Association of Ficolin-3 with severity and outcome of chronic heart failure

Prohászka, Zoltán; Munthe‐Fog, Lea; Gombos, Tímea; Skjoedt, Mikkel‐Ole; Förhécz, Zsolt; Pozsonyi, Zoltán; Jánoskúti, Lívia; Füst, George; Garred, Peter

doi:10.1016/j.molimm.2011.06.263

Cited by 4 publications

(5 citation statements)

References 28 publications

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“…34 Consumption of ficolins has been associated with ischemic conditions in different organs. 36 Now, we show that patients with SAH with ischemic lesions are characterized by a decrease in ficolin-3 concentration and LCP activity, again in line with the idea that cellular damage may trigger the deposition of LCP components on the injured tissue. Ischemic stroke patients show lower acute and follow-up ficolin-3 levels compared with controls, 9 and deposition of LCP components on the ischemic brain endothelium has been recently shown in mouse ischemia.…”

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confidence: 85%

Ficolin-3–mediated lectin complement pathway activation in patients with subarachnoid hemorrhage

et al. 2014

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confidence: 85%

Ficolin-3–mediated lectin complement pathway activation in patients with subarachnoid hemorrhage

et al. 2014

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“…Low ficolin‐3 level is a major initiator of the ficolin–lectin pathway in complement activation . We also showed a correlation between low ficolin‐3 level, the severity and the unfavourable outcome of acute ischaemic stroke and CHF . We further presumed that as an integrative marker of cellular damage, complement activation might be an independent predictor of mortality in post‐cardiac arrest patients.…”

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confidence: 55%

Complement Activation and its Prognostic role in Post‐cardiac Arrest Patients

et al. 2014

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Cardiac arrest causes generalized ischaemia/hypoxia, and subsequent resuscitation inflicts reperfusion injury, the pathology of which is not fully understood. Moreover, predicting the prognosis of comatose, post-cardiac arrest patients is a complex clinical challenge. We hypothesized that the extent of complement activation might be a reliable predictor of mortality in this population. Forty-six comatose cardiac arrest patients were enrolled into our prospective cohort study, conducted in a tertiary care university clinic. All subjects were cooled to 32-34°C body temperature for 24 h and then allowed to rewarm to normothermia. All patients underwent diagnostic coronary angiography. On admission, at 6 and 24 h, blood samples were taken from the arterial catheter. In these, complement products (C3a, C3, C4d, C4, SC5b9 and Bb) were measured by ELISA in blood samples. Patients were followed up for 30 days; 22 patients (47.8%) died by the end of this period. We observed that complement activation (determined as the C3a to C3 ratio) was higher in non-survivors than in survivors at each time point. In the multivariate Cox regression analysis, the C3a/C3 ratio determined 24 h after the initiation of therapeutic hypothermia predicted 30-day mortality regardless of age, sex and the APACHE II score. Complement activation occurs in post-cardiac arrest patients, and its extent correlates with 30-day survival. The C3a/C3 ratio might prove useful for estimating the prognosis of comatose postcardiac arrest patients.

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“…Low ficolin-3 concentration in serum has already been associated with the pathophysiology of sarcoidosis [20], chemotherapy-related infections in children [21], Crohn's disease [22] and heart failure [23]. On the other hand, high ficolin-3 levels were associated with Systemic Lupus Erythematosus [24], ovarian tumors [25] and seem to be a risk factor for shorter graft survival in kidney transplantation [26].…”

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confidence: 99%

Association of a new FCN3 haplotype with high ficolin-3 levels in leprosy

et al. 2017

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Leprosy is a chronic inflammatory disease caused by Mycobacterium leprae that mainly affects the skin and peripheral nervous system, leading to a high disability rate and social stigma. Previous studies have shown a contribution of genes encoding products of the lectin pathway of complement in the modulation of the susceptibility to leprosy; however, the ficolin-3/FCN3 gene impact on leprosy is currently unknown. The aim of the present study was to investigate if FCN3 polymorphisms (rs532781899: g.1637delC, rs28362807: g.3524_3532insTATTTGGCC and rs4494157: g.4473C>A) and ficolin-3 serum levels play a role in the susceptibility to leprosy. We genotyped up to 190 leprosy patients (being 114 (60%) lepromatous), and up to 245 controls with sequence-specific PCR. We also measured protein levels using ELISA in 61 leprosy and 73 controls. FCN3 polymorphisms were not associated with disease, but ficolin-3 levels were higher in patients with FCN3 *2B1 (CinsA) haplotype (p = 0.032). Median concentration of ficolin-3 was higher in leprosy per se (26034 ng/mL, p = 0.005) and lepromatous patients (28295 ng/mL, p = 0.016) than controls (18231 ng/mL). In addition, high ficolin-3 levels (>33362 ng/mL) were more common in leprosy per se (34.4%) and in lepromatous patients (35.5%) than controls (19.2%; p = 0.045 and p = 0.047, respectively). Our results lead us to suggest that polymorphisms in the FCN3 gene cooperate to increase ficolin-3 concentration and that it might contribute to leprosy susceptibility by favoring M. leprae infection.

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Association of Ficolin-3 with severity and outcome of chronic heart failure

Cited by 4 publications

References 28 publications

Ficolin-3–mediated lectin complement pathway activation in patients with subarachnoid hemorrhage

Ficolin-3–mediated lectin complement pathway activation in patients with subarachnoid hemorrhage

Complement Activation and its Prognostic role in Post‐cardiac Arrest Patients

Association of a new FCN3 haplotype with high ficolin-3 levels in leprosy

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