Interleukin-1 enhances pain reflexes. Mediation through increased prostaglandin E2 levels

Schweizer, A.; Feige, Ulrich; Fontana, Adriano; Müller, Klaus; Dinarello, Charles A.

doi:10.1007/bf01965025

Cited by 103 publications

(48 citation statements)

References 12 publications

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“…It follows that cyclooxygenase products generated by IL-1p in the vicinity of afferent nerve endings are responsible for the enhancement of the hyperaemic response to capsaicin. This inference is in keeping with the reported involvement of prostaglandins in the IL-IP-induced hyperalgesia in the rat paw (Ferreira et al, 1988) and rabbit ear (Schweizer et al, 1988) but-does not negate the possibility that other mediators could also participate (Follenfant et al, 1989). …”

Section: Discussionsupporting

confidence: 59%

Interleukin‐1β enhances capsaicin‐induced neurogenic vasodilatation in the rat skin

Herbert

Holzer

1994

British J Pharmacology

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This study examined the effect of interleukin‐1β (IL‐1β) on the capsaicin‐induced increase in cutaneous blood flow of anaesthetized rats as measured by laser Doppler flowmetry. The substances were administered by intraplantar subcutaneous injection of 10 μl‐volumes, saline being injected into one hindpaw and IL‐1β into the other. IL‐1β (0.5–500 pg) was without effect on blood flow on its own but dose‐dependently enhanced the hyperaemic response to intraplantar capsaicin (0.3 μg) up to 180% (P < 0.05) of the response seen in saline‐treated paws. Il‐1β‐(163–171), a fragment devoid of proinflammatory activity, failed to enhance capsaicin‐induced hyperaemia when given at a dose of 50 pg. Indomethacin (10 mg kg−1, i.p.) did not alter the capsaicin‐induced vasodilatation but prevented IL‐1β (50 pg) from augmenting the hyperaemic response to capsaicin. The hyperaemia evoked by intraplantar calcitonin gene‐related peptide (0.038–3.8 ng) was not altered by IL‐1β (50 pg). These data indicate that IL‐1β enhances the cutaneous hyperaemic response to afferent nerve stimulation with capsaicin in a prostaglandin‐dependent manner. This proinflammatory action of the cytokine appears to arise from sensitization of afferent nerve endings.

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Section: Discussionsupporting

confidence: 59%

Interleukin‐1β enhances capsaicin‐induced neurogenic vasodilatation in the rat skin

Herbert

Holzer

1994

British J Pharmacology

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“…However, it is worth mentioning that IL-6 has both pro-inflammatory and anti-inflammatory properties (13). IL-1β excites the nociceptive dorsal root ganglia (57), increases the production of substance P and prostaglandin E2 by neuronal and glial cells (58,59), and causes hyperalgesia.…”

Section: Discussionmentioning

confidence: 99%

Immune responses following McKenzie lumbar spine exercise in individuals with acute low back pain: A preliminary study

Al‐Obaidi

Mahmoud

2014

AMA

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Objective. This study explores the immune responses following 4 weeks of McKenzie lumbar spine exercise in individuals with acute low back pain (ALBP). Patients and methods. Fifteen patients with ALBP and 15 healthy individuals volunteered in this study. Ten ml of peripheral blood were obtained from each patient before and after exercise sessions, and from healthy individuals at the beginning of the study.

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“…These neuropeptides are released from the central terminals of C-fibres and have excitatory effects on dorsal horn neurones controlling the gain of nociceptive transmission (Woolf, 1991 (Movat, 1987;Dinarello, 1991;Bianchi et al, 1992). IL-1i is produced by activated macrophages and a large variety of other cell types including B-lymphocytes and endothelial cells (Libby et al, 1986;Dinarello, 1991) and its administration causes hyperalgesia (Ferreira et al, 1988;Schweizer et al, 1988;Ferreira, 1993;Fukuoka et al, 1994;Watkins et al, 1994). IL-10 can, in addition, induce NGF production in a number of cell types Heumann et al, 1987;Lindholm et al, 1987;Matsuoka et al, 1991;Yoshida & Gage, 1992 Sivilotti & Woolf, 1994 (Shive & Thrall, 1991;Thompson et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

Contribution of interleukin‐1β to the inflammation‐induced increase in nerve growth factor levels and inflammatory hyperalgesia

Safieh‐Garabedian

Poole

Allchorne

et al. 1995

British J Pharmacology

551

324

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Peripheral inflammation is associated with the local production of neuroactive inflammatory cytokines and growth factors. These may contribute to inflammatory pain and hyperalgesia by directly or indirectly altering the function or chemical phenotype of responsive primary sensory neurones. To investigate this, inflammation was produced by the intraplantar injection of complete Freund's adjuvant (CFA) in adult rats. This resulted in a significant elevation in interleukin‐ip (IL‐1β) and nerve growth factor (NGF) levels in the inflamed tissue and of the peptides, substance P and calcitonin gene‐related peptide (CGRP) in the L4 dorsal root ganglion 48 h post CFA injection. The effects of a steroidal (dexamethasone) and a non‐steroidal (indomethacin) anti‐inflammatory drug on the levels of NGF and IL‐1β in inflamed tissue were investigated and compared with alterations in behavioural hyperalgesia and neuropeptide expression in sensory neurones. Systemic dexamethasone (120 μg kg−1 per day starting the day before the CFA injection) had no effect on the inflammatory hyperalgesia. When the dose was administered 3 times daily, a reduction in mechanical and to a lesser extent thermal sensitivity occurred. Indomethacin at 2 mg kg−1 daily (i.p.) had no effect on the hyperalgesia and a dose of 4 mg kg−1 daily was required to reduce significantly mechanical and thermal hypersensitivity. The increase in NGF produced by the CFA inflammation was prevented by both dexamethasone and indomethacin, but only at the higher dose levels. Dexamethasone at the lower and higher dose regimes diminished the upregulation of IL‐1β whereas indomethacin had an effect only at the higher dose. The increase in SP and CGRP levels produced by the CFA inflammation was prevented by dexamethasone and indomethacin at the lower and higher dose regimes. Intraplantar injections of IL‐1β (0.01, 0.1 and 1 ng) produced a brief (6 h) thermal hyperalgesia and an elevation in cutaneous NGF levels which was prevented by pretreatment with human recombinant IL‐1 receptor antagonist (IL‐1 ra) (0.625 μg, i.v.). The thermal hyperalgesia but not the NGF elevation produced by intraplantar IL‐1β (1 ng) was prevented by administration of a polyclonal neutralizing anti‐NGF serum. IL‐1 ra significantly reduced the mechanical hyperalgesia produced by CFA for 6 h after administration as well as the CFA‐induced elevation in NGF levels. Anti‐NGF pretreatment substantially reduced CFA‐induced mechanical and thermal hyperalgesia without reducing the elevation in IL‐1β. Intraplantar NGF (0.O2, 0.2 and 2 μg) injections produced a short lasting thermal and mechanical hyperalgesia but did not change IL‐1β levels in the hindpaw skin. Our results demonstrate that IL‐1β contributes to the upregulation of NGF during inflammation and that NGF has a major role in the production of inflammatory pain hypersensitivity.

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Interleukin-1 enhances pain reflexes. Mediation through increased prostaglandin E2 levels

Cited by 103 publications

References 12 publications

Interleukin‐1β enhances capsaicin‐induced neurogenic vasodilatation in the rat skin

Interleukin‐1β enhances capsaicin‐induced neurogenic vasodilatation in the rat skin

Immune responses following McKenzie lumbar spine exercise in individuals with acute low back pain: A preliminary study

Contribution of interleukin‐1β to the inflammation‐induced increase in nerve growth factor levels and inflammatory hyperalgesia

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