Inhaled Fine Particles Induce Alveolar Macrophage Death and Interleukin-1α Release to Promote Inducible Bronchus-Associated Lymphoid Tissue Formation. Academic Article uri icon

Overview

abstract

  • Particulate pollution is thought to function as an adjuvant that can induce allergic responses. However, the exact cell types and immunological factors that initiate the lung-specific immune responses are unclear. We found that upon intratracheal instillation, particulates such as aluminum salts and silica killed alveolar macrophages (AMs), which then released interleukin-1α (IL-1α) and caused inducible bronchus-associated lymphoid tissue (iBALT) formation in the lung. IL-1α release continued for up to 2 weeks after particulate exposure, and type-2 allergic immune responses were induced by the inhalation of antigen during IL-1α release and iBALT formation, even long after particulate instillation. Recombinant IL-1α was sufficient to induce iBALTs, which coincided with subsequent immunoglobulin E responses, and IL-1-receptor-deficient mice failed to induce iBALT formation. Therefore, the AM-IL-1α-iBALT axis might be a therapeutic target for particulate-induced allergic inflammation.

publication date

  • December 20, 2016

Research

keywords

  • Bronchi
  • Interleukin-1alpha
  • Lymphoid Tissue
  • Macrophages, Alveolar
  • Particulate Matter

Identity

Scopus Document Identifier

  • 85006827094

Digital Object Identifier (DOI)

  • 10.1016/j.immuni.2016.11.010

PubMed ID

  • 28002730

Additional Document Info

volume

  • 45

issue

  • 6