Respiratory syncytial virus upregulates expression of the substance P receptor in rat lungs

Giovanni Piedimonte, Maria M. Rodriguez, Katherine A. King, Stafford McLean, Xiaobo Jiang

Research output: Contribution to journalArticlepeer-review

100 Scopus citations


Respiratory syncytial virus (RSV) is a major respiratory pathogen in infants. The first goal of this study was to determine whether the infection following endotracheal inoculation of Rsv in Fischer 344 rats results in increased inflammatory responses to substance P (SP) either released by capsaicin from sensory nerves or injected into the circulation. Five days after inoculation, the extravasation of Evans blue-labeled albumin after capsaicin or Sp was significantly greater in Rsv-infected airways than in pathogen-free controls. The peptide-degrading activity of the regulatory enzyme neutral endopeptidase was unaffected by Rsv. However, Sp(NK1) receptor mRNA levels increased fivefold in Rsv-infected lungs, and the density of Sp binding sites in the bronchial mucosa increased threefold. These data suggest that Rsv makes the airways abnormally susceptible to the proinflammatory effects of SP by upregulating SP(NK1) receptor gene expression, thereby increasing the density of these receptors on target cells. This effect may contribute to the inflammatory reaction to the virus and could be a target for the therapy of RSV disease and its sequelae.

Original languageEnglish (US)
Pages (from-to)L831-L840
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Issue number4 21-4
StatePublished - Oct 1999


  • Airway inflammation
  • Asthma
  • Bronchiolitis
  • Neurokinin receptors
  • Sensory nerves

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Cell Biology
  • Physiology
  • Physiology (medical)


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