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Parainfluenza 3 virus induces increased cough sensitivity, tracheal BDNF expression, and vagal sensory TRPV1 expression
Author(s) -
Zaccone Eric,
Lieu TinaMarie,
Muroi Yukikko,
Canning Brendan,
Gao Peisong,
Undem Bradley
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.775.6
Subject(s) - trpv1 , sensory system , medicine , neuroscience , biology , transient receptor potential channel , receptor
Parainfluenza virus type 3 (PIV3) infection causes excessive coughing and croup in children, and is associated with exacerbation of asthma. We infected guinea pigs intranasally with PIV3 and quantified the cough response in conscious animals. The guinea pigs infected with PIV3 (day 4) coughed nearly three times more than those treated with the viral growth medium (control) in response to either capsaicin or bradykinin (P<0.05). In an ex vivo perfused guinea pig tracheal preparation, we found that within 8 hr of infusion PIV3 resulted in a ~10‐fold increase in brain‐derived neurotrophic factor (BDNF) mRNA (qPCR) in the tissue. We have previously reported that tracheal BDNF is an effective inducer of transient receptor potential cation channel, subfamily V, member 1 (TRPV1) in nodose Aδ tracheal cough neurons that normally do not express this channel (Am J Physiol; 302:L941‐8). Consistent with this, PIV3 infection (day 4) increased TRPV1 expression in tracheal‐specific nodose Aδ neurons. In vehicle treated animals only 20±10% of the tracheal‐specific nodose neurons expressed TRPV1 (single neuron rt‐PCR), whereas 4 days after PIV3 infection 60±2% of the neurons expressed TRPV1 (n=6 ganglia ~60 neurons; P<0.05). In summary, PIV3 infection in guinea pigs evokes BDNF expression in the trachea and this increased de novo TRPV1 expression in tracheal specific cough nodose neurons, and a heightened cough response to capsaicin and bradykinin. Supported by NIH.