Brain research · 2026
EAE models of neuropathic pain in multiple sclerosis do not require pertussis toxin.
СтатьяНазвание и аннотация: Перевод в очереди
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Lamerand Sydney R, Basu Paramita, Gakii Nina E, Steber Skyy S, Taylor Bradley K
Аннотация
BACKGROUND: Experimental autoimmune encephalomyelitis (EAE) is a preclinical model of multiple sclerosis (MS), typically induced with two inoculations of myelin oligodendrocyte glycoprotein (MOG35-55) emulsified in complete Freund's adjuvant (CFA), and supplemented with pertussis toxin (PTX). Although PTX has been considered essential, recent studies suggest that EAE pathology can develop without it.
OBJECTIVES: Indices of clinical disease and neuropathic pain were evaluated in a conventional model of EAE that included PTX (EAE-PTX) and one that lacked PTX (EAE-nPTX), as well as in multiple control groups that lacked MOG35-55 (CFA-PTX and CFA-nPTX).
METHODS: A battery of behavioral tests were used to evaluate motor dysfunction and hypersensitivity to mechanical, cold, and heat stimuli with a repeated-measures design in male and female C57BL/6 mice. One month after the first EAE inoculation, fluoromyelin staining was used to evaluate demyelination in spinal cord, cortex, and peripheral nerve, while ATF3 was used as a marker of injury in sensory neurons of lumbar L4-L5 dorsal root ganglia (DRG).
RESULTS: Compared to CFA-PTX and CFA-nPTX controls, both EAE-PTX and EAE-nPTX groups developed motor dysfunction, behavioral hypersensitivity, and demyelination in ventral spinal cord but not cortex. Spinal demyelination was greater in EAE-nPTX than in EAE-PTX. ATF3 was detected in lumbar DRG of all EAE and CFA control groups, suggesting that systemic inflammation, rather than MOG35-55-driven neuropathology, contributes to neuron damage.
CONCLUSIONS: PTX is not required for the manifestation of motor dysfunction and neuropathic pain in MOG35-55-based EAE models. Newer EAE-nPTX models have the distinct advantage of mimicking MS disease while avoiding confounding effects of pertussis toxin.
OBJECTIVES: Indices of clinical disease and neuropathic pain were evaluated in a conventional model of EAE that included PTX (EAE-PTX) and one that lacked PTX (EAE-nPTX), as well as in multiple control groups that lacked MOG35-55 (CFA-PTX and CFA-nPTX).
METHODS: A battery of behavioral tests were used to evaluate motor dysfunction and hypersensitivity to mechanical, cold, and heat stimuli with a repeated-measures design in male and female C57BL/6 mice. One month after the first EAE inoculation, fluoromyelin staining was used to evaluate demyelination in spinal cord, cortex, and peripheral nerve, while ATF3 was used as a marker of injury in sensory neurons of lumbar L4-L5 dorsal root ganglia (DRG).
RESULTS: Compared to CFA-PTX and CFA-nPTX controls, both EAE-PTX and EAE-nPTX groups developed motor dysfunction, behavioral hypersensitivity, and demyelination in ventral spinal cord but not cortex. Spinal demyelination was greater in EAE-nPTX than in EAE-PTX. ATF3 was detected in lumbar DRG of all EAE and CFA control groups, suggesting that systemic inflammation, rather than MOG35-55-driven neuropathology, contributes to neuron damage.
CONCLUSIONS: PTX is not required for the manifestation of motor dysfunction and neuropathic pain in MOG35-55-based EAE models. Newer EAE-nPTX models have the distinct advantage of mimicking MS disease while avoiding confounding effects of pertussis toxin.