Air pollution and tobacco smoke contain oxidants that when inhaled can cause damage to the lungs and contribute to diseases such as asthma and chronic obstructive pulmonary disease (COPD). In a study that appears in the March issue of the Journal of Clinical Investigation, researchers from the Harvard School of Public Health, Boston, identify a new mechanism by which mice are protected against inhaled oxidants.
Lester Kobzik and colleagues observed that immune cells in the lungs (known as alveolar macrophages) of mice resistant to lung damage caused by the oxidant ozone expressed more of a protein known as MARCO than the alveolar macrophages of mice susceptible to ozone-induced lung damage. Consistent with a role for MARCO in protection from oxidant-induced lung damage, mice lacking MARCO showed more lung damage when exposed to either ozone or another oxidant than mice expressing normal amounts of MARCO. MARCO provided protection by enabling alveolar macrophages to take up lipids in the lung modified by the oxidant that would initiate an inflammatory reaction if not removed. A similar role in the removal of lipids in the lung modified by these oxidants was identified for another protein related to MARCO, SR-AI/II. As discussed in an accompanying commentary by Edward Postlethwait from the University of Alabama at Birmingham, it is now important to determine whether similar functions can be ascribed to these and other related proteins (all of which are known as scavenger receptors) in humans because of the extensive morbidity associated with lung diseases such as asthma and COPD.