interferon abstract

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Nihon Kyobu Shikkan Gakkai Zasshi 1995 Apr;33(4):389-94

[A possible mechanism of interstitial pneumonia during interferon therapy

with sho-saiko-to]

[Article in Japanese]

Murakami K, Okajima K, Sakata K, Takatsuki K.

Department of Internal Medicine and Laboratory Medicine, Kumamoto

University Medical School, Japan.

Interstitial pneumonia has been reported to be a side effect of treatment

with interferon, and Sho-saiko-to (Xiao-Chai-Hu-Tang) may enhance this

side effect. It is well known that activated neutrophils are important

mediators of pulmonary fibrosis, so we studied the effects of interferon

and Sho-saiko-to on neutrophil activation. Homogenized lung

myeloperoxidase (MPO) activity was assayed after intraperitoneal injection

of interferon with or without pretreatment with Sho-saiko-to. Although

Sho-saiko-to alone did not change the lung MPO content, MPO in the lung

was significantly increased by interferon administration. The increase was

enhanced further by pretreatment with Sho-saiko-to. When the accumulated

neutrophils are activated by some cytokines, such as TNF alpha or IL-1

beta from monocytes/macrophages, they may damage lung tissue. We therefore

studied the effects of Sho-saiko-to and interferon on TNF alpha production

in freshly isolated human monocytes. Sho-saiko-to increased the production

of TNF alpha, but interferon did not. In addition, Sho-saiko-to

significantly increased the production of TNF alpha by monocytes

stimulated by lipopolysaccharide. Taken together, these data indicate that

interferon causes neutrophils to accumulate in the lung. Sho-saiko-to

alone may not injure lung tissue, but it increases the effect of

interferon. When stimulated by some antigen, Sho-saiko-to may

overstimulate the neutrophils. Granulocytes elastase and oxygen radicals

released from activated neutrophils may damage lung tissue. The

fibroblasts that repair the damaged tissue may increase the risk of

pulmonary fibrosis.

 

 

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