ACR Meeting Abstracts

ACR Meeting Abstracts

  • Home
  • Meetings Archive
    • ACR Convergence 2020
    • 2020 ACR/ARP PRSYM
    • 2019 ACR/ARP Annual Meeting
    • 2018 ACR/ARHP Annual Meeting
    • 2017 ACR/ARHP Annual Meeting
    • 2017 ACR/ARHP PRSYM
    • 2016-2009 Meetings
    • Download Abstracts
  • Keyword Index
  • Advanced Search
  • Your Favorites
    • Favorites
    • Login
    • Register
    • View and print all favorites
    • Clear all your favorites
  • Meeting Resource Center

Abstract Number: 1069

The Effects of TNF Stimulation On Control of Apoptosis in Neutrophils

Direkrit Chiewchengchol1, Connie Lam1, Kate Roberts1, Helen Wright1, Huw Thomas1, Robert Moots2 and Steven Edwards1, 1Institute of Integrative Biology, University of Liverpool, Liverpool, United Kingdom, 2University Hospital Aintree, Liverpool, United Kingdom

Meeting: 2012 ACR/ARHP Annual Meeting

Keywords: Apoptosis, neutrophils and signal transduction

  • Tweet
  • Email
  • Print
Save to PDF
Session Information

Session Title: Innate Immunity and Rheumatic Disease

Session Type: Abstract Submissions (ACR)

Background/Purpose: TNF is a key regulator of immune function and plays a pivotal role in inflammatory conditions such as rheumatoid arthritis. Human neutrophils express and release TNF, and are activated by it. Neutrophil responses to TNF are bimodal: low concentrations of TNF (~10 ng/mL) delay apoptosis but higher concentrations (>20 ng/mL) accelerate apoptosis. When neutrophils are activated to express TNF, complex regulatory mechanisms must control their response to both autocrine and paracrine signalling. This study investigated the mechanisms by which neutrophils respond to anti-apoptotic concentrations of TNF and control apoptosis delay. 

Methods: Human neutrophils were exposed to 10 ng/mL of TNF: apoptosis was determined by flow cytometry (annexin V/PI binding); gene expression was determined by analysis of mRNA levels, flow cytometery and western blotting. 

Results: Transcriptome analysis revealed that TNF signalling significantly increased mRNA levels for TNF, ICAM1, TNFAIP3, CD40, BFL1 plus several genes associated with NF-kB signalling. In contrast, mRNA levels of TNF receptor 1, TNF receptor 2, FADD, Bax and Caspase 8 were all significantly down-regulated. Many of these changes in mRNA levels were paralleled by changes in protein levels. These data indicate that neutrophils contribute to TNF-mediated signalling pathways via activated secretion of this cytokine. In parallel, they up-regulate genes that delay apoptosis (e.g. BFL1) but down-regulate expression of pro-apoptotic genes such as Bax and FADD. 

Conclusion: These data shed important new insights into understanding the function of neutrophils in inflammation and inflammatory diseases; neutrophils contribute to TNF-mediated inflammation and in doing so become more resistant to apoptosis.


Disclosure:

D. Chiewchengchol,
None;

C. Lam,
None;

K. Roberts,
None;

H. Wright,
None;

H. Thomas,
None;

R. Moots,
None;

S. Edwards,
None.

  • Tweet
  • Email
  • Print
Save to PDF

« Back to 2012 ACR/ARHP Annual Meeting

ACR Meeting Abstracts - https://acrabstracts.org/abstract/the-effects-of-tnf-stimulation-on-control-of-apoptosis-in-neutrophils/

Advanced Search

Your Favorites

You can save and print a list of your favorite abstracts by clicking the “Favorite” button at the bottom of any abstract. View your favorites »

ACR Convergence: Where Rheumatology Meets. All Virtual. November 5-9.

ACR Pediatric Rheumatology Symposium 2020

© COPYRIGHT 2021 AMERICAN COLLEGE OF RHEUMATOLOGY

Wiley

  • Home
  • Meetings Archive
  • Advanced Search
  • Meeting Resource Center
  • Online Journal
  • Privacy Policy
  • Permissions Policies
loading Cancel
Post was not sent - check your email addresses!
Email check failed, please try again
Sorry, your blog cannot share posts by email.
This site uses cookies: Find out more.