The concept of the
inflammasome, a macromolecular complex sensing cell stress or danger signals and initiating
inflammation, was first introduced approximately a decade ago. Priming and activation of these intracellular
protein platforms trigger the maturation of pro-inflammatory
chemokines and
cytokines, most notably, interleukin-1β (IL-1β) and
IL-18, to promulgate innate immune defenses. Although classically studied in models of
gout, Type II diabetes,
Alzheimer's disease, and
multiple sclerosis, the importance and mechanisms of action of
inflammasome priming and activation have recently been elucidated in cells of the respiratory tract where they modulate the responses to a number of inhaled pathogenic particles and fibres. Most notably,
inflammasome activation appears to regulate the balance between tissue repair and
inflammation after inhalation of pathogenic
pollutants such as
asbestos, crystalline
silica (CS), and
airborne particulate matter (PM). Different types of fibres and particles may have distinct mechanisms of
inflammasome interaction and outcome. This review summarizes the structure and function of
inflammasomes, the interplay between various
chemokines and
cytokines and cell types of the lung and pleura after
inflammasome activation, and the events leading to the development of non-malignant (allergic airway disease and
chronic obstructive pulmonary disease (
COPD),
asbestosis,
silicosis) and
malignant (mesothelioma,
lung cancer) diseases by pathogenic particulates. In addition, it emphasizes the importance of communication between cells of the immune system, target cells of these diseases, and components of the extracellular matrix (ECM) in regulation of
inflammasome-mediated events.