Epigenetic mechanisms of alveolar macrophage activation in chemical-induced acute lung injury

Front Immunol. 2024 Nov 8:15:1488913. doi: 10.3389/fimmu.2024.1488913. eCollection 2024.

Abstract

Airways, alveoli and the pulmonary tissues are the most vulnerable to the external environment including occasional deliberate or accidental exposure to highly toxic chemical gases. However, there are many effective protective mechanisms that maintain the integrity of the pulmonary tissues and preserve lung function. Alveolar macrophages form the first line of defense against any pathogen or chemical/reactant that crosses the airway mucociliary barrier and reaches the alveolar region. Resident alveolar macrophages are activated or circulating monocytes infiltrate the airspace to contribute towards inflammatory or reparative responses. Studies on response of alveolar macrophages to noxious stimuli are rapidly emerging and alveolar macrophage are also being sought as therapeutic target. Here such studies have been reviewed and put together for a better understanding of the role pulmonary macrophages in general and alveolar macrophage in particular play in the pathogenesis of disease caused by chemical induced acute lung injury.

Keywords: chemical; epigenetics; halogen; inhaled; lung; macrophage.

Publication types

  • Review

MeSH terms

  • Acute Lung Injury* / chemically induced
  • Acute Lung Injury* / immunology
  • Animals
  • Epigenesis, Genetic*
  • Humans
  • Macrophage Activation* / immunology
  • Macrophages, Alveolar* / immunology
  • Macrophages, Alveolar* / metabolism

Grants and funding

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. Funding by the CounterACT Program grants, National Institutes of Health Office of the Director (NIH OD), the National Institute of Environmental Health Sciences (NIEHS) Grants U01ES028182 (SA), U01ES033263 (SA), R21ES030525 (SA), R21ES032353 (AA), and R56ES034423 (AA&SA) are gratefully acknowledged.