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. 2017 Nov 3;8:1463. doi: 10.3389/fimmu.2017.01463

Figure 1.

Figure 1

Nociceptor activation promotes Th2 but not Th1 airway inflammation. In the aluminum hydroxide (AlOH)/ovalbumin (OVA) sensitized mice (A–C), a standard model of airway Th2-driven inflammation, OVA-challenge do not significantly increase the numbers of ILC2 cells (A) in the lung but did enhance their production of IL-5 (B) as well as the numbers of inflammatory dendritic cells (DCs) in bronchoalveolar lavage fluid (BALF) (C). Silencing lung sensory neurons with aerosolized QX-314 (0.003%, 20 min nebulization, 20 psi) decreased these Th2 immune cell responses. By contrast, silencing nociceptors in a Th1-driven lung inflammation model [complete Freund’s adjuvant (CFA)]/OVA sensitized mice; (D–F), had no impact on the OVA-challenge induced increases in BALF CD3+ (D), eosinophils (E), and macrophages (F). Mean ± SEM; Two-tailed unpaired Welsh’s t-test (n = 5–12 animals/group; 1–2 cohorts).