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Microbiota and Resolvins in Arthritis

Total Cost €


EC-Contrib. €






Project "MaRiA" data sheet

The following table provides information about the project.


Organization address
address: 327 MILE END ROAD
city: LONDON
postcode: E1 4NS

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country United Kingdom [UK]
 Total cost 195˙454 €
 EC max contribution 195˙454 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2016
 Funding Scheme MSCA-IF-EF-RI
 Starting year 2017
 Duration (year-month-day) from 2017-09-21   to  2020-02-21


Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    QUEEN MARY UNIVERSITY OF LONDON UK (LONDON) coordinator 195˙454.00


 Project objective

The proposed work will investigate the regulation of pro-resolving lipid mediators (LM) by pathobionts and dysbiotic microbiota in rheumatoid arthritis (RA).

RA is a chronic inflammatory disease with considerable socioeconomic impact. Most treatment options carry severe side effects including immunosuppression. Recent studies found associations between RA and dysbiosis of the microbiota, with the underlying mechanisms leading to this dysbiosis remaining of interest. In addition, I recently found that in both mice during pathobiont-driven inflammatory arthritis and in plasma from patients with RA the levels of a novel family of host protective LM, termed n-3 docosapentaenoic acid-derived Resolvins (RvDn-3 DPA), were significantly altered.

The novel hypothesis of this action is that pathobionts and pathobiont-induced gut-dysbiosis trigger local inflammatory responses and impair the production of RvDn-3 DPA, resulting in exacerbation and chronicity of local inflammation.

This novel hypothesis will be addressed using a multi-pronged approach to:

1) Characterise the role of Porphyromonas gingivalis and Prevotella copri in regulating RvDn-3 DPA, local inflammation and their effects on intestinal microbiota and gut barrier function.

2) Assess the regulation of inflammatory arthritis and RvDn-3 DPA by RA patients’ microbiota.

3) Establish the protective actions of RvDn-3 DPA in pathobiont-driven inflammatory arthritis.

This will provide insights into mechanisms of pathobiont- and dysbiotic microbiota-triggered arthritic inflammation, the regulation of tissue LM profiles and identify potential novel diagnostic markers for early RA-detection. In addition, this work will establish the therapeutic potential of RvDn-3 DPA in regulating exacerbated inflammation and dysbiosis in inflammatory arthritis, providing novel therapeutic opportunities for RA treatment.


year authors and title journal last update
List of publications.
2020 E. Muñoz-Atienza, M.B. Flak, J. Sirr, N.A. Paramonov, J. Aduse-Opoku, C. Pitzalis, M.A. Curtis
The P. gingivalis Autocitrullinome Is Not a Target for ACPA in Early Rheumatoid Arthritis
published pages: 456-462, ISSN: 0022-0345, DOI: 10.1177/0022034519898144
Journal of Dental Research 99/4 2020-04-15
2019 Magdalena B. Flak, Romain A. Colas, Estefanía Muñoz-Atienza, Michael A. Curtis, Jesmond Dalli, Costantino Pitzalis
Inflammatory arthritis disrupts gut resolution mechanisms, promoting barrier breakdown by Porphyromonas gingivalis
published pages: , ISSN: 2379-3708, DOI: 10.1172/jci.insight.125191
JCI Insight 4/13 2020-04-15

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The information about "MARIA" are provided by the European Opendata Portal: CORDIS opendata.

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