title: Heparin protects BALB/c mice from mite-induced airway allergic inflammation.
abstract: More and more studies have demonstrated the anti-inflammatory effects of heparin. However, in the aspect of allergic airway inflammation, data about its daily use in animal model is scarce. To evaluate the efficacy of 22-day intranasal heparin administration in mite-induced airway allergic inflammation in BALB/c mice, the murine model of house dust-mite allergen-induced asthma was used to assess the effect of heparin (h) and low molecular weight heparin (l mwh) administered intra-nasally (IN) throughout the full study period (22 days). Effects were monitored by histopathology, cell counts in broncho-alveolar lavage fluid (BALF), local cytokine production, serum, specific antibody levels, and airway resistance measurements. Compared to the positive control group, both hIN and lmwhIN groups had lower peri-bronchiolar/alveolar inflammatory pathology score and lower goblet cell scores (p less than 0.01); lower eosinophil and neutrophil counts in BALF (p less than 0.0001); and lower cytokine levels including IL-17A/F, IL-5, IL-13, IL-8 and eotaxin in lung tissue (p less than 0.001). Serum Der p-specific IgE level was also lower in heparin-treated groups (p less than 0.004). The two heparin-treated groups also revealed lower value of Penh after Mch stimulation. In conclusion, heparin and lmw heparin decrease serum Der p-specific IgE level and possess anti-inflammatory effects on mite-induced airway allergic inflammation model in BALB/c mice.
authors.affiliation: Pediatric Department, Taichung Veterans General Hospital, Taichung, Taiwan.
authors.forename: L S
authors.initials: LS
authors.lastname: Fu
authors.forename: J J
authors.initials: JJ
authors.lastname: Tsai
authors.forename: Y J
authors.initials: YJ
authors.lastname: Chen
authors.forename: H K
authors.initials: HK
authors.lastname: Lin
authors.forename: M C
authors.initials: MC
authors.lastname: Tsai
authors.forename: M D T
authors.initials: MD
authors.lastname: Chang
mesh_terms: D000281:Administration, Intranasal; D000403:Airway Resistance / Q000187:drug effects; D000485:Allergens / Q000276:immunology*; D000818:Animals; D018926:Anti-Allergic Agents / Q000008:administration & dosage / Q000494:pharmacology*; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage / Q000494:pharmacology*; D039741:Antigens, Dermatophagoides / Q000276:immunology*; D060829:Arthropod Proteins / Q000276:immunology*; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D004334:Drug Administration Schedule; D006493:Heparin / Q000008:administration & dosage / Q000494:pharmacology*; D007073:Immunoglobulin E / Q000097:blood; D018836:Inflammation Mediators / Q000378:metabolism; D008168:Lung / Q000187:drug effects* / Q000276:immunology / Q000473:pathology / Q000503:physiopathology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D012130:Respiratory Hypersensitivity / Q000097:blood / Q000276:immunology / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D013997:Time Factors
chemical_list: D000485:Allergens; D018926:Anti-Allergic Agents; D000893:Anti-Inflammatory Agents; D039741:Antigens, Dermatophagoides; D060829:Arthropod Proteins; D016207:Cytokines; D018836:Inflammation Mediators; D007073:Immunoglobulin E; D006493:Heparin