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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 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.
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fig4: 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.

Mentions: Elevated levels of IgE have been reported to be important in the development of an allergic pulmonary response, and evidence suggests that IL-9 can alter the in vitro differentiation of B cells and enhance Ig production (27, 8). We measured total IgE and OVA-specific IgE in sera from KO and WT mice after allergen challenge. Both groups of mice showed significantly enhanced production of total and antigen specific IgE after allergen challenge (Fig. 4) . IL-9 deficiency had no significant effect on the production of total IgE. Levels of OVA-specific IgE were slightly lower in the absence of IL-9, indicating that the antigen-specific Ig response was perhaps less efficient.


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 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.
© Copyright Policy
Related In: Results  -  Collection

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

fig4: 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.
Mentions: Elevated levels of IgE have been reported to be important in the development of an allergic pulmonary response, and evidence suggests that IL-9 can alter the in vitro differentiation of B cells and enhance Ig production (27, 8). We measured total IgE and OVA-specific IgE in sera from KO and WT mice after allergen challenge. Both groups of mice showed significantly enhanced production of total and antigen specific IgE after allergen challenge (Fig. 4) . IL-9 deficiency had no significant effect on the production of total IgE. Levels of OVA-specific IgE were slightly lower in the absence of IL-9, indicating that the antigen-specific Ig response was perhaps less efficient.

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