Nerve injury and immune response

Author(s):  
Claudia Sommer
Keyword(s):  
2009 ◽  
Vol 220 (2) ◽  
pp. 320-327 ◽  
Author(s):  
Andrew D. Gaudet ◽  
Margaret Leung ◽  
Françoise Poirier ◽  
Toshihiko Kadoya ◽  
Hidenori Horie ◽  
...  

2018 ◽  
Vol 15 (1) ◽  
Author(s):  
Jane A. Lindborg ◽  
Jon P. Niemi ◽  
Madeline A. Howarth ◽  
Kevin W. Liu ◽  
Christian Z. Moore ◽  
...  
Keyword(s):  

2021 ◽  
Vol 14 ◽  
Author(s):  
Andrei V. Chernov ◽  
Veronica I. Shubayev

Peripheral nerve injury induces genome-wide transcriptional reprogramming of first-order neurons and auxiliary cells of dorsal root ganglia (DRG). Accumulating experimental evidence suggests that onset and mechanistic principles of post-nerve injury processes are sexually dimorphic. We examined largely understudied aspects of early transcriptional events in DRG within 24 h after sciatic nerve axotomy in mice of both sexes. Using high-depth RNA sequencing (>50 million reads/sample) to pinpoint sexually dimorphic changes related to regeneration, immune response, bioenergy, and sensory functions, we identified a higher number of transcriptional changes in male relative to female DRG. In males, the decline in ion channel transcripts was accompanied by the induction of innate immune cascades via TLR, chemokine, and Csf1-receptor axis and robust regenerative programs driven by Sox, Twist1/2, and Pax5/9 transcription factors. Females demonstrated nerve injury-specific transcriptional co-activation of the actinin 2 network. The predicted upstream regulators and interactive networks highlighted the role of novel epigenetic factors and genetic linkage to sex chromosomes as hallmarks of gene regulation post-axotomy. We implicated epigenetic X chromosome inactivation in the regulation of immune response activity uniquely in females. Sexually dimorphic regulation of MMP/ADAMTS metalloproteinases and their intrinsic X-linked regulator Timp1 contributes to extracellular matrix remodeling integrated with pro-regenerative and immune functions. Lexis1 non-coding RNA involved in LXR-mediated lipid metabolism was identified as a novel nerve injury marker. Together, our data identified unique early response triggers of sex-specific peripheral nerve injury regulation to gain mechanistic insights into the origin of female- and male-prevalent sensory neuropathies.


1995 ◽  
Vol 7 (4) ◽  
pp. 193-198
Author(s):  
K. Jovanova-Nešić ◽  
V. Savić

2015 ◽  
Vol 36 (1) ◽  
pp. 37-46 ◽  
Author(s):  
Ciro De Luca ◽  
Leonilde Savarese ◽  
Anna Maria Colangelo ◽  
Maria Rosaria Bianco ◽  
Giovanni Cirillo ◽  
...  

2020 ◽  
Author(s):  
Ashley L Kalinski ◽  
Choya Yoon ◽  
Lucas D Huffman ◽  
Patrick C Duncker ◽  
Rafi Kohen ◽  
...  

2021 ◽  
pp. 154596832110010
Author(s):  
John M. Daines ◽  
Lauren Schellhardt ◽  
Matthew D. Wood

Following traumatic peripheral nerve injury, adequate restoration of function remains an elusive clinical goal. Recent research highlights the complex role that the immune system plays in both nerve injury and regeneration. Pro-regenerative processes in wounded soft tissues appear to be significantly mediated by cytokines of the type 2 immune response, notably interleukin (IL)-4. While IL-4 signaling has been firmly established as a critical element in general tissue regeneration during wound healing, it has also emerged as a critical process in nerve injury and regeneration. In this context of peripheral nerve injury, endogenous IL-4 signaling has recently been confirmed to influence more than leukocytes, but including also neurons, axons, and Schwann cells. Given the role IL-4 plays in nerve injury and regeneration, exogenous IL-4 and/or compounds targeting this signaling pathway have shown encouraging preliminary results to treat nerve injury or other neuropathy in rodent models. In particular, the exogenous stimulation of the IL-4 signaling pathway appears to promote postinjury neuron survival, axonal regeneration, remyelination, and thereby improved functional recovery. These preclinical data strongly suggest that targeting IL-4 signaling pathways is a promising translational therapy to augment treatment approaches of traumatic nerve injury. However, a better understanding of the type 2 immune response and associated signaling networks functioning within the nerve injury microenvironment is still needed to fully develop this promising therapeutic avenue.


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