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Published on: April 2, 2014
Airway function and reactivity, leukocyte influx and nitric oxide after inoculation with parainfluenza-3 virus:
T J Toward1, F J Johnson, J E Boult
1Division of Pharmacology, Welsh School of Pharmacy, Cardiff University, King Edward VII Avenue, Cathays Park, Cardiff CF10 3XF, UK. toby.toward@abbott.com
Abstract:
Guinea-pigs were inoculated with parainfluenza type 3 (PI3) virus (5.2 x 10(7)) or medium (125 microl each nostril). The PDE4-inhibitor, rolipram (1 mg kg(-1)), the corticosteroid, dexamethasone (20 mg kg(-1)), or vehicle were administered (i.p.) 24 h and 0.5 h before inoculation and for 4 days thereafter. Respiratory function, recorded in conscious guinea-pigs as specific airways conductance (sGaw) by whole-body plethysmography, was unaffected over 4 days by inoculation with medium or PI3. Inhaled histamine (nose-only, 1 mM, 20 s) 24 h before inoculation produced no response but 4 days after PI3 inoculation, a significant (P<0.001) bronchoconstriction occurred, indicating airway hyperreactivity (AHR). Dexamethasone or rolipram treatment inhibited the AHR. Four days after PI3- or medium-inoculation, animals underwent bronchoalveolar lavage (BAL) for total and differential (macrophages, eosinophils and neutrophils) cell counts and determination of nitric oxide (NO) as nitrite and nitrate. Compared with medium-inoculated animals, BAL fluid removed 4 days after PI3 inoculation had significantly increased macrophages, eosinophils and neutrophils. Dexamethasone or rolipram significantly (P<0.05) reduced the PI3-induced airways influx of macrophages (by 40% and 47%), eosinophils (79% and 84%) and neutrophils (58% and 61%). PI3-inoculation significantly (P<0.05) increased BALF combined NO metabolites (84.8+/-2.2 microM 100 microl(-1)), compared with medium-inoculated (56.0+/-5.8) or naive animals (45.7+/-2.0). Treating the PI3-infected guinea-pigs with dexamethasone or rolipram significantly (P<0.001) reduced the raised NO metabolites by 34% and 37%, respectively. These results support a role for steroids and PDE4-inhibitors in the management of inflammation and airways hyperreactivity arising from viral infection of the airways.
Insights
Parainfluenza type 3 virus infection in guinea pigs caused airway hyperreactivity and inflammation. Both dexamethasone and rolipram treatments effectively reduced these effects, suggesting their therapeutic potential in viral airway infections.
Area of Science:
- Respiratory Medicine
- Immunology
- Pharmacology
Background:
- Viral respiratory infections, such as those caused by parainfluenza type 3 (PI3) virus, can lead to significant airway inflammation and hyperreactivity.
- Understanding the mechanisms underlying these responses is crucial for developing effective therapeutic strategies.
Purpose of the Study:
- To investigate the effects of PI3 virus inoculation on airway function and inflammation in guinea pigs.
- To evaluate the therapeutic potential of a corticosteroid (dexamethasone) and a PDE4-inhibitor (rolipram) in mitigating PI3-induced airway hyperreactivity and inflammation.
Main Methods:
- Guinea pigs were inoculated with PI3 virus or a control medium.
- Respiratory function was assessed using whole-body plethysmography after histamine challenge.
- Bronchoalveolar lavage (BAL) was performed to analyze inflammatory cell counts and nitric oxide (NO) metabolites.
Main Results:
- PI3 inoculation induced significant airway hyperreactivity (AHR) and increased inflammatory cells (macrophages, eosinophils, neutrophils) in BAL fluid.
- Both dexamethasone and rolipram treatments significantly inhibited PI3-induced AHR and reduced inflammatory cell influx.
- PI3 infection led to elevated levels of NO metabolites in BAL fluid, which were significantly reduced by dexamethasone and rolipram treatment.
Conclusions:
- These findings demonstrate that PI3 virus infection causes airway inflammation and hyperreactivity in guinea pigs.
- Corticosteroids and PDE4-inhibitors show promise as therapeutic agents for managing viral-induced airway inflammation and hyperreactivity.
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