Airway Microbiota-Host Interactions Regulate Secretory Leukocyte Protease Inhibitor Levels and Influence Allergic Airway Inflammation.

Airway Microbiota-Host Interactions Regulate Secretory Leukocyte Protease Inhibitor Levels and Influence Allergic Airway Inflammation.
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DOI:
10.1016/j.celrep.2020.108331
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发表时间:
2020-11-03
期刊:
影响因子:
8.8
通讯作者:
Kau AL
Kau AL
中科院分区:
生物学1区
文献类型:
--
作者:
Jaeger N;McDonough RT;Rosen AL;Hernandez-Leyva A;Wilson NG;Lint MA;Russler-Germain EV;Chai JN;Bacharier LB;Hsieh CS;Kau AL

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Homeostatic mucosal immune responses are fine-tuned by naturally evolved interactions with native microbes, and integrating these relationships into experimental models can provide new insights into human diseases. Here, we leverage a murine-adapted airway microbe, Bordetella pseudohinzii (Bph), to investigate how chronic colonization impacts mucosal immunity and the development of allergic airway inflammation (AAI). Colonization with Bph induces the differentiation of interleukin-17A (IL-17A)-secreting T-helper cells that aid in controlling bacterial abundance. Bph colonization protects from AAI and is associated with increased production of secretory leukocyte protease inhibitor (SLPI), an antimicrobial peptide with anti-inflammatory properties. These findings are additionally supported by clinical data showing that higher levels of upper respiratory SLPI correlate both with greater asthma control and the presence of Haemophilus, a bacterial genus associated with AAI. We propose that SLPI could be used as a biomarker of beneficial host-commensal relationships in the airway. Asthma is known to be modified by airway microbes. Jaeger et al. use a murine-adapted bacterium to show that airway colonization evokes a Th17 response associated with increased SLPI, an antimicrobial peptide, and protection from lung inflammation. In people, SLPI was correlated with airway microbiota composition.
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