ArticleRespiratory research2003
Attenuated allergic airway hyperresponsiveness in C57BL/6 mice is associated with enhanced surfactant protein (SP)-D production following allergic sensitization.
Article in Respiratory research, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 67 citations in OpenAlex.
- Genetic background and microbiome drive susceptibility to epicutaneous sensitization and food allergy in adjuvant-free mouse model.Frontiers in immunology · 2024Article
- Regulation of Surfactant Protein Gene Expression byMicroorganisms · 2023Article
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- Ozone-Induced Oxidative Stress, Neutrophilic Airway Inflammation, and Glucocorticoid Resistance in Asthma.Frontiers in immunology · 2021Review
- Surfactant Protein D Recognizes Multiple Fungal Ligands: A Key Step to Initiate and Intensify the Anti-fungal Host Defense.Frontiers in cellular and infection microbiology · 2020Review
- Ozone Inhalation Attenuated the Effects of Budesonide onFrontiers in immunology · 2019Article
- Protective Role of Surfactant Protein-D Against Lung Injury and Oxidative Stress Induced by Nitrogen Mustard.Toxicological sciences : an official journal of the Society of Toxicology · 2018Article
- Surfactant Protein D in Respiratory and Non-Respiratory Diseases.Frontiers in medicine · 2018Review
- Host Soluble Mediators: Defying the Immunological Inertness ofJournal of fungi (Basel, Switzerland) · 2017Review
- Comparative study of fertilization rates of C57BL/6NKorl and C57BL/6N mice obtained from two other sources.Laboratory animal research · 2017Article
- NKT cells contribute to basal IL-4 production but are not required to induce experimental asthma.PloS one · 2017Article
- A pathogenic role for the integrin CD103 in experimental allergic airways disease.Physiological reports · 2016Article
- Group 2 innate lymphoid cells mediate ozone-induced airway inflammation and hyperresponsiveness in mice.The Journal of allergy and clinical immunology · 2016Article
- Eosinophil-associated lung diseases. A cry for surfactant proteins A and D help?American journal of respiratory cell and molecular biology · 2014Review
- Oncostatin M overexpression induces matrix deposition, STAT3 activation, and SMAD1 Dysregulation in lungs of fibrosis-resistant BALB/c mice.Laboratory investigation; a journal of technical methods and pathology · 2014Article
- Innate and adaptive immune response to pneumonia virus of mice in a resistant and a susceptible mouse strain.Viruses · 2013Article
- Prolonged injury and altered lung function after ozone inhalation in mice with chronic lung inflammation.American journal of respiratory cell and molecular biology · 2012Article
- The effect of lipoprotein-associated phospholipase A2 deficiency on pulmonary allergic responses in Aspergillus fumigatus sensitized mice.Respiratory research · 2012Article
- Innate Immunity and the Role of Epithelial Barrier During Aspergillus fumigatus Infection.Current immunology reviews · 2012Article
- KLF13 sustains thymic memory-like CD8(+) T cells in BALB/c mice by regulating IL-4-generating invariant natural killer T cells.The Journal of experimental medicine · 2011Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundC57BL/6 mice have attenuated allergic airway hyperresponsiveness (AHR) when compared with Balb/c mice but the underlying mechanisms remain unclear. SP-D, an innate immune molecule with potent immunosuppressive activities may have an important modulatory role in the allergic airway response and the consequent physiological changes. We hypothesized that an elevated SP-D production is associated with the impaired ability of C57BL/6 mice to develop allergic AHR.
methodsSP-D mRNA and protein expression was investigated during development of allergic airway changes in a model of Aspergillus fumigatus (Af)-induced allergic inflammation. To study whether strain dependency of allergic AHR is associated with different levels of SP-D in the lung, Balb/c and C57BL/6 mice were compared.
resultsSensitization and exposure to Af induced significant airway inflammation in both mouse strains in comparison with naïve controls. AHR to acetylcholine however was significantly attenuated in C57BL/6 mice in spite of increased eosinophilia and serum IgE when compared with Balb/c mice (p < 0.05). Af challenge of sensitized C57BL/6 mice induced a markedly increased SP-D protein expression in the SA surfactant fraction (1,894 +/- 170% of naïve controls) that was 1.5 fold greater than the increase in Balb/c mice (1,234 +/- 121% p < 0.01). These changes were selective since levels of the hydrophobic SP-B and SP-C and the hydrophilic SP-A were significantly decreased following sensitization and challenge with Af in both strains. Further, sensitized and exposed C57BL/6 mice had significantly lower IL-4 and IL-5 in the BAL fluid than that of Balb/c mice (p < 0.05).
conclusionsThese results suggest that enhanced SP-D production in the lung of C57BL/6 mice may contribute to an attenuated AHR in response to allergic airway sensitization. SP-D may act by inhibiting synthesis of Th2 cytokines.
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