Neutrophils in Tuberculosis-Associated Inflammation and Lung Pathology

Front Immunol. 2020 May 27:11:962. doi: 10.3389/fimmu.2020.00962. eCollection 2020.

Abstract

Protective immunity to Mycobacterium tuberculosis (Mtb)-the causative agent of tuberculosis (TB)-is not fully understood but involves immune responses within the pulmonary airways which can lead to exacerbated inflammation and immune pathology. In humans, this inflammation results in lung damage; the extent of which depends on specific host pro-inflammatory processes. Neutrophils, though increasingly linked to the development of inflammatory disorders, have been less well studied in relation to TB-induced lung pathology. Neutrophils mode of action and their specialized functions can be directly linked to TB-specific lung tissue damage observed on patient chest X-rays at diagnosis and contribute to long-term pulmonary sequelae. This review discusses aspects of neutrophil activity associated with active TB, including the resulting inflammation and pulmonary impairment. It highlights the significance of neutrophil function on TB disease outcome and underlines the necessity of monitoring neutrophil function for better assessment of the immune response and severity of lung pathology associated with TB. Finally, we propose that some MMPs, ROS, MPO, S100A8/A9 and Glutathione are neutrophil-related inflammatory mediators with promising potential as targets for developing host-directed therapies for TB.

Keywords: inflammatory mediators; lung damage; neutrophils; sequelae; tuberculosis.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / therapeutic use
  • Antitubercular Agents / therapeutic use
  • Host-Pathogen Interactions
  • Humans
  • Lung / drug effects
  • Lung / immunology*
  • Lung / metabolism
  • Lung / microbiology
  • Mycobacterium tuberculosis / drug effects
  • Mycobacterium tuberculosis / immunology*
  • Mycobacterium tuberculosis / pathogenicity
  • Neutrophils / drug effects
  • Neutrophils / immunology*
  • Neutrophils / metabolism
  • Neutrophils / microbiology
  • Pneumonia / drug therapy
  • Pneumonia / immunology*
  • Pneumonia / metabolism
  • Pneumonia / microbiology
  • Signal Transduction
  • Tuberculosis, Pulmonary / drug therapy
  • Tuberculosis, Pulmonary / immunology*
  • Tuberculosis, Pulmonary / metabolism
  • Tuberculosis, Pulmonary / microbiology

Substances

  • Anti-Inflammatory Agents
  • Antitubercular Agents