Influences of innate immunity, autophagy, and fibroblast activation in the pathogenesis of lung fibrosis

Author:

O'Dwyer David N.1,Ashley Shanna L.12,Moore Bethany B.13ORCID

Affiliation:

1. Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan;

2. Graduate Program in Immunology, University of Michigan, Ann Arbor, Michigan; and

3. Department of Microbiology and Immunology, University of Michigan, Ann Arbor, Michigan

Abstract

Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease characterized by accumulation of extracellular matrix (ECM) and impaired gas exchange. The pathobiological mechanisms that account for disease progression are poorly understood but likely involve alterations in innate inflammatory cells, epithelial cells, and fibroblasts. Thus we seek to review the most recent literature highlighting the complex roles of neutrophils and macrophages as both promoters of fibrosis and defenders against infection. With respect to epithelial cells and fibroblasts, we review the data suggesting that defective autophagy promotes the fibrogenic potential of both cell types and discuss new evidence related to matrix metalloproteinases, growth factors, and cellular metabolism in the form of lactic acid generation that may have consequences for promoting fibrogenesis. We discuss potential cross talk between innate and structural cell types and also highlight literature that may help explain the limitations of current IPF therapies.

Funder

HHS | NIH | National Heart, Lung, and Blood Institute (NHBLI)

HHS | NIH | National Institute of Allergy and Infectious Diseases (NIAID)

United Negro College Fund Special Programs Corporation-MERCK

Publisher

American Physiological Society

Subject

Cell Biology,Physiology (medical),Pulmonary and Respiratory Medicine,Physiology

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