sPECAM-1 and sVCAM-1: role in pathogenesis and diagnosis of chronic hepatitis C and association with response to antiviral therapy

Kukla, Michał; Żwirska-Korczala, K; Gabriel, Andrzej; Janczewska, Ewa; Berdowska, Agnieszka; Wiczkowski, Andrzej; Rybus-Kalinowska, Barbara; Kalinowski, Mariusz; Ziółkowski, Adam; Woźniak-Grygiel, Elżbieta; Waluga, Marek; Nowak, Błażej

doi:10.1177/1756283x08100666

Cited by 11 publications

(14 citation statements)

References 42 publications

(66 reference statements)

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“…Visfatin may also induce VCAM-1 and ICAM-1 synthesis directly in endothelial cells and leukocytes by activation of nuclear factor (NF)-κB (25,51). Both these adhesion molecules are significantly increased in CHC (47,52), and serum ICAM-1 concentration is associated with the inflammatory activity grade (47). These findings suggest that visfatin directly, together with TNFα, or through induction of TNFα, may enhance production of adhesion molecules and therefore may have a pivotal role in the regulation of the necro-inflammatory process in the liver and facilitates migration of immune cells to the site of inflammation.…”

Section: Visfatin and Necro-inflammatory Activity In Chronic Hepatitismentioning

confidence: 99%

Potential Role of Leptin, Adiponectin and Three Novel Adipokines—Visfatin, Chemerin and Vaspin—in Chronic Hepatitis

Kukla

Mazur

Bułdak

et al. 2011

Mol Med

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Chronic hepatitis C (CHC) is generally a slowly progressive disease, but some factors associated with rapid progression have been identified. Steatosis, independently of its metabolic or viral origin, leads to liver injury and fibrosis. It is suggested that hepatitis C virus may contribute to a wide spectrum of metabolic disturbances-namely, steatosis, insulin resistance, increased prevalence of impaired glucose tolerance, type 2 diabetes mellitus and lipid metabolism abnormalities. Adipokines, which are produced mainly by adipose tissue, may influence the inflammatory response and insulin sensitivity and contribute to the development of metabolic abnormalities in CHC and also regulate fibrogenesis and angiogenesis. Visfatin was described as an adipokine with immunomodulating and proinflammatory properties that promotes B-cell maturation and enhances activation of leukocytes, synthesis of adhesion molecules and production of proinflammatory cytokines. Visfatin exerts insulin-mimetic effects, decreases plasma glucose levels and regulates cell energy balance. Chemerin stimulates chemotaxis of dendritic cells, macrophages and natural killer (NK) cells toward the site of inflammation. On the other hand, it inhibits synthesis of proinflammatory mediators and enhances adiponectin production, influences adipocyte differentiation and maturation and regulates glucose uptake in adipocytes. Vaspin expression in human adipose tissue seems to be a compensatory mechanism associated with obesity and insulin resistance. Vaspin suppresses leptin, tumor necrosis factor (TNF)-α and resistin expression. Leptin protects against liver steatosis but accelerates fibrosis progression and exacerbates the inflammatory process. In contrast, adiponectin exerts a hepatoprotective effect. In this report, data indicating a possible role of these adipokines in the pathogenesis of chronic hepatitis are summarized.

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Section: Visfatin and Necro-inflammatory Activity In Chronic Hepatitismentioning

confidence: 99%

Potential Role of Leptin, Adiponectin and Three Novel Adipokines—Visfatin, Chemerin and Vaspin—in Chronic Hepatitis

Kukla

Mazur

Bułdak

et al. 2011

Mol Med

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“…Other authors have indicated that patients with HCV infection who were treated with interferon had decreased circulating levels of ICAM-I if they attained an SVR [21,22]. In contrast, a 2009 study assessed the levels of this marker in patients with HCV before and after antiviral treatment and revealed that sVCAM-I levels were higher in patients with more advanced stages of fibrosis, but the levels did not predict treatment response [15]. Subsequently, another study [23] including 134 patients with chronic liver disease concluded that the VCAM level is related to a Child-PughC.…”

Section: Discussionmentioning

confidence: 99%

“…HCV infection leads to inflammatory processes of different grades that involve the activation of adhesion molecules and cytokines that facilitate the recruitment of leukocytes to areas of inflammation [15]. Liver fibrosis follows hepatic inflammation as a result of hepatocyte injury [16].…”

Section: Discussionmentioning

confidence: 99%

Serum markers of apoptosis and inflammation in patients with chronic hepatitis c virus

Ferronato¹,

Leão²,

Schacher³

et al. 2017

Int J Recent Sci Res

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Background: Our study aimed to elucidate the possible relationship between apoptosis, inflammation, and fibrosis in hepatitis C virus (HCV) patients. Methods: Patients aged 18 to 60 years with HCV were included and underwent clinical and pathological examinations. Patients with chronic renal failure, malignancies, alcohol abuse, or pregnancy and/or those who were taking immunosuppressant agents were excluded. Body mass index, glucose, insulin, HOMA-IR, lipid profile, and the extent of fibrosis (METAVIR) were determined, as were the serum levels of CK-18 (M30-Apoptosense, ELISA -Lausen, Switzerland), Fas, Fas-L, I-CAM, V-CAM, MIF, and PAI (HSEP-63k, Milliplex, Millipore, Copenhagen, Denmark). Results: Of the 55 patients, 23 were treatment-naïve, 15 demonstrated a sustained virologic response (SVR) and 17 were non-responders (NR). The levels of CK-18 did not differ between the groups. Inflammation, as assessed by sVCAM, was directly associated with advanced fibrosis (p = 0.009). sFas-L and sVCAM were increased in the SVR group compared with the treatment-naïve group (p = 0.006 and 0.019, respectively). sVCAM was associated with both sFas-L (r s = 0.778, p < 0.001) and MIF (r s = 0.621, p < 0.001). MIF and sFas-L were also correlated (r s = 0.526, p = 0.001). Conclusions: Advanced fibrosis was positively correlated with inflammation according to the levels of sVCAM. Furthermore, apoptosis, as assessed by the levels of sFas-L, and inflammation, as determined by sVCAM, were increased in the patients who achieved viral clearance compared with the treatment-naïve patients. The patients with advanced fibrosis were also more likely to present with higher levels of MIF.

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“…sICAM-1, sVCAM-1, and sE-selectin levels are higher in the anti-HCV-positive group of hemodialysis patients. [14,26,27] …”

Section: Discussionmentioning

confidence: 99%

“…Studies have reported that the sVCAM-1 level does not differ significantly between healthy volunteers and asymptomatic chronic hepatitis C carriers with minimal inflammatory grade. [26,28] The sVCAM-1 level increased only in the advanced fibrosis stage of HCV infection. Although patients with hemophilia A in this study did not exhibit symptoms of liver fibrosis, we nevertheless attempted to rule out the suspicion of chronic hepatitis C interference in sVCAM-1 levels.…”

Section: Discussionmentioning

confidence: 99%

Soluble vascular cell adhesion molecular-1 is a potential biological indicator of hemophilic arthropathy

et al. 2016

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Hemophilic arthropathy is the most common chronic complication in patients with hemophilia. The pathogenesis of hemophilic arthropathy involves the inflammatory processes associated with rheumatoid arthritis (RA). Determining the severity and/or progression of joint damage is crucial when evaluating the effect of treatment modalities. Identifying reliable biomarkers in the peripheral blood of patients with hemophilic arthropathy may be beneficial in clinical practice. Circulating soluble vascular cell adhesion molecule-1 (sVCAM-1), E-selectin, and P-selectin levels are elevated in patients with RA. Our study investigated whether these soluble adhesion molecules can be used as biological indicators in the course of joint damage in patients with hemophilia A.Patients with hemophilia A (mild, moderate, and severe) were enrolled. The plasma levels of sVCAM-1, E-selectin, and P-selectin in patients with hemophilia A and control were measured using specific enzyme-linked immunosorbent assay kits. Joint damages were evaluated using Pettersson scores.No statistically significant differences were observed in E-selectin and P-selectin levels between patients and controls. The sVCAM-1 level was significantly higher in patients with hemophilia A than in controls. The differences remained significant in patients with severe hemophilia A but not in patients with mild or moderate hemophilia A. The degree of hemophilic arthropathy was evaluated using Pettersson scores, and a score higher than 5 indicated marked arthropathy. Patients with more than 1 joint with marked arthropathy showed significantly higher sVCAM-1 levels.sVCAM-1 levels in patients with hemophilia A are associated with the severity of hemophilic arthropathy.

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sPECAM-1 and sVCAM-1: role in pathogenesis and diagnosis of chronic hepatitis C and association with response to antiviral therapy

Cited by 11 publications

References 42 publications

Potential Role of Leptin, Adiponectin and Three Novel Adipokines—Visfatin, Chemerin and Vaspin—in Chronic Hepatitis

Potential Role of Leptin, Adiponectin and Three Novel Adipokines—Visfatin, Chemerin and Vaspin—in Chronic Hepatitis

Serum markers of apoptosis and inflammation in patients with chronic hepatitis c virus

Soluble vascular cell adhesion molecular-1 is a potential biological indicator of hemophilic arthropathy

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