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

Lambert, N; Lescoulié, P L; Yassine‐Diab, Bader; Enault, Geneviève; Mazières, B; Préval, C. de; Cantagrel, Alain

doi:10.1046/j.1365-2249.1998.00621.x

Cited by 46 publications

(28 citation statements)

References 29 publications

(27 reference statements)

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“…Further evidence that the FLS samples did not contain monocytes or macrophages was provided in the response of such cultures to sCD154. Although monocytes/ macrophages and FLS can share expression of CD40 (25,26), the FLS cultures could not be induced to express enhanced levels of BAFF by sCD154, which is in contrast to monocytes or macrophages. As such, it is unlikely that the BAFF mRNA detected in our serial passaged FLS lines was derived from contaminating myelomonocytic cells.…”

Section: Discussionmentioning

confidence: 86%

Fibroblast-Like Synoviocytes of Mesenchymal Origin Express Functional B Cell-Activating Factor of the TNF Family in Response to Proinflammatory Cytokines

Ohata

Zvaifler

Nishio

et al. 2005

The Journal of Immunology

193

127

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Immunohistochemical analysis revealed that the intimal lining cells of synovial tissue of inflamed joints of patients with rheumatoid arthritis differed from that of normal joints or of diseased joints in osteoarthritis in that they stained with mAb specific for the B cell-activating factor of the TNF family (BAFF; also called BLyS). We generated fibroblast-like synoviocytes (FLS) cell lines that were bereft of myelomonocytic cells to examine whether mesenchymal-derived FLS could express this critical B cell survival factor. We found that FLS expressed low amounts of BAFF mRNA relative to that of myelomonocytic cells. However, when various cytokines/factors were added to such FLS cell lines, we found that IFN-γ or TNF-α were unique in that they could induce significant increases in BAFF mRNA and protein. Even minute amounts of IFN-γ primed FLS for TNF-α, allowing the latter to stimulate significantly higher levels of BAFF mRNA and protein than could TNF-α alone. Consistent with this, B cells cocultured with IFN-γ and/or TNF-α-treated FLS had a significantly greater viability than B cells cocultured with nontreated FLS. The enhanced protection of B cells afforded by IFN-γ/TNF-α-treated FLS was inhibited by the addition of BAFF-R:Fc fusion protein. We conclude that the proinflammatory cytokines IFN-γ and TNF-α can induce mesenchymal-derived FLS to express functional BAFF in vitro. The induced expression of BAFF on FLS by proinflammatory cytokines may enhance the capacity of such cells to protect B cells from apoptosis in inflammatory microenvironments in vivo.

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Section: Discussionmentioning

confidence: 86%

Fibroblast-Like Synoviocytes of Mesenchymal Origin Express Functional B Cell-Activating Factor of the TNF Family in Response to Proinflammatory Cytokines

Ohata

Zvaifler

Nishio

et al. 2005

The Journal of Immunology

193

127

View full text Add to dashboard Cite

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“…Lymph node FDC express CD106 (VCAM-1) which is a survival and differentiation factor for GC B cells [38,39]. In addition, complement decay-accelerating factor (DAF) and complement receptor 2 (CR2) are important molecules expressed by lymph node FDC that prevent complement deposition and promote B cell survival [40,41]. FDC also trap antigens at their cell surfaces for long periods of time allowing them to act as an antigenic sink for B cells [40][41][42].…”

Section: Other Synoviocyte Interactions With B Cellsmentioning

confidence: 99%

“…In addition, complement decay-accelerating factor (DAF) and complement receptor 2 (CR2) are important molecules expressed by lymph node FDC that prevent complement deposition and promote B cell survival [40,41]. FDC also trap antigens at their cell surfaces for long periods of time allowing them to act as an antigenic sink for B cells [40][41][42]. To date, only CR2 expression has been reported on the FDC found in RA synovium [37].…”

Section: Other Synoviocyte Interactions With B Cellsmentioning

confidence: 99%

Synovial biology and T cells in rheumatoid arthritis

2005

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Events that occur in rheumatoid arthritis synovial tissues are responsible for the signs and symptoms of joint inflammation and for the eventual destruction of articular and periarticular structures that lead to joint dysfunction and disability. The three most abundant cell populations in RA synovium are synovial macrophages (type A synoviocytes), synovial fibroblasts (type B synoviocytes) and infiltrating T lymphocytes. Other important cell populations include B lymphocytes, dendritic cells, plasma cells, mast cells and osteoclasts. Our current understanding of rheumatoid arthritis is moving beyond previous concepts that view this disease as the consequence of a specific and focused humoral or cellular autoimmune response to a single autoantigen. Rather, a new view of rheumatoid arthritis is emerging, which seeks to understand this disease as the product of pathologic cell-cell interactions occurring within a unique and defined environment, the synovium. T lymphocytes in rheumatoid arthritis synovium interact closely with dendritic cells, the most potent antigen-presenting cell population in the immune system. T cells also interact with monocytes and macrophages and cytokine-activated T cells may be, especially, suited to trigger production of the important cytokine TNFα by synovial macrophages. Recent evidence also suggests a potent bidirectional interaction between synovial T cells and synovial fibroblasts, which can lead to activation of both cell types. An important role for synovial B lymphocytes has been emphasized recently, both by experimental data and by results of clinical interventions. B cells in synovium can interact with fibroblasts as well as with other cells of the immune system and their potential role as antigen-presenting cells in the joint is as yet underexplored. Rheumatoid arthritis synovium may be one of the most striking examples of pathologic, organ-specific interactions between immune system cells and resident tissue cell populations. This view of rheumatoid arthritis also leads to the prediction that novel approaches to treatment will more logically target the intercellular communication systems that maintain such interactions, rather than attempt to ablate a single cell population.

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“…SP is produced by afferent neurons and a variety of immune cells, including eosinophils, monocytes, macrophages (17,30), lymphocytes (9), and dendritic cells (23). Numerous studies have directly associated SP with exacerbated inflammation (22,25,26,29,31,32,44). SP has been shown to affect inflammation by mediating vasodilation, thereby enhancing cell trafficking, as well as by affecting the cellular events involved in proliferation and cytokine and growth factor synthesis (3-5, 7, 11, 24, 28, 36).…”

mentioning

confidence: 99%

Neutralizing Anti-F Glycoprotein and Anti-Substance P Antibody Treatment Effectively Reduces Infection and Inflammation Associated with Respiratory Syncytial Virus Infection

Haynes

Tonkin

Anderson

et al. 2002

J Virol

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Respiratory syncytial virus (RSV) is the most important virus mediating lower respiratory tract illness in infants and young children. RSV infection is associated with pulmonary inflammation and increased levels of substance P (SP), making the airways and leukocytes that express SP receptors susceptible to the proinflammatory effects of this peptide. This study examines combining neutralizing anti-F glycoprotein and anti-SP antibody treatment of RSV-infected BALB/c mice to inhibit RSV replication and inflammation associated with infection. BALB/c mice were prophylactically treated with antibody prior to RSV infection or were therapeutically treated at day 2 or 6 post-RSV infection. Prophylactic or therapeutic treatment with anti-SP antibodies promptly reduced pulmonary inflammatory cell infiltration and decreased the number of cells expressing proinflammatory cytokines, while anti-F antibody treatment reduced virus titers. The results suggest that combined anti-viral and anti-SP antibody treatment may be effective in treating RSV disease.Respiratory syncytial virus (RSV) is the leading cause of lower respiratory tract disease in infants and young children worldwide. A member of the Paramyxoviridae family, RSV is an enveloped virus containing a negative-sense single-stranded RNA genome. The protective immune response to RSV infection is primarily directed against the two major surface viral glycoproteins, i.e., the G (attachment) and F (fusion) glycoproteins. The F glycoprotein appears to be most important for induction of protective immunity and is associated with a high serum neutralizing antibody response (6, 37) and activation of CD14 and Toll-like receptor-4 (21). Some monoclonal antibodies against the F glycoprotein provide passive protection against RSV disease (8,13,18,42); therefore, the F glycoprotein has been the focus for therapeutic intervention in RSV disease.At present, there is no RSV vaccine available, and the only options to address disease are prophylactic administration of enriched anti-RSV human immune globulin (Respigam) or anti-F glycoprotein monoclonal antibodies (palivizumab [Synagis]), both of which are recommended only for young children at high risk for RSV disease. In addition, ribavirin (Virazole), the only specific antiviral agent approved for RSV infection, has limited efficacy (10, 19, 41; M. I. Marks and J. McBride, abstract from Ribavirin Therapy for Respiratory Syncytial Virus Infections: a Scientific Workshop, Sept., 1989, Pediatr. Infect. Dis. J. 9:S84, 1990), and its use is limited for treatment of RSV infection in immune-compromised patients (10, 43).Treatment with anti-RSV human immune globulin or anti-F glycoprotein neutralizing antibodies is effective in decreasing the titer of virus but does not appear to ameliorate the disease process, suggesting that a substantial portion of disease is associated with the host response to infection (27). The importance of the host response to infection is also suggested by the prominence of obstructed-airway disease and wheezing durin...

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

Cited by 46 publications

References 29 publications

Fibroblast-Like Synoviocytes of Mesenchymal Origin Express Functional B Cell-Activating Factor of the TNF Family in Response to Proinflammatory Cytokines

Fibroblast-Like Synoviocytes of Mesenchymal Origin Express Functional B Cell-Activating Factor of the TNF Family in Response to Proinflammatory Cytokines

Synovial biology and T cells in rheumatoid arthritis

Neutralizing Anti-F Glycoprotein and Anti-Substance P Antibody Treatment Effectively Reduces Infection and Inflammation Associated with Respiratory Syncytial Virus Infection

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