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. 2019 May 31;10:1203. doi: 10.3389/fimmu.2019.01203

Figure 1.

Figure 1

Commensal bacteria mediated innate immunity to respiratory pathogens. Commensal bacteria stimulate various innate immune cells, particularly alveolar macrophages (Mϕ), mucosa-associated invariant T (MAIT) cells, group 3 innate lymphoid cells (ILC3), and natural killer (NK) cells, to induce early protection. These bacteria promote pathogen killing via granulocyte–macrophage colony-stimulating factor (GM-CSF), which stimulates pathogen killing and clearance by alveolar macrophages (Mϕ) through phagocytosis, reduced reactive oxygen species (RO), and extracellular signal regulated kinase (ERK) signaling. Intrapulmonary GM-CSF production in response to infection is regulated by the microbiota via interleukin-17A (IL-17A). Pattern recognition receptor (PRR) expressed by Mϕ recognizes PRR ligands, such as nod-like receptor ligands (NOD RL), leading to the activation of Mϕ. NK and MAIT cells when activated by commensal bacteria produce large quantities of IL-17A, whereas ILC3 cells secrete IL-22, aiding in inhibition/killing of various respiratory pathogens.