First-Breath-Induced Type 2 Pathways Shape the Lung Immune Environment | Zendy

Simona Saluzzo | Zendy; Anna-Dorothea Gorki | Zendy; Batika M.J. Rana | Zendy; Rui Martins | Zendy; Seth Thomas Scanlon | Zendy; Philipp Starkl | Zendy; Karin Lakovits | Zendy; Anastasiya Hladik | Zendy; Ana Korosec | Zendy; Omar Sharif | Zendy; Joanna Warszawska | Zendy; Helen E. Jolin | Zendy; Ildikó Mesteri | Zendy; Andrew N. J. McKenzie | Zendy; Sylvia Knapp | Zendy

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First-Breath-Induced Type 2 Pathways Shape the Lung Immune Environment

Author(s) -

Simona Saluzzo,

Anna-Dorothea Gorki,

Batika M.J. Rana,

Rui Martins,

Seth Thomas Scanlon,

Philipp Starkl,

Karin Lakovits,

Anastasiya Hladik,

Ana Korosec,

Omar Sharif,

Joanna Warszawska,

Helen E. Jolin,

Ildikó Mesteri,

Andrew N. J. McKenzie,

Sylvia Knapp

Publication year - 2017

Publication title -

cell reports

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 6.264

H-Index - 154

eISSN - 2639-1856

pISSN - 2211-1247

DOI - 10.1016/j.celrep.2017.01.071

Subject(s) - homeostasis , lung , immune system , phenotype , biology , immunology , innate lymphoid cell , macrophage polarization , downregulation and upregulation , progenitor cell , microbiology and biotechnology , innate immune system , macrophage , alveolar macrophage , stem cell , medicine , gene , genetics , in vitro

From birth onward, the lungs are exposed to the external environment and therefore harbor a complex immunological milieu to protect this organ from damage and infection. We investigated the homeostatic role of the epithelium-derived alarmin interleukin-33 (IL-33) in newborn mice and discovered the immediate upregulation of IL-33 from the first day of life, closely followed by a wave of IL-13-producing type 2 innate lymphoid cells (ILC2s), which coincided with the appearance of alveolar macrophages (AMs) and their early polarization to an IL-13-dependent anti-inflammatory M2 phenotype. ILC2s contributed to lung quiescence in homeostasis by polarizing tissue resident AMs and induced an M2 phenotype in transplanted macrophage progenitors. ILC2s continued to maintain the M2 AM phenotype during adult life at the cost of a delayed response to Streptococcus pneumoniae infection in mice. These data highlight the homeostatic role of ILC2s in setting the activation threshold in the lung and underline their implications in anti-bacterial defenses.

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