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

McMillan SJ, Bishop B, Townsend MJ, McKenzie AN, Lloyd CM - J. Exp. Med. (2002)

Bottom Line: 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.Goblet cell hyperplasia and immunoglobulin (Ig) E production were also unaffected by the lack of IL-9.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.

View Article: PubMed Central - PubMed

Affiliation: Leukocyte Biology Section, Division of Biomedical Sciences, Faculty of Medicine, Imperial College of Science, Technology, and Medicine, London SW7 2AZ, England.

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.

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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.
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fig1: 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.

Mentions: AHR is a cardinal feature of the pulmonary allergic response and has been linked with the development of robust Th2 responses. To determine whether deficiency in IL-9 has a direct effect on development of airway dysfunction, AHR was measured by whole body plethysmography 24 h after the final, serial OVA challenge in knockout (KO) and WT mice. Fig. 1 shows that increasing doses of methacholine elicited a similar response in IL-9–deficient mice compared with their WT littermates. There was no difference in the response to methacholine in unsensitized (alum/PBS) wild–type mice or IL-9 KO over the dose range studied. However, both OVA-sensitized WT and IL-9–deficient mice showed significantly enhanced response to methacholine after allergen challenge, as compared with the unsensitized control groups.


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

McMillan SJ, Bishop B, Townsend MJ, McKenzie AN, Lloyd CM - J. Exp. Med. (2002)

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.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2196020&req=5

fig1: 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.
Mentions: AHR is a cardinal feature of the pulmonary allergic response and has been linked with the development of robust Th2 responses. To determine whether deficiency in IL-9 has a direct effect on development of airway dysfunction, AHR was measured by whole body plethysmography 24 h after the final, serial OVA challenge in knockout (KO) and WT mice. Fig. 1 shows that increasing doses of methacholine elicited a similar response in IL-9–deficient mice compared with their WT littermates. There was no difference in the response to methacholine in unsensitized (alum/PBS) wild–type mice or IL-9 KO over the dose range studied. However, both OVA-sensitized WT and IL-9–deficient mice showed significantly enhanced response to methacholine after allergen challenge, as compared with the unsensitized control groups.

Bottom Line: 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.Goblet cell hyperplasia and immunoglobulin (Ig) E production were also unaffected by the lack of IL-9.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.

View Article: PubMed Central - PubMed

Affiliation: Leukocyte Biology Section, Division of Biomedical Sciences, Faculty of Medicine, Imperial College of Science, Technology, and Medicine, London SW7 2AZ, England.

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.

Show MeSH
Related in: MedlinePlus