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. 2005 Jan 20;115(2):313–325. doi: 10.1172/JCI22433

Figure 4.

Figure 4

Blockade of mIL-6R through i.n. application of anti–IL-6R antibodies ameliorates AHR and induces IFN-γ and IL-10 levels in BALF in a mouse model of asthma after OVA sensitization. (A) Eight to 10 BALB/c mice per group were sensitized to OVA-alum (OVA-sensitized mice) followed by local treatment with OVA alone or treatment with OVA plus either gp130-Fc, IgG, or anti–IL-6R antibody. Control mice were sensitized with saline-alum and exposed to saline aerosol (saline). Transpulmonary resistance was performed 24 hours after the last local treatment in all mice, as specified in Methods. Dose-response curves to MCh were obtained after administering indicated doses of intravenous MCh. OVA-sensitized mice reacted with an increase of airway resistance at low doses of MCh as compared to that of mice given saline. Anti–IL-6R–treated, OVA-sensitized mice were more protected from the development of AHR compared to untreated (P = 0.049) or IgG-treated, OVA-sensitized mice. Moreover, blockade of sIL-6R by gp130-Fc was less effective compared to anti–IL-6R antibody treatment. (B and C) Local anti–IL-6R antibody treatment induced significant release of IFN-γ (P = 0.048) (B) and IL-10 (P = 0.020) (C) in BALF of OVA-senstitized mice as compared to untreated, OVA-sensitized mice (5 < n < 15). Mean values ± SEM are shown. *P < 0.05.