The IL-1 receptor antagonist prevented ozone-induced airway hyperreactivity 3 days, but not 1 day, after ozone exposure. nerves and prevented ozone-induced deposition of extracellular eosinophil major basic protein in airways. These data demonstrate that IL-1 mediates ozone-induced airway hyperreactivity at 3 days, but not 1 day, after ozone exposure. Furthermore, avoiding hyperreactivity was accompanied by decreased eosinophil major basic protein deposition within the lung, suggesting that IL-1 affects eosinophil activation 3 days after ozone exposure. test. Baseline and histology data were analyzed by multiple one-way ANOVAs with Atenolol Bonferroni correction. A value of less than 0.05 was considered significant. Analyses were made with Kaleidagraph (version 4.01; Synergy Software, Reading, PA) or StatView 4.5 (Abacus Ideas, Berkeley, CA). RESULTS Three days after ozone exposure, IL-1 concentration in bone marrow was almost doubled (Number 1), while 1 day after ozone exposure IL-1 was improved slightly. In contrast, IL-1 was below the limit of detection (2 pg/ml) in BALF from both ozone- and air-exposed guinea pigs (data not shown). Open in a separate window Number 1. Atenolol IL-1 was present in bone marrow of control guinea pigs (= 0.057 from control. Data are means SE, = 5. Ozone exposure significantly improved baseline pulmonary inflation pressure 1 day after ozone exposure (Table 1). Pretreatment with the IL-1 receptor antagonist did not impact baseline pulmonary inflation pressure 1 day after ozone exposure. Neither ozone nor the IL-1 receptor antagonist affected resting heart rate 1 or 3 days after ozone exposure. Resting blood pressure was not affected by ozone or from the IL-1 receptor antagonist. Vehicle treatment did not impact baseline parameters compared with settings. TABLE 1. BASELINE CARDIOVASCULAR AND PULMONARY Guidelines next to respective controls). *The entire rate of recurrence response after ozone exposure is definitely significantly different from that of air-exposed guinea pigs. ?The entire frequency response in the presence of IL-1 receptor antagonist is significantly different from ozone-exposed guinea pigs. Data are indicated as means SE, = 3C7. Ozone slightly, but not significantly, improved bronchoconstriction in response to intravenous acetylcholine at 1 and 3 days (Numbers 3A and Rabbit Polyclonal to Cyclin H 3B). This increase probably does not contribute to ozone-induced airway hyperreactivity, since it was small compared with ozone’s potentiation of Atenolol vagally induced bronchoconstriction. The IL-1 receptor antagonist improved smooth muscle mass responsiveness to acetylcholine, but the effect was not significant and occurred regardless of whether animals were exposed to air flow or ozone (Number 3C). Vehicle treatment did not impact acetylcholine-induced bronchoconstriction Atenolol in either air flow- or ozone-exposed animals (Number 3B). Open in a separate window Number 3. Blocking IL-1 receptors raises airway smooth muscle mass contraction to intravenous acetylcholine. Acetylcholine-induced bronchoconstriction was measured in vagotomized guinea pigs as an increase in pulmonary inflation pressure. (next to respective settings). ?The entire frequency response in the presence of IL-1 receptor antagonist is significantly different from that of ozone-exposed guinea pigs. Data are indicated as means SE, = 4C7. In the heart, ozone exposure improved acetylcholine-induced bradycardia, although not significantly, compared with air-exposed controls 1 day after ozone exposure (Number 4C). Ozone did not impact either vagally induced or intravenous acetylcholine-induced bradycardia after 3 days (Numbers 4B and 4D). Pretreatment with the IL-1 receptor antagonist didn’t influence bradycardia in atmosphere- or ozone-exposed pets also. Automobile.