Rhinorrhea associated with viral upper respiratory tract infections or reaction to aeroallergens affects all human beings and has been associated with loss of quality of life. Pulmonary fluid accumulation in acute lung injury is a leading cause of hospital admission and death from lower respiratory tract infection and sepsis.

Methods:

In this narrative review, evidence supporting the hypotheses that both rhinorrhea and inflammation-related pulmonary fluid accumulation are due to the dysfunction of the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) is presented, and novel concepts of the patho-mechanisms involved are explained.

Results: Upper and lower airway as well as alveolar surface liquid volumes are shown to be dependent on CFTR. Its function is regulated directly by cytokines in allergic- and infection-related inflammation and through increased hydrostatic tissue pressure secondary to vasodilatation in enclosed spaces within the upper airway and in heart failure in pulmonary interstitial spaces. The regulation of upper airway fluid secretion manifested in allergic inflammation and viral infections by rhinovirus and respiratory syncytial virus can be explained by CFTR activation and alveolar fluid accumulation by the inactivation of CFTR through cytokine-induced microRNA and Na/K ATPase inhibition. Therapeutic interventions reducing CFTR dysfunction through anti-inflammatory and CFTR modulating strategies are introduced.

Conclusions: Excessive fluid secretion in the upper respiratory tract induced by viruses and allergy as well as increased lung water in local and systemic inflammation can be explained by CFTR dysfunction opening avenues for supportive treatment.