SERUM CYTOKINES (IL-6, TNF-α, IL-1β AND IFN-γ) IN ANKYLOSING SPONDYLITIS: A CLOSE CORRELATION BETWEEN SERUM IL-6 AND DISEASE ACTIVITY AND SEVERITY

Gratacós, Jordi; Collado, Antonio; Filella, X; Sanmartí, Raimón; Cañete, Juan D.; Llena, J. F.; Molina, Rafael; Ballesta, Antonio M.; Múñoz-Gómez, J

doi:10.1093/rheumatology/33.10.927

Cited by 314 publications

(198 citation statements)

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“…Since TNF-α is initially expressed on the cell surface before being cleaved off by TACE, a wide range of cells, including T cells, may be susceptible. Indeed, preliminary reports appear to confirm this in vivo, with a decrease in absolute numbers of peripheral blood CD4+ T cells (which express interferon γ and TNF-α) in patients with ankylosing spondylitis treated with infliximab and a reciprocal increase with etanercept [116,117]. All these substantial differences might explain why etanercept is more effective than infliximab in asthma and COPD.…”

Section: A C C E P T E D Article In Pressmentioning

confidence: 86%

TNF-α inhibitors in asthma and COPD: We must not throw the baby out with the bath water

Matera

Calzetta

Cazzola

2010

Pulmonary Pharmacology & Therapeutics

117

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Tumor necrosis factor (TNF)-α, a pleiotropic cytokine that exerts a variety of effects, such as growth promotion, growth inhibition, angiogenesis, cytotoxicity, inflammation, and immunomodulation, has been implicated in several inflammatory conditions. It plays a significant role in many inflammatory diseases of lung. Given that there is significant literature supporting the pathobiologic role of TNF-α in asthma, mainly in severe refractory asthma, and COPD, TNF-α inhibitors (infliximab, golimumab and etanercept) are now regarded as potential new medications in asthma and COPD management. The studies reported in literature indicate that TNF-α inhibitors are effective in a relatively small subgroup of patients with severe asthma, possibly defined by an increased TNF axis, but they seem to be ineffective in COPD, although an observational study demonstrated that TNF-α inhibitors were associated with a reduction in the rate of COPD hospitalisation among patients with COPD receiving these agents to treat their rheumatoid arthritis. These findings require a smart approach because there is still good reason to target TNF-α, perhaps in a more carefully selected patient group. TNF-α treatment should therefore not be thrown out, or abandoned. Indeed, since severe asthma and COPD are heterogeneous diseases that have characteristics that occur with different phenotypes remained poorly characterized and little known about the underlying pathobiology contributing to them, it is likely that definition of these phenotypes and choice of the right outcome measure will allow us to understand which kind of patients can benefit from TNF-α inhibitors.

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Section: A C C E P T E D Article In Pressmentioning

confidence: 86%

TNF-α inhibitors in asthma and COPD: We must not throw the baby out with the bath water

Matera

Calzetta

Cazzola

2010

Pulmonary Pharmacology & Therapeutics

117

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“…Most studies have focused on T helper cytokines, consistently demonstrating an impaired IFN␥ signature in SpA T cells (27)(28)(29)(30). With regard to macrophage-derived mediators, only a limited number of studies have analyzed serum levels of proinflammatory cytokines in SpA, indicating an increase in IL-6 and TNF␣, but not IL-1␤, in SpA patients as compared with healthy controls (31)(32)(33). Of interest, this profile appeared to be more pronounced in patients with peripheral arthritis than in those with pure axial SpA (26).…”

Section: Discussionmentioning

confidence: 99%

Absence of a classically activated macrophage cytokine signature in peripheral spondylarthritis, including psoriatic arthritis

Vandooren¹,

Noordenbos²,

Ambarus³

et al. 2009

Arthritis & Rheumatism

152

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Objective. Peripheral spondylarthritis (SpA) is characterized by macrophages that express CD163, a marker of alternative activation (M2). The purpose of this study was to assess whether this differential infiltration with macrophage subsets was associated with a different local inflammatory milieu in SpA as compared with rheumatoid arthritis (RA).Methods Conclusion. The local inflammatory milieu is clearly different in SpA as compared with RA peripheral arthritis. Synovitis in SpA, including that in PsA, is characterized by a selective decrease in M1-derived proinflammatory mediators, such as TNF␣ and IL-1␤.

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“…AS is an autoimmune disorder, and increased levels of inflammatory factors (such as interleukin-6 and tumor necrosis factor-a), and MMPs in serum of AS patients, are correlated with the activity of the disease. [16][17][18] MMPs may destroy the normal structure of ligaments, reduce proteoglycan production and induce collagen exposure. Without the mechanical support of proteoglycans, the collagen fibrils may become irregularly arranged.…”

Section: Pathological Changes Of Spinal Tissues In As Patientsmentioning

confidence: 99%

Histopathological changes in supraspinous ligaments, ligamentum flava and paraspinal muscle tissues of patients with ankylosing spondylitis

Zhang

et al. 2014

Int J of Rheum Dis

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Objective: To examine the histopathological changes in spinal tissues of ankylosing spondylitis (AS) patients.Methods: Tissue samples from 10 AS patients and 10 control subjects were obtained. Hematoxylin and eosin, picrosirius, Masson and van Gieson stainings were utilized to determine the pathological changes in tissues. Ultrastructural alterations were examined by electronic microscopy. Proteoglycan levels were assessed by enzyme-linked immunosorbent assays (ELISA). Matrix metalloproteinase-3 (MMP-3), transforming growth factor-b1 (TGF-b1) and tumor necrosis factor-a (TNF-a) levels were evaluated by immunohistochemistry.Results: Our results demonstrate that the density of collagen fibrils was reduced in the supraspinous ligaments of AS tissue and fibrils were loosely and irregularly organized as compared to a regular distribution of collagen fibrils in controls. In ligamentum flava from AS patients, activated fibroblasts with enlarged nuclei were detected, while the number of elastic fibers was greatly decreased. Paraspinal muscle tissues of AS patients exhibited increased collagen fibril accumulation and atrophy. Significantly decreased proteoglycan and elevated MMP-3 levels were found in supraspinous ligament samples from AS patients (P < 0.01). Additionally, the levels of TGF-b1 in ligamentum flava and paraspinal muscle tissues of AS patients were increased (P < 0.01). The expression of TNF-a was also upregulated in the ligamentum flavum (P < 0.01), with no significant difference in the paraspinal muscle between control and AS patients (P > 0.05).Conclusions: Our findings reveal histopathological changes that occur in certain spinal tissues of AS patients and suggest that increased levels of MMP-3 and TGF-b1 may contribute to the pathogenesis of AS.

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SERUM CYTOKINES (IL-6, TNF-α, IL-1β AND IFN-γ) IN ANKYLOSING SPONDYLITIS: A CLOSE CORRELATION BETWEEN SERUM IL-6 AND DISEASE ACTIVITY AND SEVERITY

Cited by 314 publications

References 0 publications

TNF-α inhibitors in asthma and COPD: We must not throw the baby out with the bath water

TNF-α inhibitors in asthma and COPD: We must not throw the baby out with the bath water

Absence of a classically activated macrophage cytokine signature in peripheral spondylarthritis, including psoriatic arthritis

Histopathological changes in supraspinous ligaments, ligamentum flava and paraspinal muscle tissues of patients with ankylosing spondylitis

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