Prostaglandin modulation of airway inflammation and hyperresponsiveness in mice sensitized without adjuvant |
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| Institution: | 1. The National Institute of Environmental Medicine, Division of Physiology, Karolinska Institutet, Stockholm, Sweden;2. The Centre for Allergy Research, Karolinska Institutet, Stockholm, Sweden;3. Firestone Institute for Respiratory Health, McMaster University, Hamilton, Canada;4. Department of Medicine, Clinical Immunology and Allergy Unit, Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden;1. Department of Obstetrics and Gynecology, Third Affiliated Hospital of Guangzhou Medical University, Key Laboratory for Major Obstetric Diseases of Guangdong Province, Guangzhou, China;2. Department of Obstetrics and Gynecology, Dongguan People’s Hospital, Dongguan,China;3. State Key Laboratory of Organic Geochemistry, Guangdong Key Laboratory of Environment and Resources, Guangzhou Institute of Geochemistry, Chinese Academy of Sciences, Guangzhou, China;1. Department of Respiratory Medicine, Saitama Medical University, Iruma-gun, Saitama, Japan;2. Allergy Center, Saitama Medical University Hospital, Iruma-gun, Saitama, Japan;3. Department of General Internal Medicine, Saitama Medical University, Iruma-gun, Saitama, Japan;1. Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, Hefei, China;2. Medical Genetics Center, Anhui Medical College, Hefei, China |
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| Abstract: | As adjuvant during sensitization may cause unspecific immune reactions, the aim of the present study was to define the role of cyclooxygenase (COX) activity on airway inflammation and airway hyperresponsiveness (AHR) in an adjuvant-free allergic mouse model.Administration of diclofenac and indomethacin (non-selective COX inhibitors), FR122047 (COX-1 inhibitor) and lumiracoxib (selective COX-2 inhibitor) enhanced AHR. Only diclofenac and lumiracoxib reduced the inflammatory cell content of bronchoalveolar lavage (BAL). Moreover, levels of prostaglandins in BAL were reduced by indomethacin and FR122047 but were unaffected by lumiracoxib. However, compared with antigen controls, none of the COX inhibitors displayed major effects on the production of cytokines, smooth muscle mass, number of goblet cells and eosinophils, or collagen deposition in the airways.These data in mice sensitized without adjuvant support the fact that COX products have a general bronchoprotective role in allergic airway inflammation. Furthermore, the data suggest that COX-1 activity predominantly generates prostanoids in BAL, whereas COX-2 activity is associated with the accumulation of inflammatory cells in BAL. This study further supports that AHR on the one hand, and the inflammatory response and generation of prostanoids on the other, are dissociated and, at least in part, uncoupled events. |
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