Abstract

BackgroundThe cytokine, interleukin (IL)-25, is thought to be critically involved in inducing a type 2 immune response which may contribute to regeneration after central nervous system (CNS) trauma. We investigated whether applying recombinant IL-25, locally or systemically, in a mouse model of spinal cord injury (SCI) improves functional and histological recovery.FindingsRepeated systemic administration of IL-25 did not influence functional recovery following SCI. In contrast, a single local administration of IL-25 significantly worsened locomotor outcome, which was evident from a decreased Basso mouse scale (BMS) score compared with phosphate-buffered saline (PBS)-treated controls. This was accompanied by a significant increase in lesion size, demyelination, and T helper cell infiltration.ConclusionsThese data show for the first time that IL-25 is either ineffective when applied systemically or detrimental to spinal cord recovery when applied locally. Our findings question the potential neuroprotective role of IL-25 following CNS trauma.Electronic supplementary materialThe online version of this article (doi:10.1186/s12974-016-0566-y) contains supplementary material, which is available to authorized users.

Highlights

  • The cytokine, interleukin (IL)-25, is thought to be critically involved in inducing a type 2 immune response which may contribute to regeneration after central nervous system (CNS) trauma

  • These data show for the first time that IL-25 is either ineffective when applied systemically or detrimental to spinal cord recovery when applied locally

  • The type 2 response can be characterized by differentiation of CD4+ T helper type 2 (Th2) cells and the production of the type 2 cytokines interleukin-4 (IL-4), IL-5, IL-9, and IL-13 [2,3,4]

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Summary

Conclusions

These data show for the first time that IL-25 is either ineffective when applied systemically or detrimental to spinal cord recovery when applied locally.

Introduction
Methods
Results and discussion
IL-25 b
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