Published online: January 10, 2018
Ozone is a major component of environmental air pollution and elicits respiratory inflammation and airways hyperresponsiveness (AHR) independent of adaptive immunity. IL-33, an alarmin that belongs to the IL-1 family of cytokines and which is expressed at steady state in tissues is released upon injury and its role in ozone induced acute respiratory inflammation is unknown.
In a recently published contribution in The Journal of Allergy and Clinical Immunology (JACI), Michaudel and co-workers investigated the role of IL-33 on epithelial barrier integrity and inflammation following ozone exposure in mice using IL-33 and IL-33 receptor/ST2 deficient mice, anti-ST2 antibody and exogenous IL-33. They found a biphasic effect with IL-33 being protective in the second phase
Authors report that a single ozone exposure (1ppm for 1h) in mice elicits, within 1h, a disruption of the respiratory barrier with desquamation of epithelial cells, leak of plasma protein and upregulation of IL-33 in the lung. This is followed (24 hrs later) by a second phase of a myeloid cell dependent inflammation with reactive oxygen species production enhancing the lung damage and AHR, which is under the control of IL-33/ST2 axis. In this phase, IL-33 is protective through its capacity to activate tight junction expression, maintain pulmonary barrier integrity and reduce neutrophil recruitment.
Thus, IL-33/ST2 signaling is critical for the maintenance of an intact epithelial barrier and control of inflammation in acute experimental ozone respiratory injury.
The Journal of Allergy and Clinical Immunology (JACI) is an official scientific journal of the AAAAI, and is the most-cited journal in the field of allergy and clinical immunology.