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Commensal microbiota stimulate systemic neutrophil migration through induction of Serum amyloid A
Author(s) -
Kanther Michelle,
Tomkovich Sarah,
Xiaolun Sun,
Grosser Melinda R.,
Koo Jaseol,
Flynn Edward J.,
Jobin Christian,
Rawls John F.
Publication year - 2014
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/cmi.12257
Subject(s) - biology , serum amyloid a , zebrafish , inflammation , immunology , myeloperoxidase , systemic inflammation , gene , genetics
Summary Neutrophils serve critical roles in inflammatory responses to infection and injury, and mechanisms governing their activity represent attractive targets for controlling inflammation. The commensal microbiota is known to regulate the activity of neutrophils and other leucocytes in the intestine, but the systemic impact of the microbiota on neutrophils remains unknown. Here we utilized in vivo imaging in gnotobiotic zebrafish to reveal diverse effects of microbiota colonization on systemic neutrophil development and function. The presence of a microbiota resulted in increased neutrophil number and myeloperoxidase expression, and altered neutrophil localization and migratory behaviours. These effects of the microbiota on neutrophil homeostasis were accompanied by an increased recruitment of neutrophils to injury. Genetic analysis identified the microbiota‐induced acute phase protein serum amyloid A ( Saa ) as a host factor mediating microbial stimulation of tissue‐specific neutrophil migratory behaviours. In vitro studies revealed that zebrafish cells respond to Saa exposure by activating NF ‐κ B , and that Saa ‐dependent neutrophil migration requires NF ‐κ B ‐dependent gene expression. These results implicate the commensal microbiota as an important environmental factor regulating diverse aspects of systemic neutrophil development and function, and reveal a critical role for a Saa ‐ NF ‐κ B signalling axis in mediating neutrophil migratory responses.

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