Abstract
Experimental autoimmune encephalomyelitis (EAE) represents the mouse model of multiple sclerosis, a devastating neurological disorder. EAE development and progression involves the infiltration of different immune cells into the brain and spinal cord. However, less is known about a potential role of eosinophil granulocytes for EAE disease pathogenesis. In the present study, we found enhanced eosinophil abundance accompanied by increased concentration of the eosinophil chemoattractant eotaxin-1 in the spinal cord in the course of EAE induced in C57BL/6 mice by immunization with MOG35-55 peptide. However, the absence of eosinophils did not affect neuroinflammation, demyelination and clinical development or severity of EAE, as assessed in ΔdblGATA1 eosinophil-deficient mice. Taken together, despite their enhanced abundance in the inflamed spinal cord during disease progression, eosinophils were dispensable for EAE development.
Competing Interest Statement
The authors have declared no competing interest.
Abbreviations
- MS
- Multiple sclerosis
- EAE
- experimental autoimmune encephalomyelitis
- CNS
- Central nervous system
- ECP
- Eosinophil cationic protein
- IL-5
- Interleukin-5
- IL-33
- Interleukin 33
- NMO
- Neuromyelitis optica
- LFB
- Luxol Fast Blue
- MOG
- myelin oligodendrocyte glycoprotein
- IFNγ
- interferon gamma
- IL-17A
- interleukin 17A
- IL-6
- Interleukin-6
- TNF
- tumour necrosis factor
- iNOS
- inducible nitric oxide synthase
- IL-1β
- interleukin 1 beta
- PRG2
- eosinophil major basic protein
- SC
- spinal cord.