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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: 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.

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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Immunohistochemistry of peribronchial tissue after sensitization and challenge with OVA. Localization of eosinophils and mast cells are  shown. +/+ mice are shown in a and c and W/Wv mice in b and d. In c and d, cells were stained with Astra Blue/Vital New Red. For a and b, staining  was with a rabbit anti–mouse MBP antibody and fluorescein-labeled goat anti–rabbit IgG. Original magnification of 500.
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Figure 3: Immunohistochemistry of peribronchial tissue after sensitization and challenge with OVA. Localization of eosinophils and mast cells are shown. +/+ mice are shown in a and c and W/Wv mice in b and d. In c and d, cells were stained with Astra Blue/Vital New Red. For a and b, staining was with a rabbit anti–mouse MBP antibody and fluorescein-labeled goat anti–rabbit IgG. Original magnification of 500.

Mentions: After staining with anti-MBP antibody, sensitization and challenge significantly increased the numbers of eosinophils per area in the peribronchial tissue of both groups of mice (Fig. 3, a and b) to 187 ± 23/mm2 in +/+ mice, 168 ± 18/mm2 in W/Wv mice (n = 4). In animals challenged alone very few eosinophils were detected in these sites (13 ± 4/mm2). Staining with Astra Blue/Vital New Red revealed the accumulation of mast cells in the submucosal tissue of the bronchi in sensitized and challenged +/+ mice (Fig. 3 c). None could be identified in any of the sections examined from W/Wv mice (Fig. 3 d).


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)

Immunohistochemistry of peribronchial tissue after sensitization and challenge with OVA. Localization of eosinophils and mast cells are  shown. +/+ mice are shown in a and c and W/Wv mice in b and d. In c and d, cells were stained with Astra Blue/Vital New Red. For a and b, staining  was with a rabbit anti–mouse MBP antibody and fluorescein-labeled goat anti–rabbit IgG. Original magnification of 500.
© Copyright Policy
Related In: Results  -  Collection

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

Figure 3: Immunohistochemistry of peribronchial tissue after sensitization and challenge with OVA. Localization of eosinophils and mast cells are shown. +/+ mice are shown in a and c and W/Wv mice in b and d. In c and d, cells were stained with Astra Blue/Vital New Red. For a and b, staining was with a rabbit anti–mouse MBP antibody and fluorescein-labeled goat anti–rabbit IgG. Original magnification of 500.
Mentions: After staining with anti-MBP antibody, sensitization and challenge significantly increased the numbers of eosinophils per area in the peribronchial tissue of both groups of mice (Fig. 3, a and b) to 187 ± 23/mm2 in +/+ mice, 168 ± 18/mm2 in W/Wv mice (n = 4). In animals challenged alone very few eosinophils were detected in these sites (13 ± 4/mm2). Staining with Astra Blue/Vital New Red revealed the accumulation of mast cells in the submucosal tissue of the bronchi in sensitized and challenged +/+ mice (Fig. 3 c). None could be identified in any of the sections examined from W/Wv mice (Fig. 3 d).

Bottom Line: 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.

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