J Vet Sci.  2024 May;25(3):e35. 10.4142/jvs.23302.

Histopathological evaluation of the Pathology lungs in experimental autoimmune encephalomyelitis

• Hong S
• Kim J
• Jung K
• Ahn M
• Moon C
• Nomura Y
• Matsuda H
• Tanaka A
• Jeong H
• Shin T

• KMID: 2556481
• DOI: http://doi.org/10.4142/jvs.23302

Abstract

Importance
Experimental autoimmune encephalomyelitis (EAE) is an animal model of multiple sclerosis characterized by inflammation within the central nervous system. However, inflammation in non-neuronal tissues, including the lungs, has not been fully evaluated.
Objective
This study evaluated the inflammatory response in lungs of EAE mice by immunohistochemistry and histochemistry.
Methods
Eight adult C57BL/6 mice were injected with myelin oligodendrocyte glycoprotein 35-55 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.
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.

Keyword

Experimental autoimmune encephalomyelitis; galectin-3; inflammation; lung; osteopontin