ACR Meeting Abstracts

ACR Meeting Abstracts

  • Meetings
    • ACR Convergence 2024
    • ACR Convergence 2023
    • 2023 ACR/ARP PRSYM
    • ACR Convergence 2022
    • ACR Convergence 2021
    • ACR Convergence 2020
    • 2020 ACR/ARP PRSYM
    • 2019 ACR/ARP Annual Meeting
    • 2018-2009 Meetings
    • Download Abstracts
  • Keyword Index
  • Advanced Search
  • Your Favorites
    • Favorites
    • Login
    • View and print all favorites
    • Clear all your favorites
  • ACR Meetings

Abstract Number: 1584

Chlamydia-Infected Macrophages: “Trojan Horses” for Dissemination of IL-23 and TNF-Mediated Inflammation in SKG Mouse Reactive Arthritis

Athan Baillet1, Zaied Ahmed Bhuyan2, Claire Douillard1, Aurélie Bozon1, Charles Armitage3, Xavier Romand1, Minh Vu Chuong Nguyen1, Bertrand Favier1, Timothy Wells2, Kenneth Beagley3 and Ranjeny Thomas2, 1Université Grenoble-Alpes, GREPI EA7408, Grenoble, France, 2The University of Queensland Diamantina Institute, Translational Research Institute, Brisbane, Australia, 3Institute of Health & Biomedical Innovation, Biomedical Sciences, Faculty of Health, Queensland University of Technology, Brisbane, Australia

Meeting: 2017 ACR/ARHP Annual Meeting

Date of first publication: September 18, 2017

Keywords: Macrophage and reactive arthritis

  • Tweet
  • Email
  • Print
Session Information

Date: Monday, November 6, 2017

Title: Spondyloarthropathies and Psoriatic Arthritis – Pathogenesis, Etiology Poster II

Session Type: ACR Poster Session B

Session Time: 9:00AM-11:00AM

Background/Purpose: The sterile inflammatory arthritis associated with spondylitis, uveitis and rash, known as reactive arthritis, commences a few weeks after certain gastrointestinal or genitourinary infections, including Salmonella and Chlamydia in genetically-susceptible patients. ZAP-70W163C mutant BALB/c mice (known as SKG) develop a syndrome highly similar to human reactive arthritis after vaginal infection with C. muridarum. In that model, Chlamydial DNA was found in splenic and lymph node CD11b+ cells distant from the site of infection. We hypothesized that monocytes and macrophages disseminate pro-inflammatory C. muridarum pathogen-associated inflammatory molecules (PAMPs) to distant sites in susceptible SKG mice to induce inflammatory cytokine-mediated pathology.

Methods: Female SKG and BALB/c mice were genitally infected with C. muridarum. Arthritis was assessed weekly for 12 weeks post-infection. Joint sections were scored after sacrifice and genital tracts were analyzed 1 week post-infection. We compared Hspa5, Tgtp1, IL-23 expression by RT-qPCR in genital tract from SKG mice before or 1 week after infection. Anti-TNF or isotype were delivered either immediately after infection or after arthritis developed. We engineered C. muridarum expressing luciferase and GFP (pGFP-Luc-CM) to monitor in vivo uptake and dissemination. We depleted macrophages from Chlamydia-infected SKG mice with clodronate liposomes.

Results: SKG but not BALB/c mice developed typical histological features of chronic reactive arthritis but remained autoantibody-negative, from 5 weeks after genital infection. When applied at infection, anti-TNF blocked C. muridarum-induced reactive arthritis in SKG mice. Seven weeks post-infection, SKG but not BALB/c mice developed inflammatory salpingitis. One week post-infection, we observed C. muridarum dissemination in the upper genital tract of SKG but not BALB/c mice. After infection with pGFP-Luc-CM, C. muridarum GFP signal was exclusively found in CD11b+Ly6g-Lyc6c+F4/80+MHC class II+ macrophages in both strains. Expression of macrophage Tgtp1 and IL23a but not Hspa5 expression was upregulated one week after C. muridarum infection and returned to baseline levels 5 weeks after infection. Tgtp1 and IL23a mRNA expression were highly correlated (Figure) in genital tract one week upon infection. Depletion of macrophages using clodronate liposomes just prior to infection prevented arthritis.

Conclusion: These data indicate that macrophages, IL-23 and TNF are required for the development of Chlamydia-induced reactive arthritis in SKG mice. Macrophages exclusively take up Chlamydia from the site of infection and, in susceptible mice/individuals, upregulate autophagy and IL-23 production and transport persistent bacteria to distant sites such as upper genital tract and joints to trigger TNF-mediated inflammatory pathology.


Disclosure: A. Baillet, None; Z. A. Bhuyan, None; C. Douillard, None; A. Bozon, None; C. Armitage, None; X. Romand, None; M. V. Chuong Nguyen, None; B. Favier, None; T. Wells, None; K. Beagley, None; R. Thomas, None.

To cite this abstract in AMA style:

Baillet A, Bhuyan ZA, Douillard C, Bozon A, Armitage C, Romand X, Chuong Nguyen MV, Favier B, Wells T, Beagley K, Thomas R. Chlamydia-Infected Macrophages: “Trojan Horses” for Dissemination of IL-23 and TNF-Mediated Inflammation in SKG Mouse Reactive Arthritis [abstract]. Arthritis Rheumatol. 2017; 69 (suppl 10). https://acrabstracts.org/abstract/chlamydia-infected-macrophages-trojan-horses-for-dissemination-of-il-23-and-tnf-mediated-inflammation-in-skg-mouse-reactive-arthritis/. Accessed .
  • Tweet
  • Email
  • Print

« Back to 2017 ACR/ARHP Annual Meeting

ACR Meeting Abstracts - https://acrabstracts.org/abstract/chlamydia-infected-macrophages-trojan-horses-for-dissemination-of-il-23-and-tnf-mediated-inflammation-in-skg-mouse-reactive-arthritis/

Advanced Search

Your Favorites

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

All abstracts accepted to ACR Convergence are under media embargo once the ACR has notified presenters of their abstract’s acceptance. They may be presented at other meetings or published as manuscripts after this time but should not be discussed in non-scholarly venues or outlets. The following embargo policies are strictly enforced by the ACR.

Accepted abstracts are made available to the public online in advance of the meeting and are published in a special online supplement of our scientific journal, Arthritis & Rheumatology. Information contained in those abstracts may not be released until the abstracts appear online. In an exception to the media embargo, academic institutions, private organizations, and companies with products whose value may be influenced by information contained in an abstract may issue a press release to coincide with the availability of an ACR abstract on the ACR website. However, the ACR continues to require that information that goes beyond that contained in the abstract (e.g., discussion of the abstract done as part of editorial news coverage) is under media embargo until 10:00 AM ET on November 14, 2024. Journalists with access to embargoed information cannot release articles or editorial news coverage before this time. Editorial news coverage is considered original articles/videos developed by employed journalists to report facts, commentary, and subject matter expert quotes in a narrative form using a variety of sources (e.g., research, announcements, press releases, events, etc.).

Violation of this policy may result in the abstract being withdrawn from the meeting and other measures deemed appropriate. Authors are responsible for notifying colleagues, institutions, communications firms, and all other stakeholders related to the development or promotion of the abstract about this policy. If you have questions about the ACR abstract embargo policy, please contact ACR abstracts staff at [email protected].

Wiley

  • Online Journal
  • Privacy Policy
  • Permissions Policies
  • Cookie Preferences

© Copyright 2025 American College of Rheumatology