Marc A. Williams¹, Chris Cheadle², Tonya Watkins², Anitaben Tailor², Smruti Killedar¹, Patrick Breysse², Kathleen C. Barnes² and Steve N. Georas¹

¹University of Rochester School of Medicine and Dentistry, Division of Pulmonary and Critical Care Medicine, Rochester, New York, U.S.A. ²Johns Hopkins University School of Medicine, Division of Allergy and Clinical Immunology, Baltimore, Maryland, U.S.A.

Abstract: In many subjects who are genetically susceptible to asthma, exposure to environmental stimuli may exacerbate their condition. However, it is unknown how the expression and function of a family of pattern-recognition receptors called toll-like receptors (TLR) are affected by exposure to particulate pollution. TLRs serve a critical function in alerting the immune system of tissue damage or infection—the so-called “danger signals”. We are interested in the role that TLRs play in directing appropriate responses by innate immunity, particularly dendritic cells (DC), after exposing them to particulate pollution. Dendritic cells serve a pivotal role in directing host immunity. Thus, we hypothesized that alterations in TLR expression could be further explored as potential biomarkers of effect related to DC exposure to particulate pollution. We show some preliminary data that indicates that inhaled particulate pollution acts directly on DC by down-regulating TLR expression and altering the activation state of DC. While further studies are warranted, we suggest that alterations in TLR2 and TLR4 expression should be explored as potential biomarkers of DC exposure to environmental particulate pollution.