Nitric Oxide Mediates Relative Airway Hyporesponsiveness to Lipopolysaccharide in Surfactant Protein A–Deficient Mice
| Autor: | Charles Giamberardino, Sambuddho Mukherjee, Simone Degan, Timothy J. McMahon, Lee A. Maddox, David A. Schwartz, Julia K. L. Walker, Barbara L. Lawson, Hongmei Zhu, Jerry P. Eu, Thomas R. Korfhagen, Mary E. Sunday, William M. Foster, Jo Rae Wright, Loretta G. Que, Amy M. Pastva, Erin N. Potts, Bethany J. Hsia |
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| Rok vydání: | 2011 |
| Předmět: |
Pulmonary and Respiratory Medicine
Innate immune system Lipopolysaccharide biology Clinical Biochemistry Cell Inflammation Cell Biology Pharmacology Nitric oxide Surfactant protein A chemistry.chemical_compound medicine.anatomical_structure chemistry Immunity Immunology medicine biology.protein medicine.symptom Protein A Molecular Biology |
| Zdroj: | American Journal of Respiratory Cell and Molecular Biology. 44:175-184 |
| ISSN: | 1535-4989 1044-1549 |
| Popis: | THIS ARTICLE WAS RETRACTED ON NOVEMBER 1, 2016. Please see www.atsjournals.org/doi/full/10.1165/rcmb.555retractionSurfactant protein A (SP-A) mediates innate immune cell responses to LPS, a cell wall component of gram-negative bacteria that is found ubiquitously in the environment and is associated with adverse health effects. Inhaled LPS induces lung inflammation and increases airway responsiveness (AR). However, the role of SP-A in mediating LPS-induced AR is not well-defined. Nitric oxide (NO) is described as a potent bronchodilator, and previous studies showed that SP-A modulates the LPS-induced production of NO. Hence, we tested the hypothesis that increased AR, observed in response to aerosolized LPS exposure, would be significantly reduced in an SP-A–deficient condition. Wild-type (WT) and SP-A null (SP-A−/−) mice were challenged with aerosolized LPS. Results indicate that despite similar inflammatory indices, LPS-treated SP-A−/− mice had attenuated AR after methacholine challenge, compared with WT... |
| Databáze: | OpenAIRE |
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