Parainfluenza virus type 3 induced alterations in tachykinin NK1 receptors, substance P levels and respiratory functions in guinea pig airways

Kudlacz, Elizabeth M.; Shatzer, S. A.; Farrell, Amy M.; Baugh, Larry E.

doi:10.1016/0926-6917(94)90004-3

Cited by 2 publications

(2 citation statements)

References 43 publications

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“…Also, epithelial damage induced by PI-3 virus can lead to loss of activity of neutral endopeptidase, which, since this enzyme degrades both bradykinin and neuropeptides, can enable these substances to have prolonged effects. Substance P release has been suggested to occur during PI-3 virus infection in guinea-pig airways (27). Moreover, depletion of sensory neuropeptides, including substance P, by capsaicin treatment prevents virus-induced AHR (25).…”

Section: Discussionmentioning

confidence: 99%

Virus- and Bradykinin-Induced Airway Hyperresponsiveness in Guinea Pigs

Folkerts

Jw²,

A³

et al. 2000

Am J Respir Crit Care Med

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The involvement of bradykinin in virus-induced airway hyperresponsiveness (AHR) in guinea pig airways in vivo was determined with the B(2)-receptor antagonist Hoe 140. The efficacy of Hoe 140 treatment was assessed through its effect on the bradykinin-induced (up to 2.5 microgram/100 g B.W. administered intravenously) decrease in blood pressure (BP). Hoe 140 (0.1 micromol/kg), administered subcutaneously twice a day for 5 d almost completely blocked bradykinin-induced changes in BP. Four days after parainfluenza-3 (PI-3) virus infection, guinea pigs showed AHR; excessive airway contraction was found with histamine-receptor stimulation. This hyperresponsiveness was completely inhibited by pretreatment with Hoe 140 (0.1 micromol/kg) administered subcutaneously twice a day for five consecutive days, starting 1 d before virus inoculation. Interestingly, nebulized delivery of bradykinin itself to captopril-treated animals induced an AHR comparable to that observed in virus-treated guinea pigs. Viral infection also caused influx of bronchoalveolar cells into the lungs. Both histologic examinations and lung lavage experiments showed that this cell influx could not be inhibited by pretreatment with Hoe 140. In summary, the results of the study show that bradykinin is involved in a cascade of events leading to AHR after a viral infection in guinea pigs, without affecting bronchoalveolar cell influx.

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Section: Discussionmentioning

confidence: 99%

Virus- and Bradykinin-Induced Airway Hyperresponsiveness in Guinea Pigs

Folkerts

Jw²,

A³

et al. 2000

Am J Respir Crit Care Med

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“…The role of sensory neuropeptides in the pathogenesis of virus-induced AHR has been addressed previously by several other groups: Kudlacz et al [27] investigated the effects of PIV-3 infection on the level of sensory neuro peptides in the guinea pig airway and found SP release during respiratory viral infection to be temporally related with AHR.…”

Section: Discussionmentioning

confidence: 99%

Role of Sensory Neuropeptides in PIV-3-lnfection-lnduced Airway Hyperresponsiveness in Guinea Pigs

Riedel

Benden²,

Philippou³

et al. 1997

Respiration

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Viral respiratory tract infections are known to induce transient airway hyperresponsiveness. The role of the nonadrenergic noncholinergic neuropeptide system on virus-induced airway hyperresponsiveness was studied in the guinea pig. Ten guinea pigs were inoculated with parainfluenza 3 virus (PIV-3,2 × 10⁶ PFU) by nasal route, 16 animals served as untreated controls. Viral infection was proven by histological changes and by demonstration of viral antigen using immunohistochemical techniques. Four days after inoculation, airway responsiveness to inhaled acetylcholine (ACH) aerosol was measured in anesthetized and tracheotomized guinea pigs. The ACH concentration which produced an increase of 100% in pulmonary resistance (PC_{100 RI}) and in dynamic elastance (PC_{100 Edyn}) was calculated from a 5-step ACH dose-response curve (0.125,0.25, 0.5, 1.0 and 2.0% ACH). Two further groups of 8 PIV-3-infected guinea pigs and 8 noninfected control animals were pretreated with capsaicin in increasing doses (50, 100, 125 and 150 mg/kg) on 4 consecutive days starting 6 days before virus inoculation. Measurements of airway responsiveness to ACH were performed 4 days after virus inoculation. Another 5 uninfected control animals were pretreated only with the solvent for capsaicin and inoculated with virus-free cell supernatant. PIV-3 infection increased airway responsiveness to ACH compared to noninfected controls [PC_{100 RI} 0.81 vs. > 2.0% ACH (median), p < 0.002; PC₁₀₀_Edyn 0.52 vs. 1.07% ACH (median), p < 0.01]. In capsaicin-pretreated PIV-3-infected animals, airway hyperresponsiveness was completely prevented compared to the virus-infected group without capsaicin pretreatment (PC_{100 RI} > 2.0 vs. 0.81% ACH, p < 0.01; PC_{100 Edyn} 1-42 vs. 0.52% ACH, p < 0.01). As neuropeptide depletion with capsaicin completely prevented the increase in airway constrictory response to ACH following virus infection, we conclude that neuropeptides are effectively involved in PIV-3-induced airway hyperresponsiveness in the guinea pig.

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Parainfluenza virus type 3 induced alterations in tachykinin NK1 receptors, substance P levels and respiratory functions in guinea pig airways

Cited by 2 publications

References 43 publications

Virus- and Bradykinin-Induced Airway Hyperresponsiveness in Guinea Pigs

Virus- and Bradykinin-Induced Airway Hyperresponsiveness in Guinea Pigs

Role of Sensory Neuropeptides in PIV-3-lnfection-lnduced Airway Hyperresponsiveness in Guinea Pigs

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