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April 9, 2021Frontiers in ImmunologyOpen Access

Inhibition of IL-6 in the LCWE Mouse Model of Kawasaki Disease Inhibits Acute Phase Reactant Serum Amyloid A but Fails to Attenuate Vasculitis

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Key result

Inhibition of STAT3 or blockade of IL-6 failed to alter disease development in the LCWE mouse model of Kawasaki disease, indicating they may be bystanders of inflammation.

Why the study?

10% of Kawasaki disease patients are resistant to front-line therapy, and interventions to address secondary complications such as myocardial fibrosis are lacking.

Does inhibition of IL-6 or STAT3 attenuate vasculitis in the LCWE mouse model of Kawasaki disease?

Population

5-week-old male mice

Comparison

LCWE alone vs LCWE with anakinra, STAT3 inhibitor, or anti-IL-6R antibody vs saline controls

Design

Preclinical animal model study

Authors

RPRebecca A. PorrittCHCarol Chase HuizarEDEdward J. Dick

Discussion

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Member takes

Overview

IL-6/STAT3 inhibition does not attenuate vasculitis in this model; leaves open their role as drivers in human Kawasaki disease.

Structured PICO

Does inhibition of IL-6 or STAT3 attenuate vasculitis in the LCWE mouse model of Kawasaki disease?

P
Population
5-week-old male mice injected with LCWE to model Kawasaki disease.
I
Intervention
Anakinra (IL-1 receptor antagonist), STAT3 small molecular inhibitor, or anti-IL-6R antibody
C
Comparator
LCWE alone or saline controls
O
Outcome
Disease development (vasculitis) and protein expression (STAT3, IL-6)surrogate

Inhibition of IL-6 or STAT3 fails to attenuate vasculitis in a mouse model of Kawasaki disease, indicating they may be bystanders rather than drivers of inflammation.

Cite This Study

Porritt et al. (2021) studied Kawasaki disease (mouse model). STAT3 small molecular inhibitor and anti-IL-6R antibody vs. LCWE alone or saline was evaluated on Disease development. Inhibition of STAT3 or blockade of IL-6 failed to alter disease development in the LCWE mouse model of Kawasaki disease, indicating they may be bystanders of inflammation.

synapsesocial.com/papers/6a20825bdf4cd797f4f42563https://doi.org/10.3389/fimmu.2021.630196
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Recent Developments on the Crosstalk Between STAT3 and Inflammation in Heart Function and Disease2018 · 74 citations
  2. 2Dectin-2–induced CCL2 production in tissue-resident macrophages ignites cardiac arteritis2019 · 82 citations
  3. 3Trial of Tocilizumab in Giant-Cell Arteritis2017 · 1,400 citations
  4. 4Interleukin-1 Beta–Mediated Sex Differences in Kawasaki Disease Vasculitis Development and Response to Treatment2020 · 65 citations
  5. 5Activation of STAT3 integrates common profibrotic pathways to promote fibroblast activation and tissue fibrosis2017 · 356 citations