Figure 3

Invariant natural killer T (iNKT) cells are essential to promote chronic obstructive pulmonary disease (COPD) features in mice. (a) Analysis of lung function decline induced by cigarette smoke (CS) in iNKT-cell-deficient mice. Age-matched wild-type (WT), Jα18^−/−, and CD1d^−/−mice were exposed to CS, 5 days a week, over a period of 12 weeks. Changes in airway resistance were measured on anesthetized, tracheotomized, intubated, and mechanically ventilated mice, in response to increasing doses of methacholine. Results are expressed as the mean±the s.e.m. Results are representative of three independent experiments. *P<0.05, **P<0.01 (WT mice vs. iNKT-cell-deficient mice). (b) Histological analysis of lung sections from mice exposed to CS. Lungs were harvested 12 weeks post-air or CS exposure and histopathological analysis was performed on lung sections. Representative hematoxylin and eosin-stained tissue sections (original magnification × 200) are shown. Note that CS exposure induced lung infiltration and destruction of alveolar walls in WT mice, whereas lung structure was not changed in (i)NKT-cell-deficient mice. (c) Absolute numbers of CD45⁺ CD11c⁻ F4/80⁻ CD11b⁺ Ly6C⁺ neutrophils and CD45⁺ TCRβ⁻ NK1.1⁺ NK cells were analyzed among lung mononuclear cells of mice exposed to CS for 12 weeks. Values represent the mean±s.e.m. (n=5). (d, e) The lungs were collected 12 weeks post-exposure, interleukin (IL)-17 (d) and Mmp12 (e) mRNA copy numbers were determined by quantitative RT–PCR. Data are normalized to expression of Gapdh and are expressed as fold increased over average gene expression in air-exposed WT mice or Jα18^−/− mice, respectively (n=5). *P<0.05, **P<0.01.

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