Biomedical subjects

N E Bianco

Publications and source records attributed to N E Bianco.

At least 19 recordsLinked to original sources

PubMed1998

Increased peroxide production by polymorphonuclear cells of chronic hepatitis C virus-infected patients.

To evaluate the oxidative burst in hepatitis C virus (HCV) infection, intracellular hydrogen peroxide (H2O2) production of polymorphonuclear (PMN) cells isolated from 15 chronic HCV-infected patients and 11 controls was assessed by flow cytometry in a time kinetic. Under nonstimulated and phorbol myristate acetate (PMA)-stimulated conditions, H2O2 production was higher in HCV-infected patients than in controls (P <0.05) at the time points of 20, 30, and 40 min. A positive correlation between H2O2 production by PMA-stimulated cells and serum levels of alanine aminotransferase and aspartate aminotransferase was found in the HCV-infected patients (r = 0.877, P <0.01 and r = 0.9351, P <0.001, respectively). RT-PCR analysis of purified mononuclear (MN) and PMN cells from HCV-infected patients revealed the presence of HCV RNA in 60% of MN and 27% of PMN cell samples. These results suggest that a functional alteration of PMN cells is manifested in this chronic viral infection which may represent an additional factor in the development of liver lesions.

Adult↗

PubMed1998

Expression of low-density lipoprotein receptors in peripheral blood and tonsil B lymphocytes.

B lymphocytes, purified from peripheral leucocytes from young normolipaemic humans, expressed and internalized low-density lipoprotein receptors (LDLR). The expression was assessed by a monoclonal anti-LDLR. The internalization of LDL was assessed by LDL labelled with 125I (125I-LDL) and 1,1'-dioctadecyl-3,3,3',3' tetramethyl-indocarboxycyanine perchlorate (LDL-DiI). The expression of LDLR, assessed by anti-LDLR, was: 38 +/- 8% (n = 5) for fresh purified cells, 60 +/- 10% (n = 12) for non-stimulated cells, 79 +/- 5% (n = 10) for IL-2 (100 U/ml)-stimulated cells and 95 +/- 5% (n = 8) for pokeweed mitogen (PWM) (1:200 dilution)-stimulated cells. The optimal concentrations of agonist were 100 U/ml of IL-2, and 1:200 dilution of PWM. IL-2 and PWM increased the internalization of LDL-DiI by 1.5-fold. The internalization of LDL-DiI was maximal at 60 microg of protein/ml (48 +/- 8%). Scatchard analysis revealed a Kd of 3.2 +/- 0.22 x 10(-8) M and 2180 +/- 190 binding sites in non-stimulated cells, a Kd of 7.73 +/- 0.36 x 10(-9) M and 12,500 +/- 430 binding sites for IL-2 (100 U/ml)-stimulated cells, and a Kd of 7.2 +/- 0.43 x 10(-9) M and 13,250 +/- 450 binding sites for PWM (1:200 dilution)-stimulated cells. Lineweaver-Burk analysis of LDL binding (LDL-DiI) revealed that the apparent Kd for non-stimulated cells was 1.3 +/- 0.11 x 10(-8) M, and 9.2 +/- 0.2 x 10(-9) M and 7.5 +/- 0.25 x 10(-9) M for IL-2- and PWM-stimulated cells, respectively. B lymphocytes from tonsils also showed a high expression of LDLR assessed with anti-LDLR (70 +/- 6%). The high expression of LDLR and the avid internalization of LDL suggest that LDL may be important for B cell physiological responses.

Adult↗

PubMed1998

Characterization of local memory cells in stage-classified pulmonary tuberculosis: preliminary observations.

Immunophenotype analysis and proliferative responses were investigated in bronchoalveolar lavage (BAL) cells from 21 patients with stage-classified tuberculosis: six with localized pulmonary infiltrate (LPI); seven with diffuse pulmonary infiltrate (DPI); and eight with pleural effusions (PE). Bronchoalveolar lavage cells from these patients contained a high number of cells/ml. The macrophage number was significantly lower in the DPI group (P < 0.05) compared to the LPI or PE groups. Conversely, neutrophils were markedly increased in DPI patients compared to LPI (P < 0.01) and PE (P < 0.01) patients. Lymphocyte infiltration (97.7 +/- 2.3% CD3+, > 83% alphabeta+ and CD4+ > CD8+) was observed in the three groups. A significant increase in the number of total lymphocytes (P < 0.01) and CD4+ cells (P < 0.05) was observed in the LPI group compared to the PE group. In the LPI group CD4+CD45RO+ cell infiltration was higher than CD4+CD45RA+ cells (P < 0.001), contrasting to similar numbers of these subpopulations in the DPI group. Lymphocytes from three out of three LPI patients (alphabeta+CD4+CD45RO+) responded against tuberculin purified protein derivative contrasting to the unresponsiveness of five patients with either DPI or PE. This impaired response was reverted in two out of five patients by using peripheral blood monocytes instead of alveolar macrophages. It is suggested that, in humans, alphabetaCD4+CD45RO cells are the main lymphocyte type involved in the initial local cell-mediated immune response against Mycobacterium tuberculosis.

Adolescent↗

PubMed1997

Nitric oxide in different types of hypertension during pregnancy.

1. Serum nitric oxide (NO) levels (determined by its products of oxidation) were assessed in non-pregnant women, normal pregnant women and patients suffering from mild pre-eclampsia (MPE), severe pre-eclampsia (SPE), chronic hypertension (CHT) and CHT with pre-eclampsia (CHT + PE). The levels of NO products were significantly reduced during pregnancy in MPE (P < 0.001), CHT + PE (P < 0.01) and SPE (P < 0.05). Significant reductions of NO products were also observed in puerperium (P < 0.001) in all groups except CHT + PE (P < 0.05). 2. In normal pregnancy, three events were related to NO levels: (1) negative correlations were found between the levels of nitrite (r = -0.73, P = 0.0003), nitrate (r = -0.53, P = 0.017) and the number of weeks of gestation; (2) in the caesarean section group, the levels of NO at puerperium were significantly lower (P < 0.05) than those during pregnancy; and (3) there was a significant reduction in NO levels in the pregnant women carrying male fetuses as compared with female fetuses (P < 0.05). 3. In SPE, the patients with a family history of hypertension had lower levels of NO compared with the patients without such a history (P < 0.05). 4. A negative correlation was observed between systolic blood pressure, diastolic blood pressure and NO levels in MPE (r = -0.62, P = 0.013 and r = -0.68, P = 0.0049 respectively) and SPE (r = -0.72, P = 0.004 and r = -0.53, P = 0.037 respectively). 5. In SPE, positive correlations were observed between platelet count and nitrite (r = 0.67, P = 0.006) and nitrate levels (r = 0.56, P = 0.028). 6. In MPE, patients with anti-hypertensive treatment showed significantly (P < 0.05) higher levels of NO compared with the non-treated patients. 7. NO may be important in the physiopathology of hypertension during pregnancy, although several factors may affect its levels.

Adult↗

PubMed1997

Impairment of natural killer (NK) cytotoxic activity in hepatitis C virus (HCV) infection.

In the present study, we evaluated the NK cell cytotoxic activity in a group of HCV-infected individuals. Although the number of NK cells present in the peripheral blood of the HCV-infected patients was comparable to non-infected individuals, spontaneous NK cytotoxicity was four-fold lower (P < 0.001) than in normal donors. This functional impairment was not overcome by depletion of adherent or B cells, and it was partially restored by short-term (18 h) stimulation with IL-2. However, long-term stimulation (72 h) with this lymphokine induced activated killer cell (LAK) activity comparable to normal controls. The reduction in NK cytotoxic response does not seem to be due to soluble suppressive factors, since incubation of normal peripheral blood mononuclear cells (PBMC) with infectious HCV serums for a 4-h period does not affect NK spontaneous cytotoxic activity. Successful in vitro infection of PBMC with HCV infectious serum also resulted in an impairment of NK cytotoxicity, suggesting that altered NK function is associated with HCV infection and may be responsible, at least in part, for the chronicity of the infection.

Adult↗

PubMed1997

Low density lipoprotein receptor expression and function in human polymorphonuclear leucocytes.

Low density lipoprotein receptors (LDLR), capable of internalizing LDL, are expressed in polymorphonuclear neutrophils (PMN). The expression was assessed using anti-LDLR antibody by flow cytometry. The internalization of LDL was assessed by: (i) quantification of the uptake of labelled LDL with 1,1'-dioctadecyl-3,3,3',3' tetramethyl-indocarboxycyanine perchlorate (DiI) by flow cytometry; and (ii) the binding of LDL-125I. In fresh purified cells, Lineweaver Burk analysis of LDL binding (LDL-DiI) revealed that the calculated Kd (internalized LDL) for PMN (15.0 x 10(-9) M) is lower than the Kd for monocytes (1.1 x 10(-7) M) and the Kd for lymphocytes (3.2 x 10(-7) M). Scatchard analysis (LDL-125I) revealed 25,000 binding sites and a Kd of 9.6 x 10(-9) M for PMN. The interaction of LDL with its receptor caused a two-fold fast (peak at 1 min) and transient increase in the oxidative burst, measured by the formation of 2',7' dicholoflurescein (DCF) by flow cytometry. This effect was not observed in monocytes or lymphocytes, and it was blocked by anti-LDLR antibody. The stimulation of LDL was optimal at 10 microg of protein/ml. LDL was able to suppress DCF formation induced by phorbol myristate acetate (PMA) and PMA was unable to further stimulate LDL-treated cells, suggesting protein kinase-C (PKC) involvement in LDL effects. Using a PKC assay, LDL was shown to induce a two-fold increase in PKC translocation to the membrane. Thus, LDL increases PMN oxidative burst through a PKC-dependent pathway.

Humans↗

PubMed1997

Secretion of cytokines by natural killer cells primed with interleukin-2 and stimulated with different lipoproteins.

Natural killer (NK) cells were shown to secrete differentially interleukins (IL), IL-1 alpha, IL-1 beta, IL-2, IL-8, interferon-gamma (IFN-gamma), tumour necrosis factor-alpha (TNF-alpha), granulocyte-macrophage colony-stimulating factor (GM-CSF), and leukaemia inhibitory factor (LIF) upon stimulation with optimal concentrations of chylomicrons (CM), very-low-density lipoprotein (VLDL), low-density lipoprotein (LDL), high-density lipoprotein (HDL) or acetyl-modified low-density lipoprotein (AcLDL). CM, VLDL, LDL and AcLDL induced LIF secretion which was absent in nonstimulated cells. CM, VLDL, and LDL did not affect IL-1 alpha secretion. CM stimulated IL-8 > TNF-alpha > IL-1 alpha > IL-2 = IFN-gamma, and decreased seventeen-fold GM-CSF secretion. VLDL stimulated IL-8 secretion > IL-1 alpha = IL-2 > IFN-gamma > TNF-alpha and decreased fivefold GM-CSF secretion. LDL stimulated IL-8 secretion > IL-1 alpha > IL-2 = IFN-gamma, it did not modify TNF-alpha and inhibited five hundred-fold GM-CSF secretion. HDL stimulated IL-2 secretion = IFN-gamma > IL-8, it decreased GM-CSF secretion > IL-1 alpha > IL-1 beta > TNF-alpha without affecting LIF. AcLDL stimulated IL-8 secretion > TNF-alpha > IL-1 alpha > IL-2 = IFN-gamma = IL-1 beta, and decreased GM-CSF secretion eightfold. When NK cells were primed with 10, 100 or 500 IU/ml of IL-2 before the addition of lipoproteins, a decrease in the secretion of cytokines was observed as compared with cells primed with IL-2 only. Differences in cytokine secretion were observed among the diverse type of lipoproteins used for cell stimulus. Thus, lipoproteins may condition NK cytokine secretion and cell activation.

Cell Culture Techniques↗

PubMed1996

Expression and function of low-density lipoprotein receptors in CD3-CD16+CD56+ cells: effect of interleukin 2.

Low-density lipoprotein receptors (LDLR) have been shown to be expressed, internalized, and transcribed in CD3-CD16+CD56+ cells. Only a low percentage (up to 12%) of NK cells express LDLR. Interleukin 2 (IL-2) (1000 IU/ml) induced a threefold increase in the expression of LDLR on the cell surface that results from, at least in part, augmentation of LDLR turnover from the cytosol to the membrane. Scatchard analysis revealed that IL-2 decreased the Kd of LDLR binding for LDL from 7.53 to 4.33 nM with an increment in the number of binding sites from 2500 up to 5000. Both the proliferative response and cytotoxic functions of these cells are affected by LDL. Low concentrations of LDL induce an increase in the proliferative response (up to eightfold) and in the cytotoxic response of NK cells (up to fivefold). High concentration (more than 60 micrograms/ml) of LDL hampers both proliferative response and cytotoxic activity of NK cells. LDL did not affect the cytotoxic functions of IL-2-activated NK cells. Overall, we have shown that LDLR is expressed on the surface of NK cells and can be augmented by IL-2. Furthermore, we propose some insights into the mechanism responsible for the enhanced expression of LDLR on NK cell surface. In addition, our data clearly delineate that LDLR plays an important role in the regulation of proliferative responses and cytotoxic activity of these cells.

CD3 Complex↗

PubMed1996

T cell hyperreactivity to IL-6 in chronic nonviremic HBV carriers despite normal IL-6 receptor or gp130 expression.

We previously showed that T cells from chronic nonviremic HBsAg carriers activated with immobilized OKT3 MAb are hyperreactive to monocyte accessory signals, mainly to interleukin-6 (IL-6). We have further characterized this T cell hyperreactivity using phytohemagglutinin (PHA) as the primary activating signal. PHA-stimulated T cells from nonviremic patients had a significantly higher response to addition of monocytes, monocyte supernatants, and IL-6 alone or combined with IL-1 beta when compared to controls. We examined if these effects could be mediated by a differential expression of IL-6 receptor (p80) or gp130 on resting or PHA-stimulated T cells. We found that PHA, IL-6, IL-1 beta, or IL-2 induced only small changes of the dull p80 expression on T cells. In contrast, we found a significant increase of gp130 expression on PHA-activated T cells compared to unstimulated T cells, which was down-regulated by the presence of IL-6. However, no significant differences in p80 or gp130 expression were detected between patients and controls within all the culture conditions tested. Our results confirm that IL-6 is involved in the in vitro T cell hyperreactivity of nonviremic HBV carriers and indicate that this effect is not mediated by disturbances of IL-6 receptor expression.

Adult↗

PubMed1996

Regulatory effects of lipoprotein lipase on proliferative and cytotoxic activity of NK cells.

Lipoprotein lipase (LPL) induced, in a dose-dependent fashion, a 2-fold and 11-fold increase in the proliferative response of peripheral blood lymphocytes (PBL) at 48 and 72 h, respectively; a 4- and 12-fold increase in natural killer (NK) cells, respectively; and a maximal 3-fold induction in interleukin-2 (IL-2)-treated NK cells at 72 h. T lymphocytes did not proliferate independently of the concentration of LPL used. LPL decreased the proliferative response of K562 and U937 cell lines. The effect on NK cells could be blocked by anti-LPL if it was added before LPL binding to the cell membrane. Contrary to its effects on NK proliferative response, LPL inhibited spontaneous cytotoxicity and lymphokine-activated killer activity (LAK). The effect was dose-dependent, target-dependent (U937 was more sensitive than K562 in LAK assays), but not LPL-binding time-dependent. Treatment of NK cells with heparinase overcame the inhibitory effect of LPL in spontaneous cytotoxicity. LPL binding to cell membranes, as assessed by flow cytometry, was as follows: K562 cells > monocytes > NK cells > LAK cells > U937 cells, absent in T lymphocytes and partially sensible to heparinase and IL-2 treatments. Protein kinase C translocation was observed upon treatment of NK cells with LPL. Three proteins in NK cell membrane (76, 57.2, and 27.2 kD), two in the cytosol (57.2 and 27.2 kD), and only one in ANA-1 cell membrane (76 kD) were precipitated with LPL-Sepharose. LPL receptors seem to be responsible for the proliferative and cytotoxic response observed in LPL-stimulated NK cells.

Cell Membrane↗

PubMed1995

Effects of different lipoproteins on the proliferative response of interleukin-2-activated T lymphocytes and large granular lymphocytes.

1. T lymphocytes and large granular lymphocytes internalized chylomicrons, very low-density lipoprotein, low-density lipoprotein, high-density lipoprotein and acetyl modified low-density lipoprotein through different receptors as assessed by flow cytometry. The observed internalization ranged from 8% to 20%. 2. All lipoproteins induced proliferative responses in T lymphocytes and large granular lymphocytes at optimum concentrations (40 micrograms of protein/ml for all lipoproteins except high-density lipoprotein). Chylomicrons, very low-density lipoprotein and low-density lipoprotein increased T-lymphocyte proliferative response by fourfold while inducing respectively a seven-, nine- and sevenfold increment in large granular lymphocytes. Similarly, high-density lipoprotein and acetyl modified low-density lipoprotein respectively induced a nine- and sevenfold increment in T cells and a 17- and eightfold increment in large granular lymphocyte proliferative response. 3. Both cell types internalized more lipoprotein when they were stimulated with interleukin 2. Chylomicrons and low-density lipoprotein internalization was increased threefold and very low-density lipoprotein internalization twofold, while high-density lipoprotein internalization was unchanged in both cell types. Acetyl modified low-density lipoprotein internalization was fourfold higher in large granular lymphocytes only. 4. The proliferative response of interleukin-2 stimulated cells was different from that of unstimulated cells. Chylomicrons and very low-density lipoprotein induced a sixfold increment in T-cell proliferative response but only a fourfold increment in large granular lymphocytes. Low-density lipoprotein and acetyl modified low-density lipoprotein induced respectively a sevenfold and eightfold increment in T cells and a eightfold and threefold increment in large granular lymphocyte proliferative response. High-density lipoprotein did not affect T-lymphocyte proliferative response while inducing a twofold increase in large granular lymphocytes. 5. Lipoproteins are important in the proliferative response of unstimulated and interleukin-2-stimulated cells.

Adolescent↗

PubMed1995

Decreased T-cell proliferative response to common environmental antigens could be an indicator of early human immunodeficiency virus-mediated lymphocyte lesions.

To evaluate CD4+/CD29+ cells and their responses to different antigens in polar stages of human immunodeficiency virus (HIV) infection, we studied 26 HIV-seropositive carriers (SPCs) and 15 patients with AIDS simultaneously with 20 healthy volunteers (HVs) and 10 seronegative homosexual and bisexual men (SNH). CD3, CD4, CD29, and CD45RA phenotypes were analyzed by two-color flow cytometry. Significant depletion of CD4+ T cells and both memory (CD4+/CD29+) and naive (CD4+/CD45RA+) T-cell subsets was found among SPCs and AIDS patients compared with the numbers of such cells in the HV and SNH groups. Responses to optimal doses of Candida albicans, streptokinase, and tetanus toxoid were explored in peripheral blood mononuclear cells and CD4(+)- and CD4+/CD29(+)-enriched cell populations. In SPCs, the response to C. albicans in peripheral blood mononuclear cells showed a statistically significant diminution compared with the response of HVs (15,308 versus 35,951 cpm). In addition, a significantly reduced response to streptokinase was evident only when cell preparations were CD4+/CD29+ enriched (3,048 versus 10,367 cpm). Furthermore, the SPC group comprised seven responders to at least one antigen and seven nonresponders to any of the selected specific antigens. Absence of a response in these latter patients was independent of the absolute counts of memory and naive T-cell populations. The response to tetanus toxoid, although diminished in SPCs, was not significantly different from that in controls. Our results suggest that defective responses to common environmental antigens, unrelated to the absolute number of CD4+/CD29+ cells, is probably an early indicator of an HIV-induced lymphocyte lesion.

Acquired Immunodeficiency Syndrome↗

PubMed1995

A double-blind, cross-over study using salbutamol, beclomethasone, and a combination of both in bronchial asthma.

A double-blind, cross-over protocol was applied to 22 asthmatic patients who were previously subjected to provocation tests with methacholine. The baseline FEV1 for mild asthma was 89.6 +/- 13.6% while for moderate asthma it was 73 +/- 6%. The initial provocation tests with methacholine revealed that the mild asthma group needed a greater accumulated dose of methacholine than that required by the moderate asthma group to lower the FEV1 by 20%, stressing the enhanced bronchial hyperreactivity present in the latter group. Significant differences in the PD20 values were obtained in both groups of patients using the combination of salbutamol plus beclomethasone. Salbutamol alone was ineffective to change the PD20 values in mild asthma while beclomethasone alone was able to change significantly the PD20 values in these patients, stressing the importance of the inflammatory component in the pathogenesis of stable asthma. Furthermore, the combination of both drugs was also more effective in the moderate asthma group than either medication alone, confirming the pharmacological control of the obstructive and inflammatory changes that are already established in patients with moderate asthma.

Adolescent↗

PubMed1995

Expression of different lipoprotein receptors in natural killer cells and their effect on natural killer proliferative and cytotoxic activity.

Natural killer (NK) cells take up chylomicrons (CM), very low density (VLDL), low density (LDL), high density (HDL) and acetyl-modified low density (AcLDL) lipoproteins through different receptors, VLDL being the lipoprotein with the highest uptake and HDL the lowest. The uptake of LDL can be selectively blocked by the anti-LDL receptor, which does not affect the uptake of CM, VLDL, HDL and AcLDL. Although the uptake of lipoproteins assessed by flow cytometry using DiI is not very high, the lipoproteins are able to induce an increase in proliferative responses, VLDL, AcLDL and HDL being the most important ones with 12- and 17-fold increments, respectively. CM, VLDL and LDL at low concentrations increase NK cytotoxic activity, while HDL and AcLDL inhibit, in a dose-dependent fashion, the killing of NK cells against K562. These results suggest the presence of four different receptors that are responsible for the cytotoxic and proliferative responses observed.

Acetylation↗

PubMed1994

CD3- and CD28-activating pathways in HCV infection.

We investigated the proliferative response and IL-2 receptor (IL-2R) expression in peripheral blood mononuclear cells (PBMC) activated with anti-CD3 mAb alone or in combination with anti-CD28 mAb in a group of hepatitis C virus (HCV)-infected patients with detectable viremia demonstrated by "nested" PCR. PBMC from HCV patients and controls showed similar proliferative responses either to anti-CD3 mAb, 64.1, and/or to anti-CD28 mAb, 9.3. No differences were found in anti-CD3 or anti-CD3 plus anti-CD28-induced proliferative responses between patients who demonstrated circulating PBMC bearing HCV-RNA when compared to those with negative HCV-RNA PBMC. Moreover, flow cytometry studies confirmed that anti-CD3 alone or in combination with anti-CD28 were able to induce a significant increase of IL-2R expression in patients or controls PBMC. Both groups showed similar basal CD28 expression. These results indicate that both CD3- and CD28-activating pathways are preserved in HCV-infected patients with chronic active liver disease.

Adult↗

PubMed1994

Lipoprotein lipase expression in natural killer cells and its role in their cytotoxic activity.

Lipoprotein lipase (LPL) is the key enzyme in the metabolism of triglyceride-rich lipoproteins. The patterns of LPL mRNA expression and secretion of the enzyme have not yet been established in natural killer (NK) cells. We show in the present communication that CD3- CD16+ cells (NK cells) transcribe LPL mRNA, express LPL on the surface and secrete the enzyme. In contrast, there is no LPL expression on the surface of highly purified B and T lymphocytes. Stimulation of NK cells with interleukin-2 (IL-2) reduced the expression of LPL on their surface and augmented the secretion of LPL by the cells. The addition of anti-LPL antibodies to NK cells in culture led to a complete abrogation of cytotoxicity of NK cells against the K562 tumour cell line. Furthermore, IL-2 stimulation of effector cells reversed the anti-LPL antibody-induced inhibition of cytotoxic activity. Overall, these findings suggest that LPL plays a key role in the cytotoxic activity of NK cells.

Base Sequence↗

PubMed1993

Anti-CD3-activated T cells from chronic nonviremic HBV carriers are hyperreactive to monocytic accessory signals.

We analyzed T cell responses through the CD3 activation pathway in a group of chronic HBV carriers. PBMC stimulated with the mAb OKT3 showed higher proliferative response in HBV-DNA(-) carriers compared to HBV-DNA(+) carriers and to controls. In contrast, no differences in proliferative responses were observed between HBV-DNA(-) carriers and controls in cell cultures stimulated with immobilized 64.1 mAb (SPB-64.1) which induces proliferation in the absence of monocytes. We further examined T cell responses in the presence of monocytes and their soluble factors to immobilized OKT3 mAb (SPB-OKT3). Purified T cells did not proliferate to SPB-OKT3. When autologous monocytes were added, higher proliferative response, IL-2 production, and IL-2 receptor expression were observed in HBV-DNA(-) carriers than in controls. An enhanced cell proliferation was also obtained when monocyte supernatants were added to T cells cultured with SPB-OKT3. Moreover, when IL-6 alone or combined with IL-1 was added to SPB-OKT3-stimulated T cell cultures, a significantly higher increase in T cell proliferation was detected in HBV-DNA(-) carriers. Our results thus show a T cell hyperreactivity to accessory signals from monocytes (mainly IL-6) in HBV-DNA(-) carriers, that is probably related to an ongoing viral clearance.

Adult↗

PubMed1992

Assessment of former and newly developed HBV assays in a Third World setting.

Newly available HBV serological assays have not been established routinely in most underdeveloped countries. Utilizing enzyme-immune assays to determine the presence of pre-S1 antigen and anti-pre-S2, and using two conventional hybridization techniques and the PCR assay to detect HBV-DNA, we studied 30 HBsAg chronic carriers and as a reference group 10 subjects whose only HBV routine marker was anti-HBc. Seventy-nine percent of the HBeAg positive carriers showed detectable HBV-DNA by a non-radioactive slot-blotting technique. The PCR assay was more sensitive than the slot-blotting technique, detecting HBV-DNA in anti-HBe positive patients with moderate or normal ALT activity. Pre-S1 antigen was mostly related to the presence of HBsAg and anti-pre-S2 was associated with active viremic state, increased ALT activity (ranges 51 to 640 IU/L), and with self-limited HBV infection. The presence of HBV-DNA in the group with anti-HBc only was detectable solely by the PCR assay. For an underdeveloped country the addition of a PCR assay or pre-S/anti-pre-S protein tests to the current assessment procedures of HBV chronic infection should be used only in selective cases. HBeAg/anti-HBe serological evaluation and HBV-DNA detection by a non-isotopic conventional hybridization technique still remain as useful tools to screen initially for the presence of viremia in chronic HBsAg carriers. The presence of HBV-DNA in individuals with anti-HBc only suggests that anti-HBc screening should be maintained and expanded to all the blood banks of less industrialized countries where the rate of HBV infection in apparently healthy people tends to be high.

Adult↗