Salah-uddin Ahmed, Ph.D.
Affiliate Professor
Division of Rheumatology

Faculty Information

Education & Training: 
Rajasthan University
Jaipur, India
Hamdard University
New Delhi, India
Hamdard University
New Delhi, India
(509) 368-6566
Mailing Address: 

Office: PBS 411
P.O. Box 1495
Washington State University
Spokane, WA 99210-1495

Research & Clinical Interests
Research Interests: 

Ahmed’s primary research focus is aimed at understanding the role of epigenetic, posttranslational, and cell signaling mechanisms orchestrated by a network of cytokines and chemokines in autoimmune and chronic inflammatory diseases, including rheumatoid arthritis (RA), osteoarthritis (OA), and gout. His current research focus is to examine the role of epigenetic and posttranslational mechanisms involved in tissue damage and inflammation induced by pro-inflammatory cytokines such as IL-6, IL-1β, and TNF-α in RA and other autoimmune diseases. Ahmed’s research lab is currently one of the active groups involved in developing novel targeted therapeutics (microRNA and small-molecule inhibitors) in the prevention and treatment of RA, gout, OA, and vascular inflammation.

Ahmed’s research is currently funded by grants from the National Institutes of Health, the Rheumatology Research Foundation.

Recent Research Support

07/12/18-06/30/2023 | “MicroRNA-based therapy for rheumatoid arthritis.”

NIAMS/NIH R01 AR063104
Principal Investigator: Salah-uddin Ahmed

08/16/19-08/15/21 | “Elucidating the Role of Sulfatase-2 in RA Pathogenesis.”

NIAMS/NIH F31 AR076204
Principal Investigator: Ruby J Siegel; Mentor: Salah-uddin Ahmed

07/01/20-06/30/21 | “Role of guanylate binding proteins in gouty arthritis.”

Rheumatology Research Foundation Medical and Graduate Student Preceptorship
Principal Investigator (Mentor): Salah-uddin Ahmed


  1. Nash KM and Ahmed S. Nanomedicine in the ROS-mediated pathophysiology: applications and clinical advances. Nanomedicine 2015:11;2033-40.
  2. Singh AK, Umar S, Riegsecker, Chourasia M, and Ahmed S. Regulation of TAK1 activation by epigallocatechin-3-gallate in RA synovial fibroblasts: Suppression of K63-linked autoubiquitination of TRAF6. Arthritis Rheumatol 2016; 68(2):347-58.
  3. Akhtar N, Singh AK, and Ahmed S. MicroRNA-17 suppresses TNF-α signaling by interfering with TRAF2 and cIAP2 association in rheumatoid arthritis synovial fibroblasts. J Immunol 2016;197(6):2219-28.
  4. Fechtner SC, Fox DA, and Ahmed S. TAK1: a potential therapeutic target in rheumatic diseases. Rheumatology 2017;56(7):1060-1068.
  5. Agere SA, Akhtar N, Watson JM, and Ahmed S. RANTES/CCL5 Induces Collagen Degradation by Activating MMP-1 and MMP-13 Expression in Human Rheumatoid Arthritis Synovial Fibroblasts. Front Immunol 2017;8:1341.
  6. Kim EY, Sudini K, Singh AK, Haque M, Leaman D, Khuder S, Ahmed S. Ursolic acid facilitates apoptosis in rheumatoid arthritis synovial fibroblasts by inducing SP-1 mediated Noxa expression and proteasomal degradation of Mcl-1. FASEB J 2018 May 25. doi: 10.1096/fj.201800425R.
  7. Singh AK, Fechtner SC, and Ahmed S. Critical role of IL-1α in IL-1β-induced inflammatory responses: cooperation with NF-κBp65 in transcriptional regulation. FASEB J 2019 Feb;33(2):2526-2536..
  8. Fechtner SC, Singh AK, and Ahmed S. Role of Cannabinoid Receptor 2 in mediating Interleukin-1β-induced inflammation in Rheumatoid Arthritis Synovial Fibroblasts Clin Exp Rheumatol 2019 Nov-Dec;37(6):1026-1035.
  9. Fechtner SC, Singh AK, Natesan S, and Ahmed S. Cannabinoid receptor 2 agonist JWH-015 inhibits Interleukin-1β-induced inflammation in Rheumatoid arthritis synovial fibroblasts and in adjuvant induced arthritis rat via glucocorticoid receptor. Front Immunol 2019 May 8;10:1027. doi: 10.3389/fimmu.2019.01027.
  10. Singh AK, Haque M, Chourasia M, and Ahmed S. Suppression of monosodium urate crystal-induced inflammation by inhibiting TGFβ-activated kinase 1-dependent signaling: Role of ubiquitin proteasome system. Cell Mol Immunol 2019 Sep 11. doi: 10.1038/s41423-019-0284-3.
  11. Siegel RJ, Bridges SL Jr., and Ahmed S. Emerging role of HLA-C in rheumatic and inflammatory diseases. ACR Open 2019 Sep 6;1(9):571-579.