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Waldiceu A. Verri

Researcher at Universidade Estadual de Londrina

Publications -  288
Citations -  12868

Waldiceu A. Verri is an academic researcher from Universidade Estadual de Londrina. The author has contributed to research in topics: Hyperalgesia & Oxidative stress. The author has an hindex of 54, co-authored 249 publications receiving 10311 citations. Previous affiliations of Waldiceu A. Verri include Universidade Estadual de Maringá & Universidade Federal de Minas Gerais.

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Nociceptor Sensory Neuron-Immune Interactions in Pain and Inflammation.

TL;DR: The dialog between nociceptor neurons and the immune system is a fundamental aspect of inflammation, both acute and chronic, and a better understanding of these interactions could produce approaches to treat chronic pain and inflammatory diseases.
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A cascade of cytokines mediates mechanical inflammatory hypernociception in mice.

TL;DR: Results extend to mice the concept that the release of primary mediators responsible for hypernociception is preceded by a cascade of cytokines.
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Hypernociceptive role of cytokines and chemokines: targets for analgesic drug development?

TL;DR: The evidence suggesting pro- and anti-inflammatory cytokines and chemokines are potential targets to develop novel drugs and therapies for the treatment of pain is emphasized, emphasizing the importance of the direct and indirect actions of cytokine actions in inflammatory and neuropathic hypernociception.
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An electronic pressure-meter nociception paw test for mice

TL;DR: The results show that the electronic pressure-meter provides a sensitive, objective and quantitative mechanical nociceptive test that could be useful to characterize new nOCiceptive inflammatory mediators and also to evaluate new peripheral analgesic substances.
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Interleukin-33 attenuates sepsis by enhancing neutrophil influx to the site of infection

TL;DR: It is shown that interleukin-33 reduces mortality in mice with experimental sepsis from cecal ligation and puncture (CLP) and reverses the TLR4-induced reduction of CXCR2 expression in neutrophils via the inhibition of expression of G protein–coupled receptor kinase-2 (GRK2), a serine-threonine protein kinase that induces internalization of chemokine receptors.