Neuroinflammatory consequences of rhinovirus infection in the human airway

The mechanism responsible for respiratory virus induced cough in humans is unknown. This research aimed to determine whether RV directly infects and alters neural function or exerts its effect indirectly via the release of inflammatory mediators from infected airway epithelium. <br><br>A human sensory neuronal model was derived from differentiation of human dental pulp stem cells towards a neuronal phenotype, termed peripheral neuronal equivalents (PNEs).

PNEs were infected for 2, 6, 24, 48 and 72 hrs with major group RV-A16, or minor group RV-A1b, at a range of multiplicities of infection (MOI) (0.01 – 100). Primary bronchial epithelial cells (PBEC) from chronic cough, COPD and healthy patients, were infected for 24 hrs with RV-A16 and at MOI 1.<br><br>PNEs expressed intracellular adhesion molecule 1 (ICAM-1), the entry receptor of major group RV. Viral titrations, Western Blotting (WB), immunocytochemistry (ICC) and flow cytometry confirm RV-A16 entry and replication in PNE when infected at MOI 1 for 24, 48 and 72 hours.