Commensal Microbes Induce Serum IgA Responses that Protect against Polymicrobial Sepsis.
Commensal Microbes Induce Serum IgA Responses that Protect against Polymicrobial Sepsis.
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DOI：
10.1016/j.chom.2018.01.005
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发表时间：
2018-03-14
影响因子：
30.3
通讯作者：
Allman D
中科院分区：
文献类型：
--
作者：
Wilmore JR;Gaudette BT;Gomez Atria D;Hashemi T;Jones DD;Gardner CA;Cole SD;Misic AM;Beiting DP;Allman D
血清IgA抗体很容易在小鼠和人体内检测到，但血清IgA诱导的机制及其在宿主保护中的作用仍不确定。我们报道，选择共生菌诱导几个方面的全身性iga介导的免疫。将常规小鼠暴露于一种独特但天然的微生物菌群中，其中包括变形菌门的几个成员，导致血清IgA水平的T细胞依赖性增加，并诱导骨髓中大量分泌IgA的浆细胞。由此产生的血清IgA与有限的细菌分类群结合，抗原特异性血清IgA抗体在与共生细菌幽门螺杆菌肠道定植后很容易诱导。最后，向富含变形菌群的微生物群迁移导致血清iga介导的对多微生物败血症的耐药性。我们得出结论，共生微生物明显影响血清IgA库，导致对细菌性败血症的构成保护。摘要：Wilmore等人证明了血清IgA在预防多微生物脓毒症中的作用。诱导T细胞依赖性血清IgA的保护浓度需要肠道定植一个复杂的微生物群，包括变形菌门的细菌。
Serum IgA antibodies are readily detected in mice and people, yet the mechanisms underlying the induction of serum IgA and its role in host protection remains uncertain. We report that select commensal bacteria induce several facets of systemic IgA-mediated immunity. Exposing conventional mice to a unique but natural microflora that included several members of the Proteobacteria phylum led to T cell-dependent increases in serum IgA levels and the induction of large numbers of IgA-secreting plasma cells in the bone marrow. The resulting serum IgA bound to a restricted collection of bacterial taxa, and antigen-specific serum IgA antibodies were readily induced after intestinal colonization with the commensal bacterium Helicobacter muridarum. Finally, movement to a Proteobacteria-rich microbiota led to serum IgA-mediated resistance to polymicrobial sepsis. We conclude that commensal microbes overtly influence the serum IgA repertoire, resulting in constitutive protection against bacterial sepsis. In Brief: Wilmore et al. demonstrate a role for serum IgA in protection against polymicrobial sepsis. Induction of protective concentrations of T cell-dependent serum IgA requires colonization of the gut with a complex microbiota that includes bacteria in the phylum Proteobacteria.
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影响因子：
32.4
作者：
Hall JA;Cannons JL;Grainger JR;Dos Santos LM;Hand TW;Naik S;Wohlfert EA;Chou DB;Oldenhove G;Robinson M;Grigg ME;Kastenmayer R;Schwartzberg PL;Belkaid Y
通讯作者：
Belkaid Y
影响因子：
64.5
作者：
Koch MA;Reiner GL;Lugo KA;Kreuk LS;Stanbery AG;Ansaldo E;Seher TD;Ludington WB;Barton GM
通讯作者：
Barton GM
影响因子：
32.4
作者：
Bunker JJ;Flynn TM;Koval JC;Shaw DG;Meisel M;McDonald BD;Ishizuka IE;Dent AL;Wilson PC;Jabri B;Antonopoulos DA;Bendelac A
通讯作者：
Bendelac A
影响因子：
4.4
作者：
Lowrey, Liam;Woodhams, Douglas C.;Salinas, Irene
通讯作者：
Salinas, Irene
影响因子：
4.4
作者：
Kamata, T;Nogaki, F;Honjo, T
通讯作者：
Honjo, T