Fungal Chitin Induces Trained Immunity in Human Monocytes during Cross-talk of the Host with Saccharomyces cerevisiae*
Fungal Chitin Induces Trained Immunity in Human Monocytes during Cross-talk of the Host with Saccharomyces cerevisiae*
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DOI：
10.1074/jbc.m115.699645
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发表时间：
2016-02
期刊：
影响因子：
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通讯作者：
L. Rizzetto;D. Ifrim;S. Moretti;N. Tocci;Shih-Chin Cheng;J. Quintin;G. Renga;Vasilis Oikonomou;C. de Filippo;Tobias Weil;B. Blok;M. Lenucci;Manuel A. S. Santos;L. Romani;M. Netea;D. Cavalieri
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作者：
L. Rizzetto;D. Ifrim;S. Moretti;N. Tocci;Shih-Chin Cheng;J. Quintin;G. Renga;Vasilis Oikonomou;C. de Filippo;Tobias Weil;B. Blok;M. Lenucci;Manuel A. S. Santos;L. Romani;M. Netea;D. Cavalieri
免疫系统对维持宿主及其微生物群和真菌群之间的相互作用至关重要。作为一种共生菌，酿酒酵母菌可能以一种重要的方式塑造免疫反应。我们观察到酿酒葡萄球菌细胞在TLR配体以及细菌和真菌共生体的二次刺激下，通过增强TNFα和IL-6的产生，以菌株依赖的方式诱导单核细胞的训练免疫。几丁质含量的差异解释了菌株之间训练特性的差异，通过增加细胞因子的产生和体外和体内的直接抗菌活性来诱导训练免疫。这些几丁质诱导的保护特性与其内化密切相关，确定了吞噬体酸化促进微生物消化的关键作用。本研究揭示了共生微生物和乘客微生物如何通过调节宿主对病原体的防御，从而影响宿主微生物-免疫系统的相互作用，在促进健康和预防粘膜疾病方面发挥重要作用。
The immune system is essential to maintain the mutualistic homeostatic interaction between the host and its micro- and mycobiota. Living as a commensal, Saccharomyces cerevisiae could potentially shape the immune response in a significant way. We observed that S. cerevisiae cells induce trained immunity in monocytes in a strain-dependent manner through enhanced TNFα and IL-6 production upon secondary stimulation with TLR ligands, as well as bacterial and fungal commensals. Differential chitin content accounts for the differences in training properties observed among strains, driving induction of trained immunity by increasing cytokine production and direct antimicrobial activity both in vitro and in vivo. These chitin-induced protective properties are intimately associated with its internalization, identifying a critical role of phagosome acidification to facilitate microbial digestion. This study reveals how commensal and passenger microorganisms could be important in promoting health and preventing mucosal diseases by modulating host defense toward pathogens and thus influencing the host microbiota-immune system interactions.