OBJECTIVE: To determine the possible involvement of vasoactive intestinal peptide (VIP) in the development of airway hyper responsiveness (AHR). METHODS: Twenty-five rabbits were randomly divided into five groups (5 animals each). Four groups were exposed to 2.0 ppm ozone 1 h/day for 1 (group B(0)), 2 (group B(1)), 4 (group B(2)), and 8 (group B(3)) days, respectively. The control group (group A) breathed only filtered room air. The changes of the VIP level and the mRNA expression of VIP receptor 1 (VIPR1) in the lung were detected at various ozone-stressing time points. In situ hybridization was performed to examine the distribution of VIPR1 in the lung. RESULTS: (1) The concentration of VIP in the lung increased slowly and were maximal at day 4, then returned to the normal level. (2) The changing pattern of the VIPR1 mRNA in the lung was similar to those observed for VIP. Increases in VIPR1 mRNA were detectable by 1 day and maximal by 2 - 4 days, and then decreased slowly. (3) In group A, VIPR1 was expressed on airway epithelium, in pulmonary interstitial and focal areas of airways and vascular smooth muscles. By days 2 to 4, hybridization staining increased and the majority of VIPR1-positive cells was located in the perivascular and peribronchiolar area. On day 8, very few positive cells were seen in the lung. CONCLUSION: VIP may play an important role in the development of AHR by binding with VIPR1.
OBJECTIVE: To determine the possible involvement of vasoactive intestinal peptide (VIP) in the development of airway hyper responsiveness (AHR). METHODS: Twenty-five rabbits were randomly divided into five groups (5 animals each). Four groups were exposed to 2.0 ppm ozone 1 h/day for 1 (group B(0)), 2 (group B(1)), 4 (group B(2)), and 8 (group B(3)) days, respectively. The control group (group A) breathed only filtered room air. The changes of the VIP level and the mRNA expression of VIP receptor 1 (VIPR1) in the lung were detected at various ozone-stressing time points. In situ hybridization was performed to examine the distribution of VIPR1 in the lung. RESULTS: (1) The concentration of VIP in the lung increased slowly and were maximal at day 4, then returned to the normal level. (2) The changing pattern of the VIPR1 mRNA in the lung was similar to those observed for VIP. Increases in VIPR1 mRNA were detectable by 1 day and maximal by 2 - 4 days, and then decreased slowly. (3) In group A, VIPR1 was expressed on airway epithelium, in pulmonary interstitial and focal areas of airways and vascular smooth muscles. By days 2 to 4, hybridization staining increased and the majority of VIPR1-positive cells was located in the perivascular and peribronchiolar area. On day 8, very few positive cells were seen in the lung. CONCLUSION:VIP may play an important role in the development of AHR by binding with VIPR1.