Pulmonary Neutrophilic Inflammation and Noncommunicable Diseases: Pathophysiology, Redox Mechanisms, Biomarkers, and Therapeutics

Abstract

Significance: Pulmonary neurophilic inflammation (PNI) is the homing and activation of neutrophil with damage to the microvasculature. This process is involved in pulmonary damage in patients exposed to airborne pollutants (exogenous stressors) and also to systemic inflammation/oxidative stress (endogenous stressors) associated with noncommunicable diseases (NCDs). Recent Advances: PNI is an important trigger of the early onset and progression of NCD in susceptible patients exposed to airborne pollutants. Irritation of the lung microvasculature by exogenous and endogenous stressors causes PNI. Circulating endogenous stressors in NCD can cause PNI. Critical Issues: Air pollution-triggered PNI causes increased circulating endogenous stressors that can trigger NCD in susceptible patients. Systemic inflammation/oxidative stress associated with NCD can cause PNI. Inflammation/end-oxidation products of macromolecules are also potential biomarkers and therapeutic targets for NCD-triggered PNI- and PNI-triggered NCD. Future Directions: Understanding the molecular mechanism of PNI triggered by exogenous or endogenous stressors will help explain the early onset of NCD in susceptible patients exposed to air pollution. It can also help undercover biomarkers and mechanism-based therapeutic targets in air pollutant-triggered PNI, PNI-triggered NCD, and NCD-triggered PNI.

Keywords: airborne pollution; biomarker; noncommunicable disease; pulmonary neutrophilic inflammation; stressor; therapeutic target.