Formaldehyde (FA) is a common chemical linked to respiratory problems such as airway hyperresponsiveness and pulmonary inflammation. Due to its toxicological effects and ease of mass production, FA is also recognized as a significant chemical threat by the U.S. Department of Homeland Security. This study investigates the role of mast cells in the pulmonary inflammatory response to acute high dose FA exposure. Using wild type (C57BL/6J) and mast cell-deficient (KitW-sh) mouse models, we assessed the impact of oropharyngeal aspiration of FA on lung pathology. Our findings reveal that C57BL/6J mice experienced significant increases in cellular infiltration, altered immune cell populations, and changes in lipid mediator profiles. In contrast, KitW-sh mice exhibited significantly reduced inflammatory responses. Notably, the presence of mast cells was associated with enhanced dendritic cell migration and differential production of bioactive lipid mediators, such as specialized pro-resolving mediators and pro-inflammatory leukotrienes in C57BL/6J mice. These results highlight the crucial role of mast cells in the immune response to formaldehyde and suggest they could be therapeutic targets for treating FA-induced lung inflammation.
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