Production of the chemokine RANTES by articular chondrocytes and role in cartilage degradation

Alaaeddine, Nada; Olee, Tsaiwei; Hashimoto, Sanshiro; Creighton‐Achermann, Lilo; Lotz, Martin

doi:10.1002/1529-0131(200107)44:7<1633::aid-art286>3.0.co;2-z

Cited by 120 publications

(73 citation statements)

References 27 publications

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“…In fact, we also agree that those patients meeting American College of Rheumatology classification criteria for fibromyalgia (1) may not have a discrete disease but are at the extreme end of a continuum of patients with chronic musculoskeletal pain. Our concern is that most who advocate abandoning the fibromyalgia construct also would like to abandon this group of patients.…”

Section: To the Editorsupporting

confidence: 66%

Pyridostigmine for fibromyalgia: Comment on the article by Paiva and a historical vignette

Wallace

2003

Arthritis & Rheumatism

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We couldn't agree more with Dr. Ehrlich's final comment that suggests we eliminate this unnecessary banter about the fibromyalgia label and "worry about the pains." In fact, we also agree that those patients meeting American College of Rheumatology classification criteria for fibromyalgia (1) may not have a discrete disease but are at the extreme end of a continuum of patients with chronic musculoskeletal pain. Our concern is that most who advocate abandoning the fibromyalgia construct also would like to abandon this group of patients. We would reiterate that regardless of whether a label is attached to these individuals, research into the physiology of chronic musculoskeletal pain is a critically important endeavor in the field of rheumatology.As with many critics of the fibromyalgia construct, Dr. Ehrlich veils his discomfort regarding patients with the fibromyalgia symptom complex by posing a legitimate concern surrounding societal or legal issues. In this case the issue raised is that assigning labels such as fibromyalgia may have an adverse impact on patient outcome. Unfortunately, there are few data that directly address whether this is the case or not. In direct opposition to Dr. Ehrlich's view, recent data reported by White et al show that assigning a label of fibromyalgia to individuals with chronic widespread pain has no meaningful adverse affect on clinical outcome over the long term (2). There are also data, however, suggesting that any disease label may have a detrimental impact on patient behavior. In a study of workers in an occupational setting, Haynes et al demonstrated more than two decades ago that detecting and labeling even an asymptomatic disease (hypertension) markedly increased absenteeism from work (3).Dr. Ehrlich seems to suggest that labels may be more harmful in cases in which the etiology of the symptoms reported by the patient has yet to be clearly understood. Stated another way, he proposes that syndromes characterized by subjective symptoms should not be given a label that implies those who have the symptoms are abnormal, perhaps in contradistinction to syndromes characterized by alterations of easily measured variables. It is not clear to us why this should be the case, unless one questions the veracity of self-reported symptoms. Furthermore, even when a variable is objective, the definition of what constitutes abnormal may change over time (e.g., hypertension, hypercholesterolemia, obesity) as new research changes our understanding of human physiology.The implications of Dr. Ehrlich's proposition to eliminate semantic terms from our clinical vernacular would be enormous. As he himself notes, the symptoms do not go away; the label only changes. If we discard the fibromyalgia label, then we should logically reject other labels such as migraine headache, dyslexia, all psychiatric disorders, etc. This would require a tremendous paradigm shift in how we practice clinical medicine, since the aggregate data suggest that approximately half of the visits to primary care physicians are fo...

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Section: To the Editorsupporting

confidence: 66%

Pyridostigmine for fibromyalgia: Comment on the article by Paiva and a historical vignette

Wallace

2003

Arthritis & Rheumatism

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“…Moderately increased expression of chemokines, including the C-C chemokine subfamily member RANTES, as well as IL-8 and GRO-␣, has been demonstrated in chondrocytes present in OA and RA cartilage (25)(26)(27)(28). Importantly, chemokine receptors, including CCR1, CCR2, CCR3, CCR5, CXCR1, and CXCR2, are also expressed by chondrocytes (29,30).…”

Section: Discussionmentioning

confidence: 99%

NF-κB Mediates the Stimulation of Cytokine and Chemokine Expression by Human Articular Chondrocytes in Response to Fibronectin Fragments

Pulai

Chen

et al. 2005

The Journal of Immunology

194

166

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Fibronectin fragments (FN-f) that bind to the α5β1 integrin stimulate chondrocyte-mediated cartilage destruction and could play an important role in the progression of arthritis. The objective of this study was to identify potential cytokine mediators of cartilage inflammation and destruction induced by FN-f and to investigate the mechanism of their stimulation. Human articular chondrocytes, isolated from normal ankle cartilage obtained from tissue donors, were treated with a 110-kDa FN-f in serum-free culture, and expression of various cytokine genes was analyzed by cDNA microarray and by a cytokine protein array. Compared with untreated control cultures, stimulation by FN-f resulted in a >2-fold increase in IL-6, IL-8, MCP-1, and growth-related oncogene β (GRO-β). Constitutive and FN-f-inducible expression of GRO-α and GRO-γ were also noted by RT-PCR and confirmed by immunoblotting. Previous reports of IL-1β expression induced by FN-f were also confirmed, while TNF expression was found to be very low. Inhibitor studies revealed that FN-f-induced stimulation of chondrocyte chemokine expression was dependent on NF-κB activity, but independent of IL-1 autocrine signaling. The ability of FN-f to stimulate chondrocyte expression of multiple proinflammatory cytokines and chemokines suggests that damage to the cartilage matrix is capable of inducing a proinflammatory state responsible for further progressive matrix destruction, which also includes the chemoattraction of inflammatory cells. Targeting the signaling pathways activated by FN-f may be an effective means of inhibiting production of multiple mediators of cartilage destruction.

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“…In humans, IL-18 has been reported to induce chemokines (1,25), raising the possibility that IL-18 may exert hematological effects through chemokines. Our analysis of macrophage inflammatory proteins 1␣ and 1␤ after the administration of IL-18 in mice showed that IL-18 in fact induced these chemokines.…”

Section: Discussionmentioning

confidence: 99%

Interleukin-18 Induces Acute Biphasic Reduction in the Levels of Circulating Leukocytes in Mice

Hosohara¹,

Ueda

Kashiwamura

et al. 2002

Clin Vaccine Immunol

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We investigated the acute hematological changes caused by interleukin-18 (IL-18) in mice. Intraperitoneal administration of IL-18 (2 g/mouse) resulted in biphasic decreases in the number of leukocytes in the blood. The first phase of decrease occurred within 2 h of IL-18 administration and was followed by a transient increase at 5 h. The second phase of decrease occurred at around 6 h, reaching a nadir which lasted for more than 24 h. In mice deficient in inducible nitric oxide (NO) synthase, the first phase of reduction of leukocytes did not occur although the second phase of decrease was observed. In mice deficient in gamma interferon (IFN-␥) or in mice depleted of natural killer cells and incapable of producing IFN-␥, IL-18 had no effect on the number of circulating leukocytes. Levels of nitrite and/or nitrate in the serum were elevated within 2 h after administration of IL-18, reaching a peak at 4 h and then decreasing gradually to the basal level over a 24-h period of time. On the other hand, serum IFN-␥ levels changed in a biphasic manner, reaching a peak at 2 h after IL-18 administration, followed by a decrease in the basal level and a second increase at 6 h. Levels of IL-18 receptor mRNAs also showed biphasic changes in correlation with the changes in serum IFN-␥ levels. These results suggest that the changes in the leukocyte number following IL-18 administration are mediated by NO and IFN-␥, with NO being involved in the first phase of reduction and IFN-␥ being involved in both phases.

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Production of the chemokine RANTES by articular chondrocytes and role in cartilage degradation

Cited by 120 publications

References 27 publications

Pyridostigmine for fibromyalgia: Comment on the article by Paiva and a historical vignette

Pyridostigmine for fibromyalgia: Comment on the article by Paiva and a historical vignette

NF-κB Mediates the Stimulation of Cytokine and Chemokine Expression by Human Articular Chondrocytes in Response to Fibronectin Fragments

Interleukin-18 Induces Acute Biphasic Reduction in the Levels of Circulating Leukocytes in Mice

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