Expanding Role of Circulating Adhesion Molecules in Assessing Prognosis and Treatment Response in Human Immunodeficiency Virus Infection

Sipsas, Nikolaos V.; Sfikakis, Petros P.

doi:10.1128/cdli.11.6.996-1001.2004

Cited by 8 publications

(8 citation statements)

References 84 publications

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“…In addition, up-regulated ICAM-1 and VCAM-1 expression in the hepatic sinusoid cells, vascular endothelial cells, and hepatocytes were reported in chronic liver disease in several studies 23–25. Circulating adhesion molecules is the proteolytically released form of membrane-bound activated molecule 26. The activation of endothelial cells has a crucial role in modulation of leukocyte functions and mediating the transmigration of inflammatory cells, which induce inflammation, tissue damage and liver cirrhosis.…”

Section: Discussionmentioning

confidence: 99%

Monocyte Adhesion Molecules Expression in Patients With Chronic Hepatitis C and Liver Cirrhosis

El-Bassiouni¹,

Mahmoud²,

Ahwani³

et al. 2013

Mediterr J Hematol Infect Dis

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BackgroundChronic viral hepatitis is histologically characterized by predominantly periportal infiltration of mononuclear cells, including lymphocytes and monocytes/macrophages. Intralobular infiltration of these inflammatory cells is an ominous sign of deterioration and a criterion for disease activity.ObjectiveTo assess the monocyte inflammatory milieu, monocytes adhesion molecules, their endothelial receptors, cytokines and chemokines in patients with HCV induced chronic liver disease, in an attempt to clarify the role of blood monocytes in induction of inflammation and fibrogenesis in chronic hepatitis C liver disease.Subjects and MethodsThe current study included 60 patients with chronic liver disease categorized into 2groups: Patients chronic hepatitis C (CHC) and patients with liver cirrhosis (LC), 15 patients each; 15 healthy subjects were included as normal controls. Immunophenotype characterization was carried out by flowcytometric analysis for identification of CD11a, CD11b and CD49d monocyte surface antigen expression in different groups studied. The circulating levels of the soluble adhesion molecules (sE-selectin, sICAM-1 and sVCAM-1), cytokines (TNF-α and IL-1) and chemokines (MCP-1) were also assessed by immunoassays.ResultsData demonstrated a significant increase (p<0.01) in the surface expression of CD11a on peripheral blood monocytes and in the circulating levels sE-selectins, sICAM-1, sVCAM-1 and TNF-α in both groups of patients compared to healthy subjects. Data also revealed a significant increase (p<0.01) in the surface expression of each of CD11b and CD49d on peripheral blood monocytes and in the circulating levels sICAM-1, sVCAM-1 and TNF-α in patients with LC compared to those with CHC. Moreover, data demonstrated that the increase in surface antigen expression of each CD11a (p<0.01), CD11b (p<0.05) and CD49d (p<0.01) on circulating peripheral blood monocytes is positively correlated with the increase in the circulating levels of each of sICAM-1 and sVCAM-1 in the both groups of patients.ConclusionsThese findings suggest that the modulation of monocyte-subset recruitment into the liver via adhesion molecules or cytokines/cytokine receptors may represent promising approaches for therapeutic interventions in human liver fibrosis. Measurement of serum soluble adhesion molecules may be useful for monitoring progression of liver inflammation and fibrosis during CHC.

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Section: Discussionmentioning

confidence: 99%

Monocyte Adhesion Molecules Expression in Patients With Chronic Hepatitis C and Liver Cirrhosis

El-Bassiouni¹,

Mahmoud²,

Ahwani³

et al. 2013

Mediterr J Hematol Infect Dis

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“…Selectins mediate the initial rolling of leukocytes on the endothelium. Elevated levels of the soluble forms of three immunoglobulin superfamily adhesion molecules, intercellular adhesion molecule-1 (ICAM-1, or CD54), vascular cellular adhesion molecule-1 (VCAM-1, or CD106), and the CD40 ligand (CD40L, or CD154), have been reported in patients with HIV infection [54] compared to normal controls. There is a strong indication that the adhesion molecules above mentioned might serve as a surrogate marker of endothelial function and elevated levels have been observed in patients with cardiovascular risk factors and may predict the development of cardiovascular disease.…”

Section: Atherosclerosis: Role Of Hs-crp and Hiv-infectionmentioning

confidence: 98%

“…HIV infection leads to a compensatory, chronic immune activation [54], resulting in altered expression of cell surface antigens and increased production of cytokines (TNF and IFN ). Cytokines, in turn, along with other factors up-regulate the expression of adhesion molecules on the surface of immune and endothelial cells, and subsequently the levels of circulating adhesion molecules are increased.…”

Section: Atherosclerosis: Role Of Hs-crp and Hiv-infectionmentioning

confidence: 99%

“…Cytokines, in turn, along with other factors up-regulate the expression of adhesion molecules on the surface of immune and endothelial cells, and subsequently the levels of circulating adhesion molecules are increased. Adhesion molecules are classified into three families: selectins, integrins and immunoglobulin superfamily [54] and are documented factors implicated in myocardial infarction and atherosclerosis [54,55]. The selectin family of adhesion molecules comprises three members: L-, P-and E-selectins.…”

Section: Atherosclerosis: Role Of Hs-crp and Hiv-infectionmentioning

confidence: 99%

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Metabolic-Inflammatory Changes, and Accelerated Atherosclerosis in HIV Patients: Rationale for Preventative Measures

Lorenzo

Collot-Teixeira²,

Boffito³

et al. 2008

CMC

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Human immunodeficiency virus (HIV)-infected patients are at a significantly higher risk from coronary heart diseases (CHD) and myocardial infarction (MI) compared to gender- and age-matched non-infected individuals. Combination antiretroviral therapy (cART) has transformed a fatal illness into a chronic stable condition. However, cART induces metabolic abnormalities in HIV-infected patients, while its role in vascular atherosclerosis is still under investigation. The use of cART is linked to inflammation - a key mechanism in atherosclerotic progression and destabilisation that precedes clinical events like MI. There is evidence of visceral fat abnormal distribution in HIV infected patients, and inflammatory changes in HIV infected patients drive the initiation, progression and, ultimately, thrombotic clinical complications induced by atherosclerosis. Visceral adipose tissue, a virtual factory for manufacturing pro-inflammatory mediators, affects the liver function. The inflamed liver promotes the development of pro-atherogenic dyslipidaemia. Pro-inflammatory cytokines released by adipocytes travel to the skeletal muscles and other peripheral tissues, worsening insulin sensitivity and leading to hyperglycaemia. Increased high sensitivity C-reactive protein (hs-CRP) inflammatory marker is associated with endothelial dysfunction in HIV-infected patients. Increased levels of monocytic nuclear factor kappa-B (NFkappa-B), a master switch in the inflammatory cascade, are documented in patients with elevated hs-CRP levels. It can be assumed that, as a result of NFkappa-B activation, hs-CRP up-regulates cytokines that contribute to MI by recruiting leukocytes and promoting thrombosis. This review focuses on the association of HIV-infection, metabolic abnormalities and known mechanisms involved in inducing accelerated atherosclerosis and inflammation in HIV-infected patients, as well as the role of lipid lowering agents in potentially preventing CHD.

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“…So the change of sLFA-3 levels is correlated with the activation of T lymphocytes. Recently, there have been more reports on the relationship between the soluble cell adhesion molecules and infection diseases [4][5][6]14], in which the cellular immune function was considered to play an important role in the mechanism of infection diseases [15,16].…”

Section: Introductionmentioning

confidence: 99%

The detection of sLFA-3 in plasma of patients with hemorrhagic fever with renal syndrome

Xie

Chen

et al. 2008

Clin Exp Med

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Hemorrhagic fever with renal syndrome (HFRS) is an acute viral disease characterized by endothelial dysfunction. The cellular immune response, especially the virus-specific CD8+ T lymphocytes, is known to attack vascular endothelial cells (VEC) and to contribute to the diffuse damage and penetrability increasing of VEC. Lymphocyte function associated antigen 3 (LFA-3) is expressed on T lymphocytes and VEC, which is contributed to the activation of T lymphocytes. The expression of LFA-3 on the activated T lymphocytes and VEC is highly increased, which can exfoliate into plasma to increase the level of soluble LFA-3 (sLFA-3) in plasma. So the change of sLFA-3 levels is correlated with the activation of T lymphocytes. In this study we detected the levels of sLFA-3 in plasma of patients with HFRS. We examined the levels of sLFA-3 in plasma samples collected from 53 HFRS patients by double antibody sandwich ELISA. We found variable, but persistently elevated levels of sLFA-3 throughout the various phases and types of the HFRS disease, which suggest that sLFA-3 levels have correlation with disease stages. Moreover, elevated sLFA-3 levels are closely correlated to the severity of HFRS and the degree of kidney damage.

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Expanding Role of Circulating Adhesion Molecules in Assessing Prognosis and Treatment Response in Human Immunodeficiency Virus Infection

Cited by 8 publications

References 84 publications

Monocyte Adhesion Molecules Expression in Patients With Chronic Hepatitis C and Liver Cirrhosis

Monocyte Adhesion Molecules Expression in Patients With Chronic Hepatitis C and Liver Cirrhosis

Metabolic-Inflammatory Changes, and Accelerated Atherosclerosis in HIV Patients: Rationale for Preventative Measures

The detection of sLFA-3 in plasma of patients with hemorrhagic fever with renal syndrome

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