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Development of eosinophilic airway inflammation and airway hyperresponsiveness in mast cell-deficient mice.

Takeda K, Hamelmann E, Joetham A, Shultz LD, Larsen GL, Irvin CG, Gelfand EW - J. Exp. Med. (1997)

Bottom Line: Their role in the development of allergen-induced airway hyperresponsiveness (AHR) is controversial and based on indirect evidence.Comparison of OVA-specific immunoglobulin E (IgE) levels in the serum and numbers of eosinophils in bronchoalveolar lavage fluid or lung digests showed no differences between the two groups of mice.Further, measurements of airway resistance and dynamic compliance at baseline and after inhalation of methacholine were similar.

View Article: PubMed Central - PubMed

Affiliation: Division of Basic Sciences and Pulmonary Medicine, Department of Pediatrics, National Jewish Medical and Research Center, Denver, Colorado, USA.

ABSTRACT
Mast cells are the main effector cells of immediate hypersensitivity and anaphylaxis. Their role in the development of allergen-induced airway hyperresponsiveness (AHR) is controversial and based on indirect evidence. To address these issues, mast cell-deficient mice (W/W v) and their congenic littermates were sensitized to ovalbumin (OVA) by intraperitoneal injection and subsequently challenged with OVA via the airways. Comparison of OVA-specific immunoglobulin E (IgE) levels in the serum and numbers of eosinophils in bronchoalveolar lavage fluid or lung digests showed no differences between the two groups of mice. Further, measurements of airway resistance and dynamic compliance at baseline and after inhalation of methacholine were similar. These data indicate that mast cells or IgE-mast cell activation is not required for the development of eosinophilic inflammation and AHR in mice sensitized to allergen via the intraperitoneal route and challenged via the airways.

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Lung resistance (A), and pulmonary dynamic compliance (B)  in sensitized and challenged mice. Rl and Cdyn values were obtained in  response to increasing concentrations of methacholine as described in  Materials and Methods. The results for each group are expressed as means  ± SEM (n = 8). *Significant differences (P <0.05) between the groups.  +Significant differences (P <0.05) between W/Wv and +/+ mice.
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Figure 4: Lung resistance (A), and pulmonary dynamic compliance (B) in sensitized and challenged mice. Rl and Cdyn values were obtained in response to increasing concentrations of methacholine as described in Materials and Methods. The results for each group are expressed as means ± SEM (n = 8). *Significant differences (P <0.05) between the groups. +Significant differences (P <0.05) between W/Wv and +/+ mice.

Mentions: We examined baseline lung function and assessed the airway response to inhaled methacholine. Baseline (before MCh challenge) measures of lung function as assessed with Rl and Cdyn are presented in Table 1. The values in all four groups were comparable. The response to aerosolized methacholine in mice that were challenged with antigen alone revealed small, dose-dependent changes in Rl and a 20–30% dose-dependent fall in Cdyn (Fig. 4). After sensitization and challenge, resistance values increased by almost fivefold and dynamic compliance was reduced by 60–70% with comparable doses of methacholine. The responses in the mast cell–deficient mice, if anything, exceeded the response in the congenic littermates, with a shift to the left in the methacholine dose–response curve for both Rl and Cdyn.


Development of eosinophilic airway inflammation and airway hyperresponsiveness in mast cell-deficient mice.

Takeda K, Hamelmann E, Joetham A, Shultz LD, Larsen GL, Irvin CG, Gelfand EW - J. Exp. Med. (1997)

Lung resistance (A), and pulmonary dynamic compliance (B)  in sensitized and challenged mice. Rl and Cdyn values were obtained in  response to increasing concentrations of methacholine as described in  Materials and Methods. The results for each group are expressed as means  ± SEM (n = 8). *Significant differences (P <0.05) between the groups.  +Significant differences (P <0.05) between W/Wv and +/+ mice.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2198995&req=5

Figure 4: Lung resistance (A), and pulmonary dynamic compliance (B) in sensitized and challenged mice. Rl and Cdyn values were obtained in response to increasing concentrations of methacholine as described in Materials and Methods. The results for each group are expressed as means ± SEM (n = 8). *Significant differences (P <0.05) between the groups. +Significant differences (P <0.05) between W/Wv and +/+ mice.
Mentions: We examined baseline lung function and assessed the airway response to inhaled methacholine. Baseline (before MCh challenge) measures of lung function as assessed with Rl and Cdyn are presented in Table 1. The values in all four groups were comparable. The response to aerosolized methacholine in mice that were challenged with antigen alone revealed small, dose-dependent changes in Rl and a 20–30% dose-dependent fall in Cdyn (Fig. 4). After sensitization and challenge, resistance values increased by almost fivefold and dynamic compliance was reduced by 60–70% with comparable doses of methacholine. The responses in the mast cell–deficient mice, if anything, exceeded the response in the congenic littermates, with a shift to the left in the methacholine dose–response curve for both Rl and Cdyn.

Bottom Line: Their role in the development of allergen-induced airway hyperresponsiveness (AHR) is controversial and based on indirect evidence.Comparison of OVA-specific immunoglobulin E (IgE) levels in the serum and numbers of eosinophils in bronchoalveolar lavage fluid or lung digests showed no differences between the two groups of mice.Further, measurements of airway resistance and dynamic compliance at baseline and after inhalation of methacholine were similar.

View Article: PubMed Central - PubMed

Affiliation: Division of Basic Sciences and Pulmonary Medicine, Department of Pediatrics, National Jewish Medical and Research Center, Denver, Colorado, USA.

ABSTRACT
Mast cells are the main effector cells of immediate hypersensitivity and anaphylaxis. Their role in the development of allergen-induced airway hyperresponsiveness (AHR) is controversial and based on indirect evidence. To address these issues, mast cell-deficient mice (W/W v) and their congenic littermates were sensitized to ovalbumin (OVA) by intraperitoneal injection and subsequently challenged with OVA via the airways. Comparison of OVA-specific immunoglobulin E (IgE) levels in the serum and numbers of eosinophils in bronchoalveolar lavage fluid or lung digests showed no differences between the two groups of mice. Further, measurements of airway resistance and dynamic compliance at baseline and after inhalation of methacholine were similar. These data indicate that mast cells or IgE-mast cell activation is not required for the development of eosinophilic inflammation and AHR in mice sensitized to allergen via the intraperitoneal route and challenged via the airways.

Show MeSH
Related in: MedlinePlus