Role of Innate Immune System in Environmental Lung Diseases.

Journal Article (Journal Article;Review)

The lung mucosa functions as a principal barrier between the body and inhaled environmental irritants and pathogens. Precise and targeted surveillance mechanisms are required at this lung-environment interface to maintain homeostasis and preserve gas exchange. This is performed by the innate immune system, a germline-encoded system that regulates initial responses to foreign irritants and pathogens. Environmental pollutants, such as particulate matter (PM), ozone (O3), and other products of combustion (NO2, SO3, etc.), both stimulate and disrupt the function of the innate immune system of the lung, leading to the potential for pathologic consequences. PURPOSE OF REVIEW: The purpose of this review is to explore recent discoveries and investigations into the role of the innate immune system in responding to environmental exposures. This focuses on mechanisms by which the normal function of the innate immune system is modified by environmental agents leading to disruptions in respiratory function. RECENT FINDINGS: This is a narrative review of mechanisms of pulmonary innate immunity and the impact of environmental exposures on these responses. Recent findings highlighted in this review are categorized by specific components of innate immunity including epithelial function, macrophages, pattern recognition receptors, and the microbiome. Overall, the review supports broad impacts of environmental exposures to alterations to normal innate immune functions and has important implications for incidence and exacerbations of lung disease. The innate immune system plays a critical role in maintaining pulmonary homeostasis in response to inhaled air pollutants. As many of these agents are unable to be mitigated, understanding their mechanistic impact is critical to develop future interventions to limit their pathologic consequences.

Full Text

Duke Authors

Cited Authors

  • Guttenberg, MA; Vose, AT; Tighe, RM

Published Date

  • May 10, 2021

Published In

Volume / Issue

  • 21 / 5

Start / End Page

  • 34 -

PubMed ID

  • 33970346

Pubmed Central ID

  • PMC8311569

Electronic International Standard Serial Number (EISSN)

  • 1534-6315

Digital Object Identifier (DOI)

  • 10.1007/s11882-021-01011-0

Language

  • eng

Conference Location

  • United States