Cough reflex sensitivity is increased in guinea pigs with parainfluenza virus infection

Abstract

The purpose of this study was to investigate for the change in cough reflex sensitivity (CRS) caused by parainfluenza virus type 3 (PIV3) infection. Guinea pigs were randomized into a vehicle control, an asthma control, or 1 of 4 PIV3-inoculated groups (referred to as postinfection day [PID] 6, 12, 28, and 42 groups). Evidence of viral protein and nucleic acid within the lung confirmed successful PIV3 infection. Plethysmography was used to assess CRS and airway reaction and airway inflammation was assessed via bronchoalveolar lavage fluid cytology and lung histopathology. Compared with the vehicle control group, CRS was significantly increased in all PID groups (P <.05) in concert with an obvious airway hyperresponsiveness in the PID 6 group. Though a small increase in CRS in the asthma control group was noted, it was not significant compared to the vehicle control group. Total cell counts from the bronchoalveolar lavage fluid of all PIV3-inoculated groups increased markedly and the number of lymphocytes was significantly increased in the PID 6 and PID 12 groups. The lung pathology of PIV3-inoculated animals showed airway inflammation without pneumonia in the acute infectious phase. The temporal and spatial variation of CRS may be the essential mechanism of cough caused by PIV3.

Airway Vagal Neuroplasticity Associated with Respiratory Viral Infections

“…Ye et al noted nearly a fourfold increase in the cough responses to capsaicin in guinea pigs that had previously been inoculated intranasally with PIV3 [39]. We too have found that PIV3 infection of the guinea pig airway epithelium leads to two to three times more coughs than those treated with the viral growth medium in response to capsaicin, BK, and citric acid.…”

Transient receptor potential (TRP) channels in the airway: role in airway disease

“…This phenomenon has been reported in the somatosensory system and can lead to phenotype changes in which neurons with low‐threshold mechanoreceptors take on a chemosensitive or nociceptor phenotype by expressing the neuropeptide substance P, which is typically limited to C‐fibre afferents (Neumanns et al ., ). This has been mimicked in animal models of disease, whereby cigarette smoke exposure, allergy and virus have been observed to cause hypersensitivity to TRPV1 agonist inhalation and in some cases a phenotypic change in the airway nerves has been proposed as the mechanism responsible (Karlsson et al ., ; Carr et al ., ; Myers et al ., ; Lewis et al ., ; Zhang et al ., ; Maher et al ., ; Grace et al ., ; Ye et al ., ; Lieu et al ., ). Phenotype changes in airway vagal Aδ‐fibres in an asthma model in sensitized guinea pigs following allergen challenge (Zhang et al ., ) have been reported.…”

TRPV1: A Potential Drug Target for Treating Various Diseases

“…The findings in humans were reproduced in animal models of respiratory diseases. For example, exposure of these animals to allergens, tobacco smoke or viral infection causes hypersensitivity to TRPV1 agonists and morphological changes in airway nerves [147,148,149,150,151,152]. …”