title: Antigen-induced airway hyperresponsiveness in absence of broncho-obstruction in sensitized guinea pigs.
abstract: BACKGROUND
  Airway obstruction after antigen challenge is not always observed in patients with allergic asthma, even if they develop hyperresponsiveness. A similar event is observed in our guinea pig model of allergic asthma. Our aim was to study this phenomenon.
  
  
  METHODS
  Sensitized guinea pigs were challenged with ovalbumin (OVA) 3 times every 10 days. Animals were divided into 2 groups: (1) Guinea pigs exhibiting airway obstruction after antigen challenge (R = responders), and (2) guinea pigs lacking airway obstruction response (NR = nonresponders). After the third antigen challenge, antigen-induced airway hyperresponsiveness (AI-AHR), serum OVA-specific immunoglobulins, bronchoalveolar lavage fluid (BALF) inflammatory cells, histamine, cysteinyl leukotrienes and thromboxane A2 (TxA2) BALF levels, and in vitro tracheal contraction induced by contractile mediators and OVA were evaluated.
  
  
  RESULTS
  R group consistently displayed a transient antigen-induced airway obstruction (AI-AO) as well as AI-AHR, high T×A2, histamine, OVA-IgG1, OVA-IgE and OVA-IgA levels, and intense granulocyte infiltration. NR group displayed no AI-AO and no changes in BALF measurements; nevertheless, AI-AHR and elevated OVA-IgG1 and OVA-IgA levels were observed. In all groups, histamine, TxA2 and leukotriene D4 induced a similar contraction. Tracheal OVA-induced contraction was observed only in R group. AI-AHR magnitude showed a direct association with OVA-IgG1 and OVA-IgA levels. The extent of AI-AO correlated directly with OVA-IgE and inversely with OVA-IgA levels.
  
  
  CONCLUSIONS
  Our data suggest that TxA2 and histamine participate in AI-AO likely through an IgE mechanism. AI-AHR might occur independently of AI-AO, contractile mediators release, and airway inflammatory cell infiltration, but IgA and IgG1 seem to be involved.
authors.affiliation: Departamento de Hiperreactividad Bronquial, Instituto Nacional de Enfermedades Respiratorias Ismael Cosio Villegas, Calzada de Tlalpan, México DF, México.
authors.forename: Patricia
authors.initials: P
authors.lastname: Ramos-Ramírez
authors.forename: María G
authors.initials: MG
authors.lastname: Campos
authors.forename: Erasmo
authors.initials: E
authors.lastname: Martínez-Cordero
authors.forename: Blanca
authors.initials: B
authors.lastname: Bazán-Perkins
authors.forename: Eduardo
authors.initials: E
authors.lastname: García-Zepeda
mesh_terms: D000402:Airway Obstruction / Q000276:immunology / Q000503:physiopathology; D000818:Animals; D000941:Antigens / Q000008:administration & dosage; D001249:Asthma / Q000209:etiology* / Q000276:immunology / Q000503:physiopathology; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology / Q000276:immunology; D004195:Disease Models, Animal; D006168:Guinea Pigs; D006632:Histamine / Q000378:metabolism; D006801:Humans; D007114:Immunization; D007136:Immunoglobulins / Q000097:blood; D017998:Leukotriene D4 / Q000378:metabolism; D008297:Male; D010047:Ovalbumin / Q000008:administration & dosage / Q000276:immunology; D012130:Respiratory Hypersensitivity / Q000276:immunology / Q000503:physiopathology; D013928:Thromboxane A2 / Q000378:metabolism
chemical_list: D000941:Antigens; D007136:Immunoglobulins; D013928:Thromboxane A2; D017998:Leukotriene D4; D006632:Histamine; D010047:Ovalbumin