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. 2002 Jan 7;195(1):51-7.
doi: 10.1084/jem.20011732.

The absence of interleukin 9 does not affect the development of allergen-induced pulmonary inflammation nor airway hyperreactivity

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The absence of interleukin 9 does not affect the development of allergen-induced pulmonary inflammation nor airway hyperreactivity

Sarah J McMillan et al. J Exp Med. .

Abstract

Interleukin (IL)-9 is a pleiotropic cytokine secreted by T helper (Th)2 cells and has been proposed as a candidate gene for asthma and allergy. We have used mice genetically deficient in IL-9 to determine the role of this cytokine in the pathophysiologic features of the allergic pulmonary response-airway hyperreactivity (AHR) and eosinophilia. We have demonstrated that IL-9 is not required for the development of a robust Th2 response to allergen in sensitized mice. IL-9 knockout mice developed a similar degree of eosinophilic inflammation and AHR to their wild-type littermates. Goblet cell hyperplasia and immunoglobulin (Ig) E production were also unaffected by the lack of IL-9. Moreover, levels of bronchoalveolar lavage (BAL) IL-4, IL-5, and IL-13 were comparable between wild-type and knockout mice. These findings indicate that IL-9 is not obligatory for the development of eosinophilia and AHR, and imply that other Th2 cytokines can act in a compensatory fashion VSports手机版. .

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Figures

Figure 1.
Figure 1.
Effect of IL-9 deficiency on AHR. AHR was measured 24 h after the final OVA challenge using a Buxco system where mice were exposed to increasing concentrations of methacholine (3–100 mg/ml). Results are shown for Penh after allergen challenge in WT mice and IL-9 KO mice either sensitized to alum/PBS or OVA/alum. Values are expressed as mean ± SEM; n = 9–13 per group in two separate experiments.
Figure 2.
Figure 2.
Differential cell counts in BAL (A) and lung tissue digest (B) from WT mice (white bars) and IL-9 KO mice (black bars). Mice were killed 24 h after the final OVA challenge. BAL and lung tissue digest cells were isolated as described in Materials and Methods. Values are expressed as mean ± SEM; n = 11–14 per group in two separate experiments.
Figure 2.
Figure 2.
Differential cell counts in BAL (A) and lung tissue digest (B) from WT mice (white bars) and IL-9 KO mice (black bars). Mice were killed 24 h after the final OVA challenge. BAL and lung tissue digest cells were isolated as described in Materials and Methods. Values are expressed as mean ± SEM; n = 11–14 per group in two separate experiments.
Figure 3.
Figure 3.
OVA-induced lung inflammation in IL-9 KO and WT mice. An assessment of pulmonary inflammation was made by determining the extent of inflammatory infiltrates in sections stained with H&E (A) or PAS (B). Stained sections were scored as described in Materials and Methods, and scores for individual WT (squares) and KO (circles) mice are represented. Bars depict means of groups, n = 8–9 per group. Representative photomicrographs of H&E- and PAS-stained lung sections from WT (i) and KO (ii) OVA-challenged mice are shown.
Figure 4.
Figure 4.
Effect of IL-9 deficiency on serum IgE levels. Mice were killed 24 h after the final OVA challenge, bled via cardiac puncture, serum collected, and analyzed by ELISA for total IgE (A) and OVA-specific IgE (B). Data are expressed as mean ± SEM; n = 4–13 per group.
Figure 4.
Figure 4.
Effect of IL-9 deficiency on serum IgE levels. Mice were killed 24 h after the final OVA challenge, bled via cardiac puncture, serum collected, and analyzed by ELISA for total IgE (A) and OVA-specific IgE (B). Data are expressed as mean ± SEM; n = 4–13 per group.
Figure 5.
Figure 5.
Effect of IL-9 deficiency on cytokine production. IL-4 (A), IL-5 (B), IL-13 (C), and eotaxin (D) levels were measured in BAL fluid (left) and lung homogenate (right shaded) by ELISA in samples from WT mice (white bars) and IL-9 KO mice (black bars) killed 24 h after the final OVA challenge. Data are expressed as mean ± SEM; n = 14 per group for BAL cytokines; n = five per group for lung cytokines and P < 0.05 in comparison to WT group using a Mann Whitney U test.

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