Autoantibodies to citrullinated proteins induce joint pain independent of inflammation via a chemokine-dependent mechanism

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AudienciaPúblico en generales_ES
CoberturaMéxicoes_ES
Fecha de ingreso2026-10-05T16:33:12Z
Fecha de publicación2016-01-01
ResumenObjective An interesting and so far unexplained feature of chronic pain in autoimmune disease is the frequent disconnect between pain and inflammation. This is illustrated well in rheumatoid arthritis (RA) where pain in joints (arthralgia) may precede joint inflammation and persist even after successful anti-inflammatory treatment. In the present study, we have addressed the possibility that autoantibodies against citrullinated proteins (ACPA), present in RA, may be directly responsible for the induction of pain, independent of inflammation. Methods Antibodies purified from human patients with RA, healthy donors and murinised monoclonal ACPA were injected into mice. Pain-like behaviour was monitored for up to 28 days, and tissues were analysed for signs of pathology. Mouse osteoclasts were cultured and stimulated with antibodies, and supernatants analysed for release of factors. Mice were treated with CXCR1/2 (interleukin (IL) 8 receptor) antagonist reparixin. Results Mice injected with either human or murinised ACPA developed long-lasting pronounced pain-like behaviour in the absence of inflammation, while nonACPA IgG from patients with RA or control monoclonal IgG were without pronociceptive effect. This effect was coupled to ACPA-mediated activation of osteoclasts and release of the nociceptive chemokine CXCL1 (analogue to human IL-8). ACPA-induced pain-like behaviour was reversed with reparixin. Conclusions The data suggest that CXCL1/IL-8, released from osteoclasts in an autoantibody-dependent manner, produces pain by activating sensory neurons. The identification of this new pain pathway may open new avenues for pain treatment in RA and also in other painful diseases associated with autoantibody production and/or osteoclast activation.es_ES
Doihttps://doi.org/10.1136/annrheumdis-2015-208094es_ES
URIhttps://riuat.uat.edu.mx/handle/123456789/5034
Idiomaenes_ES
EditorialBMJ PUBLISHING GROUPes_ES
RelaciónAnnals of the Rheumatic Diseaseses_ES
URL relacionadohttps://doi.org/10.1136/annrheumdis-2015-208094es_ES
DerechosAcceso abierto (Metadatos de producción científica)es_ES
Licenciahttp://purl.org/coar/access_right/c_abf2es_ES
FuenteAnnals of the Rheumatic Diseases
TítuloAutoantibodies to citrullinated proteins induce joint pain independent of inflammation via a chemokine-dependent mechanismes_ES
TipoArtículoes_ES
ArbitradoHa sido Arbitradoes_ES
AutorWigerblad, Gustaf
AutorBas, Duygu B.
AutorFernades-Cerqueira, Catia
AutorKrishnamurthy, Akilan
AutorNandakumar, Kutty Selva
AutorRogoz, Katarzyna
AutorKato, Jungo
AutorSandor, Katalin
AutorSu, Jie
AutorMiguel Jimenez-Andrade, Juan
AutorFinn, Anja
AutorFarinotti, Alex Bersellini
AutorAmara, Khaled
AutorLundberg, Karin
AutorHolmdahl, Rikard
AutorJakobsson, Per-Johan
AutorMalmstrom, Vivianne
AutorCatrina, Anca I.
AutorKlareskog, Lars
AutorSvensson, Camilla I.
AutorWigerblad, Gustafes_ES
AutorBas, Duygu B.es_ES
AutorFernades-Cerqueira, Catiaes_ES
AutorKrishnamurthy, Akilanes_ES
AutorNandakumar, Kutty Selvaes_ES
AutorRogoz, Katarzynaes_ES
AutorKato, Jungoes_ES
AutorSandor, Katalines_ES
AutorSu, Jiees_ES
AutorMiguel Jimenez-Andrade, Juanes_ES
AutorFinn, Anjaes_ES
AutorFarinotti, Alex Bersellinies_ES
AutorAmara, Khaledes_ES
AutorLundberg, Karines_ES
AutorHolmdahl, Rikardes_ES
AutorJakobsson, Per-Johanes_ES
AutorMalmstrom, Viviannees_ES
AutorCatrina, Anca I.es_ES
AutorKlareskog, Larses_ES
AutorSvensson, Camilla I.es_ES
InstituciónUniversidad Autónoma de Tamaulipas
InstituciónUniversidad Autónoma de Tamaulipases_ES
Número4es_ES
Rango de páginas730-738es_ES
URL relacionadahttps://doi.org/10.1136/annrheumdis-2015-208094
Tipo de artículoIndexado
Tipo de artículoIndexadoes_ES
Volumen75es_ES

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