Production of PAF-acether by synovial fluid neutrophils in rheumatoid arthritis

Hilliquin, P.; Dulioust, Anne; Gregoir, C.; Menkès, Charles-Joël

doi:10.1007/bf01796260

Cited by 5 publications

(1 citation statement)

References 18 publications

(12 reference statements)

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“…A strong theory to date is that the inflammatory load among the patients with RA affects the arteries and gives rise to a subclinical vascular inflammation. An increased level of Lp-PLA2 among patients with RA was shown several years ago, when it was presented as a marker of disease activity among such patients [ 35 , 36 ]. However, more recently published studies on other inflammatory diseases, as well as on the general population, suggest that Lp-PLA2 cannot be regarded as a marker of a systemic inflammation but as a mere biomarker of atherosclerosis [ 19 ].…”

Section: Discussionmentioning

confidence: 99%

Is Lipoprotein-Associated Phospholipase A2 a Link between Inflammation and Subclinical Atherosclerosis in Rheumatoid Arthritis?

Södergren

Karp

Bengtsson

et al. 2015

BioMed Research International

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Objective. Lipoprotein-associated phospholipase A2 (Lp-PLA2), a marker of vascular inflammation, is associated with cardiovascular disease. This prospective study of an inception cohort aimed to investigate whether the level of Lp-PLA2 is associated with subclinical atherosclerosis in patients with rheumatoid arthritis (RA). Methods. Patients from northern Sweden diagnosed with early RA were consecutively recruited into an ongoing prospective study. From these, all patients ≤60 years (n = 71) were included for measurements of subclinical atherosclerosis at inclusion (T0) and five years later (T5). Forty age- and sex-matched controls were included. The patients were clinically assessed, SCORE, Reynolds Risk Score, and Larsen score were calculated, and blood samples were drawn from all individuals at T0 and T5. Results. There was no significant difference in the level of Lp-PLA2 between patients with RA and controls (p > 0.05). In simple linear regression models among patients with RA, Lp-PLA2 at T0 was significantly associated with intima media thickness (IMT) at T0 and T5, flow mediated dilation (FMD) at T0 and T5, ever smoking, male sex, HDL-cholesterol (inversely), non-HDL-cholesterol, SCORE, Reynolds Risk Score, and Larsen score (p < 0.05). Conclusion. In this cohort of patients with early RA, the concentration of Lp-PLA2 was associated with both subclinical atherosclerosis and disease severity.

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Section: Discussionmentioning

confidence: 99%

Is Lipoprotein-Associated Phospholipase A2 a Link between Inflammation and Subclinical Atherosclerosis in Rheumatoid Arthritis?

Södergren

Karp

Bengtsson

et al. 2015

BioMed Research International

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Pathological Aspects of Platelet-Activating Factor (PAF)

Bruchhausen¹

1997

Platelets and Their Factors

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The role of PAF/PAFR signaling in zymosan-induced articular inflammatory hyperalgesia

Guerrero

Zaperlon

Vieira

et al. 2012

Naunyn-Schmiedeberg's Arch Pharmacol

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Platelet-activating factor (PAF) and its receptor (PAFR) have been shown to be involved in several inflammatory events, including neutrophil chemoattraction and nociception. The present study addressed the role of PAF in the genesis of articular hyperalgesia in a model of joint inflammation. Zymosan-induced articular hyperalgesia, oedema and neutrophil migration were dose-dependently reduced following pretreatment with selective PAFR antagonists, UK74505 (5, 10 and 20 mg/kg) and PCA4248 (3, 10, 30 mg/kg). These parameters were also reduced in PAF receptor-deficient mice (PAFR(-/-)). The hyperalgesic action of PAF was further confirmed by the demonstration that joint injection of PAF induces a dose- (0.3, 1 and 3 μg/joint), time- and PAFR-dependent articular hyperalgesia and oedema. The PAF hyperalgesic mechanisms were dependent on prostaglandins, leukotrienes and neutrophils, as PAF-induced articular hyperalgesia was inhibited by indomethacin (COX inhibitor), MK886 (leukotrienes synthesis inhibitor) or fucoidan (leukocyte rolling inhibitor). Furthermore, PAF-induced hyperalgesia was reduced in 5-lypoxigenase-null mice. In corroboration of these findings, intra-articular injection of PAF promotes the production of LTB(4) as well as the recruitment of neutrophils to the joint. These results suggest that PAF may participate in the cascade of events involved in the genesis of articular inflammatory hyperalgesia via stimulation of prostaglandins, leukotrienes and neutrophil migration. Finally, targeting PAF action (e.g., with a PAFR antagonist) might provide a useful therapeutic approach to inhibit articular inflammatory hyperalgesia.

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Production of PAF-acether by synovial fluid neutrophils in rheumatoid arthritis

Cited by 5 publications

References 18 publications

Is Lipoprotein-Associated Phospholipase A2 a Link between Inflammation and Subclinical Atherosclerosis in Rheumatoid Arthritis?

Is Lipoprotein-Associated Phospholipase A2 a Link between Inflammation and Subclinical Atherosclerosis in Rheumatoid Arthritis?

Pathological Aspects of Platelet-Activating Factor (PAF)

The role of PAF/PAFR signaling in zymosan-induced articular inflammatory hyperalgesia

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