Heme Oxygenase-1 May Cut Lung Injury from Silicosis

Upregulation of HO-1 may suppress damage caused by silica-induced reactive oxygen species

TUESDAY, Oct. 17 (HealthDay News) -- The oxidative damage to lung associated with chronic exposure to silica can be suppressed by upregulation of the antioxidant heme oxygenase-1 (HO-1) and may suggest a novel strategy for treatment of the disease, according to a report in the Oct. 15 issue of the American Journal of Respiratory and Critical Care Medicine.

Yoshiaki Ishigatsubo, M.D., of Yokohama City University in Yokohama, Japan, and colleagues looked at levels of HO-1 in mice experimentally exposed to silica and in the lungs of 46 male patients diagnosed with silicosis. Twenty-seven patients with chronic obstructive pulmonary disease and 42 healthy male volunteers were used as controls.

HO-1 was highly expressed in serum and lung tissue of both patients and mice exposed to silica, especially at sites adjacent to silica deposits. Higher serum HO-1 correlated with better lung function and reduced levels of reactive oxygen species (ROS) levels. And in mice, an activator of HO-1 could suppress inflammation associated with silicosis, while an HO-1 inhibitor exacerbated inflammation.

"The present study shows that HO-1 is persistently expressed in the lung lesions of patients with silicosis," the authors write. "This appears to reflect the induction of ROS by silica, leading to an elevation in serum HO-1 levels. The increased HO-1 can protect the host by suppressing silica-induced ROS activity."

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