The research activities focus on the cellular biology of the lung with emphasis on the phagocytic and regulatory role of the alveolar macrophages and the immune mechanisms of the lung parenchyma. Work is directed toward determining the modulatory role of air pollutants and therapeutic agents on maintaining the homeostasis of the lungs and resistance to respiratory infections.

A second research activity is directed toward developing models and elucidating the mechanisms by which respiratory infections and air pollutants interact to initiate and exacerbate acute and chronic lung disease. Specific projects focus on inhalation exposure to oxidants, particle-gas combinations, silica, and respiratory infections in causing acute and chronic lung injury.

Through studies on the basic cellular defenses on the lung and the mechanisms by which they are breached in health and disease, the research program is unraveling the cause-effect relationships, the pathophysiological consequences, and the mechanisms involved in the development of acute and chronic disease processes of the lungs.

cellular biology of the lung with emphasis on the phagocytic and regulatory role of the alveolar macrophages and the immune mechanisms of the lung parenchyma

Jakab GJ, Hmieleski R, Zarba A, Hemenway DR, Groopman JD (1994). Respiratory aflatoxicosis: suppression of pulmonary and systemic host defenses. Toxicol Appld Pharmacol 125:198-205.

Jakab GJ, Spannhake EW, Canning BJ, Kleeberger SR, Gilmour MI (1995). The effects of ozone on immune function. Env Health Perspect 103( Suppl 2):77-89.

Hemenway DR, Clarke R, Frank R, Jakab GJ (1996). Factors governing the mass loading of carbon black with sulfates, inhalation exposure, and alveolar macrophage phagocytic function. Inhalation Toxicol 8:679-694.

Jakab GJ, Clarke RW, Hemenway DR, Longphre MV, Kleeberger SR, Frank R (1996). Inhalation of acid coated carbon black particles impairs alveolar macrophage phagocytosis. Toxicol Letters 88:243-248.

Kleeberger SR, Zhang L, Jakab GJ (1996). Differential susceptibility to oxidant exposure in inbred strains of mice: nitrogen dioxide versus ozone. In halation Toxicol,