C
Charles A. Dinarello
Researcher at University of Colorado Denver
Publications - 1073
Citations - 152254
Charles A. Dinarello is an academic researcher from University of Colorado Denver. The author has contributed to research in topics: Interleukin & Cytokine. The author has an hindex of 190, co-authored 1058 publications receiving 139668 citations. Previous affiliations of Charles A. Dinarello include University of Guadalajara & Pennsylvania State University.
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Journal ArticleDOI
Transcriptional and inflammasome-mediated pathways for the induction of IL-1beta production by Mycobacterium tuberculosis.
Johanneke Kleinnijenhuis,Leo A. B. Joosten,Frank L. van de Veerdonk,Nigel D. L. Savage,Reinout van Crevel,Bart Jan Kullberg,André J. A. M. van der Ven,Tom H. M. Ottenhoff,Charles A. Dinarello,Jos W. M. van der Meer,Mihai G. Netea +10 more
TL;DR: The present study has deciphered the pathways leading from recognition of Mycobacterium tuberculosis to the production and release of IL‐1β, the most important member of the IL-1 family, by stimulating cells defective in various pattern recognition receptors and demonstrated that IL‐ 1β production is induced by M. tuberculosis.
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Neutralization of IL-18 attenuates lipopolysaccharide-induced myocardial dysfunction.
Christopher D. Raeburn,Charles A. Dinarello,Michael A. Zimmerman,Casey M. Calkins,Pomerantz Benjamin,Robert C. McIntyre,Alden H. Harken,Xianzhong Meng +7 more
TL;DR: It is hypothesized that neutralization of IL-18 would attenuate lipopolysaccharide (LPS)-induced cardiac dysfunction and was associated with reduced myocardial IL-1beta production and ICAM-1/VCAM- 1 expression, but myocardia TNF-alpha levels were not influenced by neutralization.
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Plasma levels of interleukin-18 and interleukin-18 binding protein are elevated in patients with chronic liver disease.
Othmar Ludwiczek,Arthur Kaser,Daniela Novick,Charles A. Dinarello,Menachem Rubinstein,Wolfgang Vogel,Herbert Tilg +6 more
TL;DR: Plasma levels of IL-18 and its antagonist,IL-18BP, are elevated in CLD and correlate with severity of disease and may not be sufficient to counteract the overwhelming proinflammatory response in end stage liver disease.
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Liposomal Delivery of Purified Inhibitory-κBα Inhibits Tumor Necrosis Factor-α–Induced Human Vascular Smooth Muscle Proliferation
Craig H. Selzman,Brian D. Shames,Leonid L. Reznikov,Stephanie A. Miller,Xianzhong Meng,Hazel A. Barton,Ariel Werman,Alden H. Harken,Charles A. Dinarello,Anirban Banerjee +9 more
TL;DR: The mitogenic effect of TNF-alpha on human arterial VSMCs is dependent on NF-kappaB activation and may be prevented by exogenously delivered IkappaBalpha, and liposomal delivery of endogenous inhibitory proteins may represent a novel, therapeutically accessible method for selective transcriptional suppression in the response to vascular injury.
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Histone deacetylase inhibition regulates inflammation and enhances Tregs after allogeneic hematopoietic cell transplantation in humans
Sung Won Choi,Erin Gatza,Guoqing Hou,Yaping Sun,Joel Whitfield,Yeohan Song,Katherine Oravecz-Wilson,Isao Tawara,Charles A. Dinarello,Pavan Reddy +9 more
TL;DR: It is demonstrated that HDAC inhibition reduces inflammatory responses of PBMC but enhances Tregs after allo-HCT, andHDAC inhibition also increased signal transducer and activator of transcription 3 acetylation and induced indoleamine-2,3-dioxygenase.