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. 2014 Feb 26;111(10):3799–3804. doi: 10.1073/pnas.1400593111

Fig. 2.

Fig. 2.

S1P1R agonist inhibition of influenza virus induced cytokine amplification is independent of endosomal and cytosolic innate sensing pathways. The 3d (A) or IPS-1−/− (B) mice were infected with 1 × 104 PFU WSN influenza virus and either vehicle (water) or CYM5442 (2 mg/kg) were administered intratracheally to mice. Proinflammatory cytokines and chemokines were measured 48 h postinfection in BALF by ELISA. (C) Total numbers of activated macrophages/monocytes, NK cells, and neutrophils were quantified from collagenase-digested lungs at 48 h postinfluenza virus infection in 3d mice. Percentage (D) and total numbers (E) of CD69 expressing macrophages in the lung of vehicle or CYM-5442 treated IPS-1+/+ or IPS-1−/− mice 48 h postinfluenza virus infection. (F) Total numbers of neutrophils in the lungs of IPS-1+/+ or IPS-1−/− mice 48 h postinfluenza virus infection. *P < 0.05, **P < 0.01, ***P < 0.005. Results are representative of two to three independent experiments and five mice per group.