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Bradykinin, Cytokines and Inflammatory Hyperalgesia

  • Chapter
Pain and Neuroimmune Interactions

Abstract

Bradykinin (BK) and related peptides are produced at sites of tissue injury and inflammation and have an important role in mediating the responses of the tissues to damage and associated pain. BK causes pain by direct stimulation of nociceptors and by sensitising sensory fibres to previously non-noxious stimuli (hyperalgesia). BK exerts its biological activities by stimulating two receptor subtypes, B1 and B2, with the latter localised to sensory neurones. The B2 receptor is believed to mediate many of the effects attributed to kinins although the B1 receptor has now been shown to have an important role in hyperalgesia, notably when the hyperalgesia is secondary to an earlier inflammatory insult.

Pro-inflammatory cytokines, e.g. interleukin-1β (IL-1β) and tumour necrosis factor α (TNFα), are potent hyperalgesic agents that constitute a link between cellular injury and the development and resolution of local and systemic manifestations of inflammation. The release of TNFα by macrophages can be induced by BK and, in a model of mechanical hyperalgesia, both BK (the preferred agonist of the B2 receptor) and its metabolite, the B1 receptor agonist [des-Arg9]BK, each initiates a cascade of cytokine release which mediates hyperalgesic responses to inflammatory agents. The cytokine cascade begins with TNFα, which stimulates production of IL-1β, IL-6, IL-8, prostaglandins (PGs) and sympathomimetics.

In the above model, B1 and B2 agonists act synergistically to cause cytokine-mediated hyperalgesia, and B1 and B2 antagonists proved to be highly effective anti-hyperalgesic drugs, especially when given together. A striking synergy between B1 and B2 receptor agonists, with each other and with IL-1β, was also described in a recent study in which B1 and B2 agonists, in the presence of IL-1β, shifted the repertoire of BK receptor subtypes from B2 to B1. Since, in addition to BK-induced IL-1β, IL-1β can induce B1 receptor-mediated hyperalgesia in models of mechanical and thermal hyperalgesia, there appear to be roles for both B1 and B2 receptors in a complex network of hyperalgesic mediators in which BK and related peptides induce cytokines and vice versa.

Another group of endogenous mediators, which includes the cytokines IL-4 and IL-1O and also lipocortin-l (LC-I), inhibit the production/action of TNFα, IL-Iβ, IL-6 and IL-8, and are now reported to have anti-hyperalgesic properties. The manipulation of the relative balance of these various proteins may permit the development of novel treatments of inflammatory hyperalgesia. In the meantime, the search for anti-hyperalgesic/analgesic drugs with novel mechanisms of action includes research on antagonists of BK B2 and, especially, B1 receptors (and possibly the combination of B1 and B2 receptor antagonists) and on the (orally active) tripeptide inhibitors of IL-Iβ-mediated hyperalgesia that have been described.

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Authors and Affiliations

  1. Division of Endocrinology, National Institute for Biological Standards and Control, Blanche Lane, South Mimms, Potters Bar, Herts, EN6 3QG

    Stephen Poole & Sergio Henriques Ferreira

  2. Department of Pharmacology, Faculty of Medicine of Ribeirão Preto, University of São Paulo, Ribeirao Preto, Brazil

    Fernando de Queiroz Cunha

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  2. Fernando de Queiroz Cunha
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  3. Sergio Henriques Ferreira
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  1. American University of Beirut, Beirut, Lebanon

    Nayef E. Saadé  & Suhayl J. Jabbur  & 

  2. SUNY Health Science Center, Syracuse, New York, USA

    A. Vania Apkarian

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Poole, S., de Queiroz Cunha, F., Ferreira, S.H. (2000). Bradykinin, Cytokines and Inflammatory Hyperalgesia. In: Saadé, N.E., Apkarian, A.V., Jabbur, S.J. (eds) Pain and Neuroimmune Interactions. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-4225-4_4

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