+1 Recommend
0 collections
      • Record: found
      • Abstract: found
      • Article: not found

      Substance P enhances cytokine-induced vascular cell adhesion molecule-1 (VCAM-1) expression on cultured rheumatoid fibroblast-like synoviocytes.

      Clinical and Experimental Immunology

      biosynthesis, Antigens, CD40, Vascular Cell Adhesion Molecule-1, pharmacology, Tumor Necrosis Factor-alpha, immunology, drug effects, cytology, Synovial Membrane, Substance P, genetics, analysis, Receptors, Tachykinin, RNA, Messenger, Interleukin-1, Interferon-gamma, Intercellular Adhesion Molecule-1, Humans, Histocompatibility Antigens Class II, Flow Cytometry, Fibroblasts, Drug Interactions, Arthritis, Rheumatoid, Antigens, CD80, Antigens, CD58

      Read this article at

          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.


          Rheumatoid arthritis (RA) is an autoimmune disease characterized by inflammation of the synovial membrane of multiple joints. This inflammatory microenvironment allows fibroblast-like synoviocytes (FLS) to express or enhance several adhesion or costimulatory molecules. This phenotypic shift, under proinflammatory cytokines, seems to be related to functional consequences for antigen presentation to T cells. The sensory neuropeptide substance P (SP), present at high levels, is able to act on FLS proliferation and enzyme secretion. These data led us to investigate whether SP could also provoke a phenotypic change of FLS. Using flow cytometry and a three-step cellular ELISA method, we determined whether SP has an influence on the expression of MHC class II, intercellular adhesion molecule-1 (ICAM-1), VCAM-1, LFA-3, CD40, B7.1 or B7.2 molecules on RA FLS incubated with interferon-gamma (IFN-gamma) or IL-1beta or tumour necrosis factor-alpha (TNF-alpha) with or without SP. Our results indicate that SP potentiates the effect of proinflammatory cytokines on the expression of VCAM-1 on RA FLS. We verified the presence of specific SP (NK1) receptor mRNA. Using reverse transcription-polymerase chain reaction, we showed that RA FLS of patients express NK1 receptor mRNA. These results suggest that SP increase of cytokine-induced VCAM-1 expression acts via this specific SP receptor. Thus, during chronic inflammation RA FLS are at the interface between the immune and the nervous systems.

          Related collections

          Author and article information



          Comment on this article