Double role of mannose-binding lectin in relation to carotid intima–media thickness in patients with rheumatoid arthritis

Troelsen, Lone N.; Garred, Peter; Christiansen, Buris; Torp‐Pedersen, Christian; Christensen, Ib Jarle; Narvestad, Eva; Jacobsen, Søren

doi:10.1016/j.molimm.2009.10.021

Cited by 35 publications

(38 citation statements)

References 34 publications

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“…32 Interestingly, the previously largest study on MBL and cIMT (n=114) reported a U-shaped association between MBL concentrations and cIMT, but that study included patients with rheumatoid arthritis and MBL concentrations were up to twice as high as in our study. 16 In line with our current findings, a smaller study in systemic lupus erythematosus patients who had MBL concentrations comparable with our study participants also reported that high plasma MBL was associated with lower cIMT. 26 In our study, participants with high plasma MBL appeared less likely to develop CVD and CVE.…”

Section: Discussionsupporting

confidence: 92%

“…Previous studies on cIMT were cross-sectional, substantially smaller, and conducted in selected populations. 16,26 We observed that high plasma MBL may protect against intimal-medial thickening, whereas the association of MBL with low-grade inflammation appeared to be nonlinear. This suggests that high MBL can have protective, as well as harmful, effects in the vasculature, which might explain why previous large studies on MBL and incident CVD have to some extent reported contradictory findings.…”

Section: Discussionmentioning

confidence: 77%

“…A previous study on cIMT reported a U-shaped association of MBL concentrations with cIMT. 16 This study was, however, rather small (n=114) and was restricted to patients with rheumatoid arthritis. Besides, factors that mediate downstream complement activation through MBL have not yet been investigated in the development of CVD.…”

mentioning

confidence: 97%

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Distinct Longitudinal Associations of MBL, MASP-1, MASP-2, MASP-3, and MAp44 With Endothelial Dysfunction and Intima–Media Thickness

Hertle

Arts

Kallen

et al. 2016

ATVB

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12associations with future CVD. When the effect of MBL on complications of established CVD was investigated, low MBL was in fact protective in most studies. [13][14][15] Thus, considerable discrepancy remains in the literature on whether MBL has beneficial or adverse effects in CVD.This reported discrepancy might be explained by a dual role of MBL in different etiologic aspects of CVD. Objective-Previous studies suggested that the lectin-complement pathway plays a complex role in cardiovascular disease (CVD). To date, no prospective human studies have investigated the relationship between the initiating factor of the lectin pathway, that is, mannose-binding lectin (MBL), and low-grade inflammation, endothelial dysfunction, or carotid intima-media thickness (cIMT). Moreover, MBL-associated proteases (MASPs) and MBL-associated proteins (MAps), which mediate downstream complement activation, have not been studied in the development of CVD. Approach and Results-In a prospective cohort (n=574; age 60±7 years; 7-year follow-up), we investigated longitudinal associations of plasma MBL, MASP-1, MASP-2, MASP-3, and MAp44 with biomarker scores that reflect low-grade inflammation and endothelial dysfunction, respectively, and with cIMT. We also investigated their associations with incident CVD (n=73). In adjusted analyses, low-grade inflammation was lowest in the middle tertile (T Middle )

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 77%

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Distinct Longitudinal Associations of MBL, MASP-1, MASP-2, MASP-3, and MAp44 With Endothelial Dysfunction and Intima–Media Thickness

Hertle

Arts

Kallen

et al. 2016

ATVB

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“…MBL deficiency has also been suggested to be associated with other autoimmune diseases, such as systemic lupus erythematosus and juvenile idiopathic arthritis [13,14]. In addition, high and low serum levels of MBL are reported to be associated with cardiovascular diseases [15]. Deficiency states arise from polymorphisms in the structural and promoter sequences of the MBL2 gene, and different combinations of the abovementioned polymorphisms result in great natural variation in the serum levels of MBL [16].…”

Section: Discussionmentioning

confidence: 99%

Recurrent infections in a rheumatoid arthritis patient with a primary immunodeficiency, treated with conventional and biologic disease-modifying anti-rheumatic drugs

Diamantopoulos

Haugeberg

2011

Mod Rheumatol

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A 64-year-old woman with longstanding rheumatoid arthritis suffered from recurrent severe infections after treatment with both synthetic and biologic disease-modifying anti-rheumatic drugs (DMARDs). She was found to have mannose-binding lectin (MBL) deficiency. MBL deficiency is associated with increased risk of infections, in particular in individuals treated with immunomodulating drugs. Patients with a history of recurrent infections in childhood, and severe infections after treatment with synthetic or biologic DMARDs, should be tested for MBL deficiency.

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“…Interestingly, it was found that both elevated and lowered levels of MBL were associated with increased carotid intima media thickness in rheumatoid arthritis as compared to those with medium MBL levels [160], illustrating the double-edged sword of complement activity. However, MBL (MBL2) genotypes have not been predictive for coronary artery disease in statin treated patients [161].…”

Section: Markers Of Innate Immunity In Cardiovascular Diseasementioning

confidence: 99%

The complement system and toll-like receptors as integrated players in the pathophysiology of atherosclerosis

et al. 2015

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Despite recent medical advances, atherosclerosis is a global burden accounting for numerous deaths and hospital admissions. Immune-mediated inflammation is a major component of the atherosclerotic process, but earlier research focus on adaptive immunity has gradually switched towards the role of innate immunity. The complement system and toll-like receptors (TLRs), and the crosstalk between them, may be of particular interest both with respect to pathogenesis and as therapeutic targets in atherosclerosis. Animal studies indicate that inhibition of C3a and C5a reduces atherosclerosis. In humans modified LDL-cholesterol activate complement and TLRs leading to downstream inflammation, and histopathological studies indicate that the innate immune system is present in atherosclerotic lesions. Moreover, clinical studies have demonstrated that both complement and TLRs are upregulated in atherosclerotic diseases, although interventional trials have this far been disappointing. However, based on recent research showing an intimate interplay between complement and TLRs we propose a model in which combined inhibition of both complement and TLRs may represent a potent anti-inflammatory therapeutic approach to reduce atherosclerosis.

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Double role of mannose-binding lectin in relation to carotid intima–media thickness in patients with rheumatoid arthritis

Cited by 35 publications

References 34 publications

Distinct Longitudinal Associations of MBL, MASP-1, MASP-2, MASP-3, and MAp44 With Endothelial Dysfunction and Intima–Media Thickness

Distinct Longitudinal Associations of MBL, MASP-1, MASP-2, MASP-3, and MAp44 With Endothelial Dysfunction and Intima–Media Thickness

Recurrent infections in a rheumatoid arthritis patient with a primary immunodeficiency, treated with conventional and biologic disease-modifying anti-rheumatic drugs

The complement system and toll-like receptors as integrated players in the pathophysiology of atherosclerosis

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