Characterization of cytokine-induced hyperalgesia

Watkins, Linda R.; Wiertelak, Eric P.; Goehler, Lisa E.; Smith, Kathrine P.; Martin, David; Maier, Steven F.

doi:10.1016/0006-8993(94)91566-0

Cited by 461 publications

(238 citation statements)

References 45 publications

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“…the skin of the back of the animal, in its relatively restrained position during UV session. These observations suggest that the hyperalgesia could be a kind of`illness induced hyperalgesia' which was described by Watkins et al (1994; following i.p. injection of endotoxin and attributed to the action of cytokines (IL-1b, in particular) on the brain.…”

Section: Discussionmentioning

confidence: 72%

“…Subsequent studies have established the contribution of neuropeptides (Substance P, CGRP) in the in¯ammatory reaction induced by UVR (Benrath et al, 1995;Gillardon et al, 1992;Scholzen et al, 1999). Furthermore, cytokines and nerve growth factor (NGF), increased during UVB-induced in¯ammation, have been shown to produce hyperalgesia following either local or systemic injections (Andreev et al, 1995;Cunha et al, 1992;Ferreira et al, 1988;Lewin & Mendell 1993;Watkins et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

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Modulation of ultraviolet‐induced hyperalgesia and cytokine upregulation by interleukins 10 and 13

Saadé

Nasr

Massaad

et al. 2000

British J Pharmacology

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1 Exposure to midrange ultraviolet radiation (UVB) is known to produce skin in¯ammation similar to sunburn. The aim of this study was to characterize the hyperalgesia and cytokine upregulation induced by UVB and their modulation by antiin¯ammatory cytokines. 2 Acute exposure of the dorsal skin of mice to UVB (200, 250 and 300 mJ cm 2 ) resulted in a dosedependent decrease in the latencies of the hot plate and tail¯ick tests, without evident signs of skin lesions. 3 The observed hyperalgesia displayed a biphasic temporal evolution with an acute phase (3 ± 6 h) and a late (48 ± 96 h) phase. 4 Exposure to UVB (300 mJ cm 2 ) elicited signi®cant upregulation of interleukin (IL)-1b, tumour necrosis factor (TNF)-a and nerve growth factor (NGF), determined by ELISA in the exposed skin. This upregulation was more important during the acute phase of hyperalgesia. 5 Daily treatment of mice, with i.p. injections of either IL-10 or IL-13 (1.5, 7.5 and 15 ng in 100 ml saline) produced a dose-dependent attenuation of the UVB-induced hyperalgesia. 6 Treatment with the highest doses of either IL-10 or IL-13, produced signi®cant attenuation of the levels of the cytokines and NGF by UVB, with relatively more pronounced e ects by IL-13. 7 Acute exposure to moderate amounts of UVB results in a systemic hyperalgesia related to the upregulation of cytokine and NGF levels, since both were prevented by treatment with antiin¯ammatory cytokines.

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Section: Discussionmentioning

confidence: 72%

Section: Introductionmentioning

confidence: 99%

Modulation of ultraviolet‐induced hyperalgesia and cytokine upregulation by interleukins 10 and 13

Saadé

Nasr

Massaad

et al. 2000

British J Pharmacology

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“…Cytokines and growth factors have been strongly implicated in the generation of pathological pain states at both peripheral and central nervous system sites (Lewin and Mendell 1993;Watkins et al, 1994) and in the development and progression of diabetic neuropathy (Skundric and Lisak 2003), although the role of cytokine transforming factors such as TGF-β . is unknown.…”

Section: Discussionmentioning

confidence: 99%

“…However, it is known that cytokines have a pain facilitatory effect following nerve injury by activating central pathways via: (1) axonal or non-axonal transport to the dorsal root ganglion, spinal cord, and brain and/or; (2) induction of central cytokines by either peripheral cytokines or glial/neuronal activation (Rutkowski and DeLeo 2002). In nerve injury, cytokines may also indirectly activate mediators of pain transmission, such as glutamate and nitric oxide, or affect neurotrophin signaling in the peripheral nerve (Rutkowski and DeLeo 2002;Watkins et al, 1994). These are similar to pathways activated in diabetic neuropathy or neuropathic pain (Russell et al, 2006b;Russell et al, 2006a;Russell and Kaminsky 2005).…”

Section: Discussionmentioning

confidence: 99%

Transforming growth factor-β induces cellular injury in experimental diabetic neuropathy

Anjaneyulu

Berent-Spillson

Inoue

et al. 2008

Experimental Neurology

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The mechanism/s leading to diabetic neuropathy are complex. Transforming growth factor-β1 (TGF-β1) has been associated with diabetic nephropathy and retinopathy but not neuropathy. In this study, changes in TGF-β isoforms were examined in-vivo and in-vitro. Two groups of animals, streptozotocin diabetic with neuropathy and non-diabetic controls were examined at 4 weeks (n=10/ group) and 12 weeks (n=8/group). In diabetic DRG using quantitative real-time PCR (QRT-PCR), TGF-β1 and TGF-β2 mRNA, but not TGF-β3, was increased at 4 and 12 weeks. In sciatic nerve TGF-β3 mRNA was primarily increased. Immunohistochemistry (DRG) and immunoblotting (sciatic nerve) showed similar differential protein expression. In sciatic nerve TGF-β formed homoand heterodimers, of which β 2 /β 3 , β 1 /β 1 , and β 1 /β 3 were significantly increased, while that of the TGF-β 2 /β 2 homodimer was decreased, in diabetic compared to non-diabetic rats. In-vitro, pretreatment of embryonic DRG with TGF-β neutralizing antibody prevents the increase in total TGF-β protein observed with high glucose using immunoblotting. In high glucose conditions, combination with TGF-β2 > β1 increases the percent of cleaved caspase-3 compared to high glucose alone and TGF-β neutralizing antibody inhibits this increase. Furthermore, consistent with the findings in diabetic DRG and nerve, TGF-β isoforms applied directly in vitro reduce neurite outgrowth, and this effect is partially reversed by TGF-β neutralizing antibody. These findings implicate upregulation of TGF-β in experimental diabetic peripheral neuropathy and indicate a novel mechanism of cellular injury related to elevated glucose levels. In combination, these findings indicate a potential new target for treatment of diabetic peripheral neuropathy.

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“…LPS stimulates the production of inflammatory mediators such as NO, TNF-α, interleukins, PGE 2 , and leukotrienes (Lee et al, 1992;Kubes and McCafferty, 2000). Moreover, LPS enhances the pain response to various somatic stimuli (Watkins et al, 1994;Yirmiya et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

Aqueous extract of Paeonia radix suppresses lipopolysaccharide-induced expressions of cyclooygenase-2 and inducible nitric oxide synthase in mouse BV2 microglial cells

Hong¹,

Kim²,

Yang³

et al. 2008

Oriental Pharmacy and Experimental Medicine

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SUMMARYPaeonia radix is the root of Paeonia aliflora Pallas, which is a perennial plant classified in the family Paeoniaceae. Paeonia radix possesses several pharmacological effects such as analgesic, antiinflammatory and anti-allergic, anti-oxidative, and anti-coagulant activities. In this study, we investigated the effect of the aqueous extract of Paeonia radix on the lipopolysaccharide-induced inflammation in mouse BV2 microglial cells. The aqueous extract of Paeonia radix at respective concentration was treated one hour before lipopolysaccharide treatment. In the present results, the aqueous extract of Paeonia radix suppressed prostaglandin E 2 synthesis and nitric oxide production by inhibiting the lipopolysaccharide-stimulated mRNA expressions of cyclooxygenase-2 and inducible nitric oxide synthase in mouse BV2 microglial cells. These results demonstrate that Paeonia radix exerts anti-inflammatory and analgesic effects probably by suppressing mRNA expressions of cyclooxygenase-2 and inducible nitric oxide synthesis. The present study demonstrates that Paeonia radix may offer a valuable mean of therapy for brain inflammatory diseases.

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Characterization of cytokine-induced hyperalgesia

Cited by 461 publications

References 45 publications

Modulation of ultraviolet‐induced hyperalgesia and cytokine upregulation by interleukins 10 and 13

Modulation of ultraviolet‐induced hyperalgesia and cytokine upregulation by interleukins 10 and 13

Transforming growth factor-β induces cellular injury in experimental diabetic neuropathy

Aqueous extract of Paeonia radix suppresses lipopolysaccharide-induced expressions of cyclooygenase-2 and inducible nitric oxide synthase in mouse BV2 microglial cells

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