Larrañaga GF, Petroni A, Deluchi G, et al. Viral load and disease progression as responsible for endothelial activation and/or injury in human immunodeficiency virus-1-infected patients. Blood Coagul Fibrinolysis 2003;14:15-18 (original) (raw)
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Blood Coagulation & Fibrinolysis, 2003
The endothelium participates in haemostasis, inflammation, blood pressure regulation and other physiological systems. Consequently, endothelial dysfunction has been related to hypertension, thrombosis and atherosclerosis. Both von Willebrand factor (vWF) and tissue-type plasminogen activator (t-PA) are synthesized by the endothelium and their plasma levels increased during endothelium activation or injury. So far, they are well-known markers of endothelial cell function. Many circumstances activate or damage the endothelium, such as viruses, bacterium and inflammation. Circulating vWF and t-PA were studied in 92 unselected human immunodeficiency virus-1 (HIV-1)-infected patients [27 patients with and 65 patients without acquired immunodeficiency syndrome (AIDS)] and correlated with plasma levels of pro-inflammatory cytokines (tumour necrosis factor-AE, interleukin-6), viral load, CD4 T-cell count and infectious status. HIV-1-infected patients had significantly higher plasma levels of vWF (152 versus 90%), tumour necrosis factor-AE (31.3 versus 9.0 pg/ml) and interleukin-6 (3.5 versus 1.9 pg/ml) but not t-PA (5.9 versus 4.2 ng/ml) than the control group. These two endothelial markers correlated significantly with viral load and interleukin-6 levels in HIV-1-infected patients. The highest levels of vWF and t-PA were found in patients with AIDS. In conclusion, endothelial cell perturbation is present in HIV infection and may be a consequence of different mechanisms such as viral load, cytokines and advanced diseases. Blood Coagul Fibrinolysis 14:15-18 & 2003 Lippincott Williams & Wilkins.
The Journal of Infectious Diseases, 1997
Tumor necrosis factor-a (TNF-a) and interleukin-1b (IL-1b) were measured by ELISA in 4.5h, lipopolysaccharide-stimulated whole blood cultures of 347 human immunodeficiency virus type 1 -infected patients and 107 healthy seronegative controls. The production of TNF-a was decreased in both AIDS and non-AIDS patients, whereas the production of IL-1b was decreased in AIDS patients only. The production of TNF-a and IL-1b was positively affected by the concentrations of CD14 / monocytes and CD8 / lymphocytes; however, in patients, the concentration of CD4 / lymphocytes and the presence of AIDS had a negative effect on cytokine production as determined by multiple linear regression analysis. It is concluded that low whole blood cytokine production is mainly caused by low numbers of cells, but a functional defect may also exist.
http://bloodjournal.hematologylibrary.org/content/93/12/4232.full.html Updated information and services can be found at: (2497 articles) Hemostasis, Thrombosis, and Vascular Biology Articles on similar topics can be found in the following Blood collections http://bloodjournal.hematologylibrary.org/site/misc/rights.xhtml#repub\_requests Information about reproducing this article in parts or in its entirety may be found online at: http://bloodjournal.hematologylibrary.org/site/misc/rights.xhtml#reprints Information about ordering reprints may be found online at: http://bloodjournal.hematologylibrary.org/site/subscriptions/index.xhtml Information about subscriptions and ASH membership may be found online at: Alterations in the vascular system and the onset of angioproliferative lesions such as Kaposi's sarcoma (KS) are common traits of human immunodeficiency virus-1 (HIV-1)-infected patients. To investigate possible factors involved in acquired immunodeficiency syndrome (AIDS)-associated vasculopathy and vascular malfunction, expression of vascular endothelial cell growth factor-A (VEGF-A) was analyzed in HUT 78 T lymphocytes upon infection with HIV-1.
Clinical & Experimental Immunology
We measured simultaneously circulating and cell-generated TNF-a and IL-I after lipopolysaccharide (LPS) stimulation of peripheral blood mononuclear cells (PBMC) by radioimmunoassay (RIA) in HIV-infected individuals at different stages of infection, classified according to CDC classification. TNF-a production, both in vitro and endogenous in sera, remained at the normal level in group II patients but was significantly increased in most patients in group IV (P< 005). Most patients of group II and IV displayed normal level of IL-1 in their sera, whereas the level of this monokine generated in vitro was significantly reduced in both groups (P < 005). The cytotoxic effect of factor(s) secreted by PBMC from HIV-infected individuals was evaluated towards a fibroblast cell line L929. The higher titre ofcytotoxicity was directly related to a higher production of TNF-a by the cells from group IV patients and the effect could be removed by pre-absorption with anti-TNF-a monoclonal antibody.
Clinical and experimental immunology, 1989
We measured simultaneously circulating and cell-generated TNF-alpha and IL-1 after lipopolysaccharide (LPS) stimulation of peripheral blood mononuclear cells (PBMC) by radioimmunoassay (RIA) in HIV-infected individuals at different stages of infection, classified according to CDC classification. TNF-alpha production, both in vitro and endogenous in sera, remained at the normal level in group II patients but was significantly increased in most patients in group IV (P less than 0.05). Most patients of group II and IV displayed normal level of IL-1 in their sera, whereas the level of this monokine generated in vitro was significantly reduced in both groups (P less than 0.05). The cytotoxic effect of factor(s) secreted by PBMC from HIV-infected individuals was evaluated towards a fibroblast cell line L929. The higher titre of cytotoxicity was directly related to a higher production of TNF-alpha by the cells from group IV patients and the effect could be removed by pre-absorption with an...
Journal of Medical Virology, 2013
The aim of this study was to evaluate the effect of antiretroviral therapy on inflammatory markers of endothelial dysfunction in HIV treatment-naïve infected patients. This was a prospective cohort study in HIV treatment-naïve infected patients. The patients were assigned to a untreated group or a treatment group according to the therapeutic strategy received. Patients in the treatment group received efavirenz or lopinavir/ritonavir, each given with zidovudine and lamivudine. HIV RNA, CD4 þ cell count, and the levels of hsCRP, sCD40L, sICAM-1, sVCAM-1, and sE-selectin were measured before and 12 weeks after treatment. Fifty patients were enrolled: 13 in the untreated group and 37 in the treatment group; 48 (96%) completed the follow-up. The mean (AESD) age was 33 AE 9 years, and 38 (79%) were men. The median pretreatment CD4 þ cell counts were 263 cells/ml (IQR 118-341) in the treatment group and 658 cells/ml (IQR 475-887) in the untreated group. In the treatment group, the median serum sVCAM-1 and sICAM-1 levels decreased by a small but significant amount (1,400 and 228 ng/ml, respectively, P < 0.05) from before to after the 12 weeks. These levels did not change in the untreated group. Antiretroviral therapy is associated with a decrease in sVCAM-1 and sICAM-1 levels after 12 weeks of treatment.
AIDS Research and Human Retroviruses, 1997
Patients infected with human immunodeficiency virus (HIV) frequently have increased production of interleukin 6 (IL-6) and tumor necrosis factor a (TNF-a), and these cytokines may in turn contribute to the disease pathogenesis. It has been hypothesized that secretion of these cytokines by HI V-exposed mononuclear cells or HIV-infected monocyte/macrophages (M/Ms) is the principal source of their overproduction in HIY infected patients, and the present study was undertaken to explore this issue. We observed that in the absence of endotoxin or cytokines, M/Ms productively infected by HIV do not produce detectable IL-6 or TNF-a. However, granulocyte-macrophage colony-stimulating factor (GM-CSF), a cytokine that enhances HIV replication in M/Ms and is frequently used to propagate monocytotropic strains of HIV, can induce the relatively long-term production of IL-6 (up to 47 U/ml) and TNF-a (up to 47 pg/ml) by M/Ms, even in the absence of HIV. Also, HIV induced production of a relatively small (<9 U/ml) quantity of IL-6 in M/Ms stimulated with macrophage-colony stimulating factor (M-CSF). Finally, while highly concentrated HIV induced production of both cytokines by either M/Ms or peripheral blood mononuclear cells (PBMCs), this production was almost completely eliminated when care was taken to avoid contamination of HIV by endotoxin. These data suggest that the excess IL-6 and TNF-a in HIV-infected patients does not simply result from their production by HIV-infected M/Ms and that alternative mechanisms are involved in this process.