Role of Inflammation and Cytokines in Peripheral Nerve Regeneration

Dubový, Petr; Jančálek, Radim; Kubek, Tomáš

doi:10.1016/b978-0-12-410499-0.00007-1

Cited by 107 publications

(89 citation statements)

References 164 publications

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“…Expression of MCP1 is reported for denervated Schwann cells, to recruit macrophages to the injury site (Deshmane et al, 2009; Tofaris et al, 2002), then assist Schwann cells in cellular debris clearing, and stimulation of axonal regrowth (Dubovy, Jancalek, & Kubek, 2013; Jessen et al, 2015). But persistent MCP1 expression produces a chronic inflammatory state, hindering nerve regeneration (Kato et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

Inflammaging impairs peripheral nerve maintenance and regeneration

et al. 2018

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The regenerative capacity of peripheral nerves declines during aging, contributing to the development of neuropathies, limiting organism function. Changes in Schwann cells prompt failures in instructing maintenance and regeneration of aging nerves; molecular mechanisms of which have yet to be delineated. Here, we identified an altered inflammatory environment leading to a defective Schwann cell response, as an underlying mechanism of impaired nerve regeneration during aging. Chronic inflammation was detected in intact uninjured old nerves, characterized by increased macrophage infiltration and raised levels of monocyte chemoattractant protein 1 (MCP1) and CC chemokine ligand 11 (CCL11). Schwann cells in the old nerves appeared partially dedifferentiated, accompanied by an activated repair program independent of injury. Upon sciatic nerve injury, an initial delayed immune response was followed by a persistent hyperinflammatory state accompanied by a diminished repair process. As a contributing factor to nerve aging, we showed that CCL11 interfered with Schwann cell differentiation in vitro and in vivo. Our results indicate that increased infiltration of macrophages and inflammatory signals diminish regenerative capacity of aging nerves by altering Schwann cell behavior. The study identifies CCL11 as a promising target for anti‐inflammatory therapies aiming to improve nerve regeneration in old age.

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Section: Discussionmentioning

confidence: 99%

Inflammaging impairs peripheral nerve maintenance and regeneration

et al. 2018

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“…The exception was for IL-6 and IL-10 that were further up-regulated by SIL treatment. IL-6 and IL-10 are part of a group of cytokines that control the inflammatory response, in part, by regulating the synthesis and release of additional cytokines [11,32]. IL-10 acts mainly as an anti-inflammatory cytokine, whereas IL-6 is pro-inflammatory and regulates the growth, survival and differentiation of peripheral neurons [33].…”

Section: Discussionmentioning

confidence: 99%

Sildenafil Attenuates Inflammation and Oxidative Stress in Pelvic Ganglia Neurons after Bilateral Cavernosal Nerve Damage

Garcia

Hlaing

Gutierrez

et al. 2014

IJMS

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Erectile dysfunction is a common complication for patients undergoing surgeries for prostate, bladder, and colorectal cancers, due to damage of the nerves associated with the major pelvic ganglia (MPG). Functional re-innervation of target organs depends on the capacity of the neurons to survive and switch towards a regenerative phenotype. PDE5 inhibitors (PDE5i) have been successfully used in promoting the recovery of erectile function after cavernosal nerve damage (BCNR) by up-regulating the expression of neurotrophic factors in MPG. However, little is known about the effects of PDE5i on markers of neuronal damage and oxidative stress after BCNR. This study aimed to investigate the changes in gene and protein expression profiles of inflammatory, anti-inflammatory cytokines and oxidative stress related-pathways in MPG neurons after BCNR and subsequent treatment with sildenafil. Our results showed that BCNR in Fisher-344 rats promoted up-regulation of cytokines (interleukin- 1 (IL-1) β, IL-6, IL-10, transforming growth factor β 1 (TGFβ1), and oxidative stress factors (Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, Myeloperoxidase (MPO), inducible nitric oxide synthase (iNOS), TNF receptor superfamily member 5 (CD40) that were normalized by sildenafil treatment given in the drinking water. In summary, PDE5i can attenuate the production of damaging factors and can up-regulate the expression of beneficial factors in the MPG that may ameliorate neuropathic pain, promote neuroprotection, and favor nerve regeneration.

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“…and TGF-β promoting nerve repair has been confirmed recently [15][16][17][18]. (3) VSD can reduce the local inflammation, relieve local hyperemia and edema [4,19], which are beneficial for nerve stabilizing within the surrounding environment and for nerve regeneration [20]. In this experiment, nerve conduction velocity, triceps recovery rate, and histological assessments indicate that VSD play a role in promoting nerve damage repair.…”

Section: International Journal Of Neurosciencementioning

confidence: 59%