Histopathological evaluation of the lungs in experimental autoimmune encephalomyelitis

实验性自身免疫性脑脊髓炎肺的组织病理学评估

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作者:Sungmoo Hong, Jeongtae Kim, Kyungsook Jung, Meejung Ahn, Changjong Moon, Yoshihiro Nomura, Hiroshi Matsuda, Akane Tanaka, Hyohoon Jeong, Taekyun Shin

Methods

Eight adult C57BL/6 mice were injected with myelin oligodendrocyte glycoprotein35-55 to induce the EAE. Lungs and spinal cords were sampled from the experimental mice at the time of sacrifice and used for the western blotting, histochemistry, and immunohistochemistry.

Objective

This study evaluated the inflammatory response in lungs of EAE mice by immunohistochemistry and histochemistry.

Results

Histopathological examination revealed inflammatory lesions in the lungs of EAE mice, characterized by infiltration of myeloperoxidase (MPO)- and galectin-3-positive cells, as determined by immunohistochemistry. Increased numbers of collagen fibers in the lungs of EAE mice were confirmed by histopathological analysis. Western blotting revealed significantly elevated level of osteopontin (OPN), cluster of differentiation 44 (CD44), MPO and galectin-3 in the lungs of EAE mice compared with normal controls (p < 0.05). Immunohistochemical analysis revealed both OPN and CD44 in ionized calcium-binding adapter molecule 1-positive macrophages within the lungs of EAE mice. Conclusions and relevance: Taken together, these findings suggest that the increased OPN level in lungs of EAE mice led to inflammation; concurrent increases in proinflammatory factors (OPN and galectin-3) caused pulmonary impairment.

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