Characterization of the Antigen-Presenting Cell and T Cell Requirements for Induction of Pulmonary Eosinophilia in a Murine Model of Asthma

Lambert, Laurie E.; Berling, Jennifer S.; Kudlacz, Elizabeth M.

doi:10.1006/clin.1996.0194

Cited by 12 publications

(8 citation statements)

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“…Far less is known about the effects of short-term smoke exposure on the lungs, especially in lungs of patients already afflicted by an allergic inflammation. Previous studies have shown that the induction of allergic airway inflammation and the accompanying AHR were associated with an increase in eosinophils (13), macrophages (14,15), and CD4 ϩ T cells in lung tissue (13,(16)(17)(18), an increase in Th2 cytokines in BAL fluid (19), and an increase in OVA-specific IgE in serum (20,21). Our model met most of these characteris- tics.…”

Section: Discussionsupporting

confidence: 58%

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Short-Term Smoke Exposure Attenuates Ovalbumin-Induced Airway Inflammation in Allergic Mice

Melgert

Postma

Geerlings

et al. 2004

Am J Respir Cell Mol Biol

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Little is known about effects of smoking on airway inflammation in asthma. We tested the hypothesis that smoking enhances established airway inflammation in a mouse model of allergic asthma. C57Bl/6j mice were sensitized to ovalbumin (OVA) and challenged with OVA (OVA-mice) or sham-sensitized to phosphate-buffered saline (PBS) and challenged with PBS aerosols (PBS-mice) for 7 wk. At 4 wk, mice were additionally exposed to air (nonsmoking controls) or mainstream smoke for 3 wk. Using whole body plethysmography, we found OVA-induced bronchoconstriction to be significantly inhibited in smoking OVA-mice as compared with nonsmoking OVA-mice (1 +/- 2% increase versus 22 +/- 6% increase in enhanced pause, respectively). Smoking did not change airway hyperresponsiveness (AHR) to methacholine in PBS-mice, yet significantly attenuated AHR in OVA-mice 24 h after OVA challenge as compared with nonsmoking mice. This was accompanied by reduced eosinophil numbers in lung lavage fluid and tissue of smoking OVA-mice compared with nonsmoking OVA-mice. In contrast to our hypothesis, short-term smoking reduced responsiveness to OVA and methacholine in OVA-mice and decreased airway inflammation when compared with nonsmoking mice. This effect of smoking may be different for long-term smoking, in which remodeling effects of smoking can be expected to interrelate with remodeling changes caused by asthmatic disease.

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Section: Discussionsupporting

confidence: 58%

“…On the first 2 d, 2 times 4 puffs of smoke from 2R1 Reference Cigarettes (University of Kentucky) were administered. Two times 6,8,10,12,15,18,21, and 24 puffs were given on subsequent days during a "break in" period. For the remainder of the 3 wk, two times 24 puffs were given daily, which equals 4 cigarettes.…”

Section: Smoke Exposure Proceduresmentioning

confidence: 99%

Short-Term Smoke Exposure Attenuates Ovalbumin-Induced Airway Inflammation in Allergic Mice

Melgert

Postma

Geerlings

et al. 2004

Am J Respir Cell Mol Biol

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“…The discrepancy in their results and our own is likely due to significant differences in the immunization and challenge protocols (55). The immunization and challenge protocol used by Xiong et al resulted in ‫%09ف‬ eosinophilia in the BAL in their WT OVA/OVA group, considerably higher than the proportion reported by us and others in models of allergeninduced airway inflammation in the mouse (7,52,(56)(57)(58)(59). The lack of a significant difference in the pulmonary resistance (R L ) response to methacholine between the NOS2-KO OVA/OVA and WT (B6) OVA/OVA mice prompted us to repeat these experiments using unanesthetized mice studied in a whole body plethysmograph.…”

Section: Discussionmentioning

confidence: 63%

Contribution of Nitric Oxide Synthases 1, 2, and 3 to Airway Hyperresponsiveness and Inflammation in a Murine Model of Asthma

Sanctis

MacLean

Hamada

et al. 1999

The Journal of Experimental Medicine

198

140

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Asthma is a chronic disease characterized by increased airway responsiveness and airway inflammation. The functional role of nitric oxide (NO) and the various nitric oxide synthase (NOS) isoforms in human asthma is controversial. To investigate the role of NO in an established model of allergic asthma, mice with targeted deletions of the three known isoforms of NOS (NOS1, 2, and 3) were studied. Although the inducible (NOS2) isoform was significantly upregulated in the lungs of ovalbumin (OVA)-sensitized and -challenged (OVA/OVA) wild-type (WT) mice and was undetectable in similarly treated NOS2-deficient mice, airway responsiveness was not significantly different between these groups. OVA/OVA endothelial (NOS3)-deficient mice were significantly more responsive to methacholine challenge compared with similarly treated NOS1 and NOS1&3-deficient mice. Airway responsiveness in OVA/OVA neuronal (NOS1)-deficient and neuronal/endothelial (NOS1&3) double-deficient mice was significantly less than that observed in similarly treated NOS2 and WT groups. These findings demonstrate an important function for the nNOS isoform in controlling the inducibility of airway hyperresponsiveness in this model of allergic asthma.

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“…L-4 and -13 induce the production of immunoglobulin (Ig)E by B cells (7)(8)(9), and IL-5 regulates the growth, differentiation, and activation of eosinophils (10). In allergen-sensitized mice, eosinophilic airway inflammation is dependent upon the presence of CD4+ T lymphocytes (11,12), and depletion of CD4 + T lymphocytes prevents the development of airway hyperreactivity and pulmonary eosinophilia in response to an inhaled allergen (13).…”

mentioning

confidence: 99%

Proinflammatory Roles of T-Cell Receptor (TCR) γδ and TCR αβ Lymphocytes in a Murine Model of Asthma

Schramm

Puddington

Yiamouyiannis

et al. 2000

Am J Respir Cell Mol Biol

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The role of lymphocytes bearing alphabeta or gammadelta T-cell receptors (TCRs) was assessed during the acute allergic response in a mouse model of asthma. The inflammatory immune response to ovalbumin (OVA) was characterized in wild-type C57BL/6J mice and congenic TCRbeta(-/-) and TCRdelta(-/-) mice by evaluation of airway eosinophilia, histopathology, serum immunoglobulin (Ig)E levels, and in vivo airway responsiveness to methacholine. OVA-challenged wild-type mice demonstrated marked pulmonary inflammation, evidenced by airway eosinophilia (68 +/- 7 x 10(4) cells), peribronchial lympho-plasmocytic infiltration, and elevated serum IgE (4.9 +/- 0.6 microg/ml). These responses were markedly attenuated in TCRdelta(-/-) animals (5.0 +/- 1.0 x 10(4) eosinophils and 1.6 +/- 0. 3 microg/ml IgE) and were completely absent in TCRbeta(-/-) mice (< 1 x 10(3) eosinophils and 0.38 +/- 0.21 microg/ml IgE). Similar results were observed in mice treated with anti-TCRgammadelta or anti-TCRalphabeta monoclonal antibodies. Airway responsiveness to aerosolized methacholine was also reduced in challenged TCRdelta(-/-) animals relative to challenged wild-type mice. These results demonstrate that acute allergic airway responses are dependent upon intact TCRalphabeta and TCRgammadelta lymphocyte function and that TCRgammadelta cells promote acute airway sensitization.

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Characterization of the Antigen-Presenting Cell and T Cell Requirements for Induction of Pulmonary Eosinophilia in a Murine Model of Asthma

Cited by 12 publications

References 0 publications

Short-Term Smoke Exposure Attenuates Ovalbumin-Induced Airway Inflammation in Allergic Mice

Short-Term Smoke Exposure Attenuates Ovalbumin-Induced Airway Inflammation in Allergic Mice

Contribution of Nitric Oxide Synthases 1, 2, and 3 to Airway Hyperresponsiveness and Inflammation in a Murine Model of Asthma

Proinflammatory Roles of T-Cell Receptor (TCR) γδ and TCR αβ Lymphocytes in a Murine Model of Asthma

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