线粒体历来被认为是细胞能量的主要来源，它通过电子传递链将脂肪酸和丙酮酸的氧化与大量三磷酸腺苷的产生结合起来。线粒体也是活性氧的主要来源。有趣的是，过去十年的研究强调，自从其整合到真核细胞中以来，这种细菌来源的细胞器不仅被免疫耐受，而且还被放置为细胞防御的中心调节器。在完整的细胞中，线粒体调节细胞对关键先天免疫受体参与的反应。下游细胞内信号通路与线粒体蛋白相互作用，并由线粒体功能调节。此外，当细胞受到应激或损伤时，线粒体成分被释放到细胞质或细胞外环境中，当它们被先天免疫受体识别时，它们作为危险信号。最后，线粒体通过调节树突状细胞和淋巴细胞之间的免疫突触的能量状态，调节炎症命运向免疫耐受或免疫原性方向发展。由于这些过程的失调最近与各种疾病有关，因此确定其潜在机制可能为调节炎症开辟新的途径。
Inflammation is a cellular and molecular response to infection and/or tissues injury. While a suited inflammatory response in intensity and time allows for killing pathogens, clearing necrotic tissue, and healing injury; an excessive inflammatory response drives various diseases in which inflammation and tissues damages/stress self-sustain each other. Microbes have been poorly implied in non-resolving inflammation, emphasizing the importance of endogenous regulation of inflammation. Mitochondria have been historically identified as the main source of cellular energy, by coupling the oxidation of fatty acids and pyruvate with the production of high amount of adenosine triphosphate by the electron transport chain. Mitochondria are also the main source of reactive oxygen species. Interestingly, research in the last decade has highlighted that since its integration in eukaryote cells, this organelle of bacterial origin has not only been tolerated by immunity, but has also been placed as a central regulator of cell defense. In intact cells, mitochondria regulate cell responses to critical innate immune receptors engagement. Downstream intracellular signaling pathways interact with mitochondrial proteins and are tuned by mitochondrial functioning. Moreover, upon cell stress or damages, mitochondrial components are released into the cytoplasm or the extra cellular milieu, where they act as danger signals when recognized by innate immune receptors. Finally, by regulating the energetic state of immunological synapse between dendritic cells and lymphocytes, mitochondria regulate the inflammation fate toward immunotolerance or immunogenicity. As dysregulations of these processes have been recently involved in various diseases, the identification of the underlying mechanisms might open new avenues to modulate inflammation.
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影响因子：
32.4
作者：
Iyer SS;He Q;Janczy JR;Elliott EI;Zhong Z;Olivier AK;Sadler JJ;Knepper-Adrian V;Han R;Qiao L;Eisenbarth SC;Nauseef WM;Cassel SL;Sutterwala FS
通讯作者：
Sutterwala FS
影响因子：
12.7
作者：
Meyer, Alain;Laverny, Gilles;Geny, Bernard
通讯作者：
Geny, Bernard
影响因子：
5.7
作者：
Min Y;Wi SM;Shin D;Chun E;Lee KY
通讯作者：
Lee KY
DOI：
10.1084/jem.20102049
发表时间：
2011-03-14
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Bulua AC;Simon A;Maddipati R;Pelletier M;Park H;Kim KY;Sack MN;Kastner DL;Siegel RM
通讯作者：
Siegel RM
影响因子：
7.3
作者：
Koshiba, Takumi;Yasukawa, Kai;Kawabata, Shun-ichiro
通讯作者：
Kawabata, Shun-ichiro