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Neutrophil ghosts worsen asthma

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Science Immunology  03 Aug 2018:
Vol. 3, Issue 26, eaau0112
DOI: 10.1126/sciimmunol.aau0112

Figures

  • Fig. 1 NETosis exacerbates allergic inflammation.

    Exposure to allergens in susceptible individuals drives TH2 cytokine production, resulting in immunoglobulin E (IgE) antibody production, eosinophilic inflammation, mucus hypersecretion, and AHR. Coincident microbial infections lead to the recruitment of PMNs and the initiation of NETosis, which releases DNA into the extracellular space and generates neutrophil cytoplasts. These cytoplasts migrate to the lymph node and, through their interactions with DCs, drive TH17 cell differentiation. The newly generated TH17 cells release IL-17A, which amplifies the neutrophilic inflammatory response through its ability to up-regulate GM-CSF, IL-8, and vascular cell adhesion molecule–1 (VCAM-1) expression, leading to increased PMN differentiation and extravasation from the bloodstream into airway tissues. Together, these processes drive exacerbation of allergic asthma.

    CREDIT: A. KITTERMAN/AAAS

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