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Biomedical subjects

A S Bansal

Publications and source records attributed to A S Bansal.

At least 19 recordsLinked to original sources
PubMed2001

Hypercalcaemia and elevated 1,25(OH)(2)D(3) levels associated with disseminated Mycobacterium avium infection in AIDS.

Hypercalcaemia may complicate granulomatous diseases, such as tuberculosis and sarcoidosis, and various AIDS-related opportunistic infections and malignancies. We report here two patients with AIDS and disseminated Mycobacterium avium infection who developed symptomatic hypercalcaemia several weeks after commencing antimycobacterial chemotherapy, and in whom inappropriately elevated 1,25(OH)(2)D(3)levels were documented. Although vitamin D supplementation may have contributed, no other cause for the hypercalcaemia was found. The biochemical and clinical similarities between these cases and other hypercalcaemic granulomatous diseases suggest a common mechanism related to macrophage activation and dysregulated vitamin D production.

AIDS-Related Opportunistic Infections↗
PubMed2001

A twin study of the etiology of prolonged fatigue and immune activation.

Risk factors to prolonged fatigue syndromes (PFS) are controversial. Pre-morbid and/or current psychiatric disturbance, and/or disturbed cell-mediated immunity (CMI), have been proposed as etiologic factors. Self-report measures of fatigue and psychologic distress and three in vitro measures of CMI were collected from 124 twin pairs. Crosstwin-crosstrait correlations were estimated for the complete monozygotic (MZ; 79 pairs) and dizygotic (DZ; 45 pairs) twin groups. Multivariate genetic and environmental models were fitted to explore the patterns of covariation between etiologic factors. For fatigue, the MZ correlation was more than double the DZ correlation (0.49 versus 0.16) indicating strong genetic control of familial aggregation. By contrast, for in vitro immune activation measures MZ and DZ correlations were similar (0.49-0.69 versus 0.42-0.53) indicating the etiologic role of shared environments. As small univariate associations were noted between prolonged fatigue and the in vitro immune measures (r = -0.07 to -0.12), multivariate models were fitted. Relevant etiologic factors included: a common genetic factor accounting for 48% of the variance in fatigue which also accounted for 4%, 6% and 8% reductions in immune activation; specific genetic factors for each of the in vitro immune measures; a shared environment factor influencing the three immune activation measures; and, most interestingly, unique environmental influences which increased fatigue but also increased markers of immune activation. PFS that are associated with in vitro measures of immune activation are most likely to be the consequence of current environmental rather than genetic factors. Such environmental factors could include physical agents such as infection and/or psychologic stress.

Age Factors↗
PubMed2000

Expression of cytokines and factors modulating apoptosis by human sinusoidal leucocytes.

BACKGROUND/AIMS: Liver sinusoids contain a large population of spontaneously cytotoxic cells (NK cells), CD8+ T cells and macrophages. The physiological role of these leucocytes remains unclear. They may participate in immune surveillance and peripheral tolerance by deleting tumour cells, virus-infected cells and activated T cells as they traffic through the liver. In order to gain further information about the function of these leucocytes within the hepatic sinusoids, we examined their production of immunomodulatory cytokines and apoptosis-related molecules. METHODS: Semi-quantitative polymerase chain reaction and immunohistochemistry were used to determine the spontaneous production of cytokines and apoptosis-related molecules by sinusoidal leucocytes isolated from donor liver preservation solution. RESULTS: In comparison with matched peripheral blood mononuclear cells, sinusoidal leucocytes produced more mRNA for IL-10, IL-15, TNF-alpha, IL-18, IFN-gamma, FasL, perforin and granzyme. IL-4 and IL-12 were not detected and IL-2 was only faintly detected in the liver-derived CD4+ population. Less bcl-2 was expressed in liver-derived CD4+ and CD8+ cells in comparison with matched peripheral blood cell populations. CONCLUSIONS: The cytokines produced spontaneously by sinusoidal leucocytes are consistent with their high level of activation and spontaneous cytotoxicity. Their strong expression of apoptosis-mediating molecules (FasL, perforin, granzyme and TNF-alpha) support a role for these cells in immune surveillance and peripheral tolerance induction.

Adjuvants, Immunologic↗
PubMed1999

Reduced IL-4 and interferon-gamma (IFN-gamma) expression by CD4 T cells in patients with chronic lymphocytic leukaemia.

CD7 co-expression by CD4 T cells has been reported to be higher in the Th1 compared with the Th2 functional subset. Clinical immunodeficiency and immune dysregulation are more prevalent in the advanced stages of B cell chronic lymphocytic leukaemia (B-CLL). To analyse this further 25 patients with B-CLL and 11 healthy subjects were examined for cell surface CD7 and intracellular IFN-gamma and IL-4 expression in the peripheral blood CD4+ T helper cell population. Significantly decreased CD7, IFN-gamma and IL-4 expression was observed in the patients with B-CLL (P < 0.001). While CD7 negativity and IL-4 expression were more frequent in the later stages of the disease, this did not attain statistical significance. These results suggest a possible explanation for the reduced cellular and humoral immunity in B-CLL.

Antigens, CD7↗
PubMed1999

Low-titre auto-antibodies predict autoimmune disease during interferon-alpha treatment of chronic hepatitis C.

BACKGROUND: In this study, we determined whether low-titre auto-antibodies are a risk factor for the development of autoimmune disease during interferon-alpha (IFNalpha) therapy for chronic hepatitis C (CHC) infection. METHODS: Eighty-three patients with circulating hepatitis C virus RNA and chronic viral hepatitis on liver biopsy, who had not received IFNalpha, were assessed for serum auto-antibodies (anti-nuclear antibodies (ANA), anti-smooth muscle antibodies, thyroid microsomal antibodies, thyroglobulin antibodies) and thyroid function tests. RESULTS: Thirty-five patients had one or more pre-existing auto-antibody. The majority were low titre ANA. Seven of the 35 patients had clinical autoimmune disease or immune-mediated disorders, predominantly thyroid disease. Twenty patients with low titre auto-antibodies received treatment with IFNalpha and of these 20 patients, six patients developed adverse effects with a possible auto-immune basis. In comparison, only five of the 48 patients without auto-antibodies had immune-mediated disorders and no patient developed autoimmune complications during therapy with IFNalpha. CONCLUSIONS: These results suggest that the presence of low-titre auto-antibodies may be a risk factor for the development of autoimmune dysfunction during IFNalpha therapy for chronic hepatitis C. Patients with no detectable auto-antibodies have a low risk for developing autoimmune complications during treatment with IFNalpha.

Adult↗
PubMed1998

Peanut allergy.

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Arachis↗
PubMed1998

Peritoneal fluid from ovarian cancer patients stimulates MUC1 epithelial mucin expression in ovarian cancer cell lines.

The MUC1 epithelial mucin is a transmembrane glycoprotein that is frequently but variably over-expressed by adenocarcinomas. It is used as a diagnostic serum tumour marker and is a candidate target for tumour immunotherapy. Peritoneal fluid (PF) samples from ovarian cancer patients were investigated for their ability to modulate MUC1 expression in 6 ovarian cancer cell lines which showed a range from very low to high endogenous MUC1 expression. Cell lines were cultured in 20% PF for 4 days, fixed in situ and MUC1 assayed by ELISA. MUC1 expression was stimulated by some PF samples in 5 of 6 lines tested. MUC1 expression in the PE04 cell line (very low endogenous expression) was increased by 35 of 36 PFs tested (p < 0.05); stimulation varied between PFs but was greater than with 100 IU/mL hu-r-gamma-interferon. Western blotting confirmed the stimulation of MUC1 in PE04 cells and FACS showed an increase in the proportion of cells expressing MUC1. The active factor was partially purified by gel filtration and was shown to stimulate PE04 cells in a dose-dependent manner. Concentrations of IL1beta, IL4, IL6, IL8, IL10, TNF-alpha, TGF-beta and GM-CSF were often very high in PF and varied substantially between different PF samples but did not correlate with the degree of MUC1 stimulatory activity.

Antigens, Neoplasm↗
PubMed1998

Histologic and immunohistochemical responses after aortic valve allografts in the rat.

BACKGROUND: Human aortic valve allografts elicit a cellular and humoral immune response. It is not clear whether this is important in promoting valve damage. We investigated the changes in morphology, cell populations, and major histocompatibility complex antigen distribution in the rat aortic valve allograft. METHODS: Fresh heart valves from Lewis rats were transplanted into the abdominal aorta of DA rats. Valves from allografted, isografted, and presensitized recipient rats were examined serially with standard morphologic and immunohistochemical techniques. RESULTS: In comparison with isografts, the allografts were infiltrated and thickened by increased numbers of CD4+ and CD8+ lymphocytes, macrophages, and fibroblasts. Thickening of the valve wall and leaflet and the density of the cellular infiltrate was particularly evident after presensitization. Endothelial cells were frequently absent in presensitized allografts whereas isografts had intact endothelium. Cellular major histocompatibility complex class I and II antigens in the allograft were substantially increased. A long-term allograft showed dense fibrosis and disruption of the media with scattered persisting donor cells. CONCLUSIONS: The changes in these aortic valve allograft experiments are consistent with an allograft immune response and confirm that the response can damage aortic valve allograft tissue.

Animals↗
PubMed1998

Serum sCD23 in patients with lepromatous and tuberculoid leprosy.

Tuberculoid and lepromatous leprosy (TL and LL) manifest exaggerated Th1 and Th2 type immunity, respectively. Serum soluble CD23, which is regulated by the stimulatory action of IL4 and inhibitory action of IFNgamma, was significantly elevated in LL relative to TL and healthy controls. These results confirm the state of cellular and humoral immunity in TL and LL.

Adult↗
PubMed1997

Serum soluble CD23 but not IL8, IL10, GM-CSF, or IFN-gamma is elevated in patients with hepatitis C infection.

The increased frequency of autoantibodies and B cell non-Hodgkins lymphoma (B-NHL) in hepatitis C virus (HCV) infection suggests dysregulated humoral immunity. Soluble CD23 (sCD23) is involved in B cell activation and proliferation and the serum levels are raised in autoimmune diseases and B cell lymphoproliferative disease. We compared the serum levels of sCD23 in patients with HCV infection with those in patients with alcoholic cirrhosis (AC) and in healthy controls. Serum levels of interleukin (IL) 8, IL10, granulocyte macrophage-colony stimulating factor, and interferon-gamma were assessed simultaneously to check for generalized nonspecific immune stimulation. In contrast to the essentially normal serum levels of these latter cytokines, the levels of sCD23 were raised in the patients with HCV compared to those with AC and the normal controls (medians 34.0, 10.1, and 11.1 arbitrary units, respectively; HCV vs AC P < 0.0004, HCV vs controls P < 0.0001, AC vs controls P > 0.8). These results confirm HCV-induced humoral immune dysregulation and invite comparison with primary Sjögrens syndrome and Epstein-Barr virus infection, both of which are also associated with raised levels of serum sCD23, autoantibodies, and B-NHL.

Adult↗
PubMed1997

An assessment of peripheral immunity in patients with sarcoidosis using measurements of serum vitamin D3, cytokines and soluble CD23.

The aetiology of the peripheral anergy in sarcoidosis is unclear. To investigate this further we measured the serum levels of several factors important in different aspects of immune regulation to obtain a profile of those factors which promote and inhibit immune activation in sarcoidosis. Thirty-seven patients with sarcoidosis and 20 healthy controls of similar sex and age comprised the study group. Serum IL-10, interferon-gamma (IFN-gamma), soluble CD23 (sCD23), IL-8, granulocyte-macrophage colony-stimulating factor (GM-CSF), IL-1beta and tumour necrosis factor-alpha (TNF-alpha) were measured using in-house ELISAs. Vitamin D3 was measured using a radioreceptor assay. Serum levels of sCD23 and IL-10 were significantly elevated in patients with sarcoidosis relative to controls (median 13.9 versus 9.5 arbitrary units/ml, P<0.01 for sCD23, and 9.6 versus 5.0 pg/ml, P<0.04 for IL-10). Regardless of steroid therapy or disease activity, serum levels of IFN-gamma, TNF-alpha, IL-1beta, GM-CSF and IL-8 were no different in patients with sarcoidosis and controls. Vitamin D3 levels were significantly higher in patients with sarcoidosis versus normal controls (medians 78.0 versus 56.0, P<0.001), active sarcoidosis (n = 20) versus inactive disease (n = 17) (medians 81.5 versus 66.0, P<0.03) and active sarcoidosis versus controls (medians 81.5 versus 56.0, P<0.0002). The levels were no different between patients with inactive sarcoidosis and controls. We suggest that IL-10 and vitamin D3 may contribute to the peripheral anergy in sarcoidosis. The elevated serum sCD23 suggests an increase in peripheral humoral immunity. Consistent with a quiescent peripheral immune system, factors capable of monocyte/macrophage activation (TNF-alpha, IFN-gamma, GM-CSF and IL-8) were not elevated in the peripheral circulation.

Adult↗
PubMed1997

The possible role of the immune system in the aetiopathogenesis of ovarian hyperstimulation syndrome.

This review examines recent evidence suggesting a role for the immune system, in particular cytokines, in the pathogenesis of ovarian hyperstimulation syndrome (OHSS). Ovarian tissue is known to contain cells capable of producing a range of immunological mediators and the concentrations of these have been shown to be elevated in serum and ascitic fluid from women with established OHSS. Available evidence points to a role for vascular endothelial growth factor and interleukin-2, possibly acting through other intermediary cytokines, in the pathogenesis of OHSS. However, each individual has a unique cytokine profile and several cytokines may share biological actions, making it difficult to interpret data on isolated cytokine concentrations from relatively small numbers of patients. Improved understanding of the role of the immune system in the development of OHSS may have implications for the prediction, prevention and management of this iatrogenic condition.

Cytokines↗
PubMed1997

Serum and blister fluid cytokines and complement proteins in a patient with Henoch Schönlein purpura associated with a bullous skin rash.

A case is presented of an adult with Henoch Schonlein purpura (HSP) with widespread bullous skin lesions in whom serum and bullous fluid (BF) cytokines and complement proteins were analysed. In both serum and BF the total haemolytic complement was subnormal. Soluble CD25 (sCD25), which is important in B cell activation and proliferation, was over 13 times higher in the BF compared with serum. The serum and BF levels of interleukin (IL) 1, IL6, IL10, tumour necrosis factor alpha and interferon gamma were within the normal serum range of 30 healthy control subjects simultaneously analysed. The raised levels of sCD23 in BF suggest dysregulated humoral immunity in the cutaneous lesions of HSP.

Adult↗