scispace - formally typeset
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.

Papers
More filters
Journal ArticleDOI

Innate Immune Response of Human Alveolar Macrophages during Influenza A Infection

TL;DR: F influenza infection induced an extensive proinflammatory response in human AM and targeting local components of innate immune response might provide a strategy for controlling influenza A infection-induced pro inflammatory response in vivo.
Journal ArticleDOI

Imbalance between interleukin-1 agonists and antagonists: relationship to severity of inflammatory bowel disease.

TL;DR: The results indicate that the proinflammatory moiety IL‐1sRI is a systemic marker of inflammation and activity in CD and local shedding of the functional antagonist IL‐ 1sRII may dampen colonic inflammation in CD, but not in UC.
Journal ArticleDOI

Triggering receptor expressed on myeloid cells-1 (TREM-1) amplifies the signals induced by the NACHT-LRR (NLR) pattern recognition receptors

TL;DR: The findings demonstrate that TREM‐1 acts on both major recognition pathways of bacterial structures: the extracellular TLR receptors, and the intracellular NLR molecules, which supports the concept that T REM‐1 provides optimal amplification of cytokine‐induced inflammation during the initiation of host defense.
Journal ArticleDOI

Hydrogen peroxide induces tumor necrosis factor α–mediated cardiac injury by a P38 mitogen-activated protein kinase–dependent mechanism

TL;DR: These results demonstrate that H2O2 alone induces myocardial TNF production, and demonstrate that P38 MPAK is an oxidant-sensitive enzyme that mediates oxidants-induced myocardials dysfunction, cardiac dysfunction, and cardiomyocyte death.