Infection-induced oxidative stress in chronic respiratory diseases

Abstract

Globally, the burden of chronic respiratory diseases (CRDs) is increasing rapidly. These include asthma, chronic respiratory obstructive diseases (COPD) and cystic fibrosis (CF). Patients with CRDs often exhibit increased levels of oxidant burden in the lungs that is primarily due to chronic exposure to deleterious particles, including cigarette smoke, air pollution, occupational exposure to chemicals and fumes and a variety of allergens. In homeostasis, a delicate balance exists between the pro-oxidant and antioxidant molecules/entities. Both structural and immune cells, when encountering these foreign particles, generally respond by triggering pro-oxidative stress-related pathways in the lungs, thereby disturbing the pulmonary redox homeostasis. Moreover, patients with CRDs are also susceptible to frequent/recurrent microbial infections that lead to worsening of disease which often requires hospitalizations. Several pathogens, such as Streptococcus pneumoniae, non-typeable Haemophilus influenzae, Mycobacterium tuberculosis, Aspergillus fumigatus, etc., have the ability to elicit pro-oxidant pathways in the respiratory tract. Also, these pathogens are equipped with enzymatic and non-enzymatic mechanisms to neutralize host-associated oxidative molecules that facilitate the persistence of these pathogens in the lungs. We will discuss the CRD/pathogen-triggered oxidative stress in the lungs. We will also discuss the microbial mechanisms that may further increase oxidative stress in patients with CRDs that potentially results in the heightened inflammatory response in the lungs. Finally, we will discuss the current treatment strategies to limit the oxidative response-associated lung pathologies.