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Biomedical subjects

J Stachowski

Publications and source records attributed to J Stachowski.

At least 37 records · Page 2Linked to original sources
PubMed1996

[Severe hemolytic-uremic syndrome complicated by cholelithiasis treated with laparoscopic cholecystectomy in a 12-year old boy].

A case of a 12-year old boy with hemolytic-uremic syndrome complicated with cholelithiasis is presented. Due to severe course of the hemolytic-uremic syndrome (enhanced catabolism, coagulation disorders) a laparoscopic cholecystectomy as a new, modern surgical technique has been considered. Postoperative period has been uncomplicated. Therefore, laparoscopic cholecystectomy proved useful and is recommended in patients with high postoperative risk.

Child↗
PubMed1995

Eleven Polish patients with microcephaly, immunodeficiency, and chromosomal instability: the Nijmegen breakage syndrome.

We report on 11 patients from 8 independent families (3 pairs of sibs) with a complex clinical pattern including microcephaly, peculiar "bird-like" face, growth retardation, and, in some cases, mild-to-moderate mental deficiency. Most of the patients have recurring respiratory tract infections. One girl has developed B-cell lymphoma. A detailed anthropometric study of 15 physical parameters, including 3 cephalic traits, was performed. It was possible to study the chromosomes of PHA-stimulated lymphocytes in all of the patients. We found structural aberrations with multiple rearrangements, preferentially involving chromosomes 7 and 14 in a proportion of metaphases in all individuals. Profound humoral and cellular immune defects were observed. Serum AFP levels were within normal range. Radioresistant DNA synthesis was strongly increased in all 8 patients who were hitherto studied in this respect. Our patients fulfill the criteria of the Nijmegen breakage syndrome, which belongs to the growing category of ataxia telangiectasia-related genetic disorders. In light of the increased predisposition to malignancy in this syndrome, an accurate diagnosis is important for the patient.

Adolescent↗
PubMed1995

Relationship between the reactivity to hepatitis B virus vaccination and the frequency of MHC class I, II and III alleles in haemodialysis patients.

To study the immunoreactivity genes in a heterogeneous human population needs a large number of individuals. Associations between HLA antigens and immunoresponse to viral or bacterial antigens have been studied with controversial results. As a homogeneous population, the MHC class I, II and III allele distribution was studied in 153 end-stage renal disease patients (ESRD, average duration of renal replacement: 8.2 + 5.1 years) immunized with a recombinant hepatitis B vaccine in accordance to the standard vaccination schedule. Thirty-four patients with an antibody titre of less than 10 U/l following the last booster injection were considered as non-responders while 119 patients with antibody titre equal to or more than 10 U/l were considered as responders. The responder group was divided into two subgroups: low responders (antibody titre: < or = 1000 U/l) and high responders (antibody titre: > 1000 U/1). Marked differences were observed between responders and non-responders in the occurrence of carriers of different MHC class I, II and III alleles. Homozygotes for HLA-A1, HLA-B8, HLA-DR3 and HLA-DQ2 were found almost exclusively in the non-responder group and significantly more heterozygotes for these alleles were found in the non-responder group compared to the responders. Similar albeit less marked differences were found in the frequency of some MHC class III alleles (C4A*6, C4A*QO, Bf*F, Bf*S0.7). Within the responder group, carriers of HLA-A2, HLA-B7 and HLA-DR4 were found to be clustered in the low responder sub-group whereas carriers of HLA-A1, HLA-B27, HLA-Cw2, C4A*6 and Bf*F were observed more frequently in the group of high responders. Similar differences were found with extended haplotypes as well. For example, the extended haplotypes HLA-A1, B8, BfS, C4AQO, C4B1, DR3, DQ2 and HLA-A1, B8, BfF, C4A6, C4B2, DR3, DQ2 were present in nine of 34 cases of non-responders but only in one of 119 case of responders (P < 0.000001). These observations indicate that the presence or absence of certain MHC alleles even in heterozygous form determine the responsiveness to hepatitis B vaccination in end-stage renal disease patients, and among responders, the intensity of antibody response is also markedly influence by immunogenetic factors.

Adult↗
PubMed1995

[Reactivity to hepatitis B vaccination (HBV) in patients with uremia: association with defined HLA antigen configuration and complement protein allotypes C4A, C4B and B factor (Bf)].

Genes, which are responsible for the effectivity of immune response are located on the chromosome 6 similarly as the genes of the class I and II of the major histocompatibility complex (MHC) together with the genes of some complement proteins (C4A, C4B, B factor/Bf/). The study investigates the interdependence between HLA configuration as well as complement protein allotypes (C4A, C4B, Bf) with the reactivity to HBV vaccination of ESRD [end stage renal disease]-patients. 153 ESRD-patients (68 females, 85 males; mean duration of hemodialysis therapy 8.2 +/- 5.1 years) were studied. Subjects were vaccinated (Gen-H-B-Vax-D; Merck, Sharp and Dohme, 40 micrograms/dosis i.m.) in the schedule at 0, 1, 2, and 6 month. Non-responders (NR) were defined when the anti-HBs antibody titer was below 10 U/liter. HLA typing was performed by means of microlymphocytotoxicity assay, whereas complement allotypes were estimated by using high voltage gel electrophoresis with subsequent specific immunofixation with antibodies against C4A, C4B and Bf. In the non-responders group [NR = 34] a) the significantly higher occurrence of single HLA-A1 and/or HLA-B8 and/or Cw4 or DR3 or DR7 or DQ2 have been found. In about 40% of NR HLA-A1, -B8, -DR3, or -DQ2 antigens occurred as homozygotes.

Adult↗
PubMed1994

The value of quantitative measurement of HBeAg and HBsAg before interferon-alpha treatment of chronic hepatitis B in children.

Serum concentrations of HBsAg, HBeAg and hepatitis B virus DNA were measured quantitatively before interferon treatment in 23 children (17 boys, 6 girls) suffering from chronic hepatitis B, and correlated to the outcome of the treatment. Five children remained HBsAg- and HBeAg-positive throughout the treatment and 6 months after the end of the treatment (non-responders), 12 children eliminated HBeAg but not HBsAg (partial responders) and six eliminated HBeAg and HBsAg (complete responders). The five non-responders had significantly higher initial HBsAg and HBeAg concentrations and significantly lower alanine aminotransferase levels than the partial or complete responders. The six complete responders had significantly lower HBsAg concentrations than the partial or non-responders, and seemed to be younger. No significant difference in HBV DNA levels was found in the three response groups. These data suggest that quantitative assays of HBsAg and HBeAg are particularly useful in selecting patients with chronic hepatitis B for interferon therapy.

Adolescent↗
PubMed1994

Non-responsiveness to hepatitis B vaccination in haemodialysis patients: association with impaired TCR/CD3 antigen receptor expression regulating co-stimulatory processes in antigen presentation and recognition.

The study was undertaken to evaluate the relationship between non-responsiveness to hepatitis B (HBV) vaccination in haemodialysed patients and HBs antigen (Ag) presentation and recognition depending on TCR/CD3 receptors expression. We have found that the cause of the blunted response to HBV vaccination is multifactorial and seems to be associated with the following: (1) A reduced number of TCR/CD3 antigen receptor complexes on freshly isolated uraemic CD4 T cells, especially in non-responders. (2) The blunted proliferative response of uraemic CD4 T cells isolated from non-responders and stimulated for 6 days by autologous monocytes presenting HBsAg was associated with the decreased density of the TCR/CD3 receptors. (3) Moreover, in uraemic non-responders the expression of adhesion and accessory molecules on monocytes (intercellular adhesion molecule-1/ICAM-1, HLA-DR/Ia/) was significantly decreased following the culture with autologous monocytes serving as HBsAg-presenting cells. CD4 molecules and lymphocyte function antigen-1 beta/LFA-1 beta/ on helper-inducer T cells were increased before and after the culture. (4) These findings were also associated with a diminished binding capacity of IL-1 beta and IL-6 to their receptors on helper-inducer T cells. (5) IL-2, IFN-gamma and IL-4 production was decreased in uraemic non-responders, especially after 72 h of the culture. (6) Inhibited proliferation of helper-inducer T cells in uraemic non-responders was only partially reversible in the presence of exogenous IL-1 beta, IL-6, IL-2 and IFN-gamma. (7) HLA typing of uraemic non-responders was associated with extended haplotype: HLA A1,B8,DR3,DR7,DQ2.

Adult↗
PubMed1993

Signalling via the TCR/CD3 antigen receptor complex in uremia is limited by the receptors number.

The TCR/CD3 receptor complex plays a key role in antigen recognition and T-cell activation. Therefore, the present study investigates TCR alpha/beta (TCR1) and CD3 receptor density (RD, number of receptors per cell) on uremic helper-inducer (CD4) T lymphocytes in relation to T-cell proliferative response induced by anti-CD3 monoclonal antibodies (mAb). We found, that: (1) the number of TCR/CD3 receptors on uremic helper-inducer (CD4) T lymphocytes is decreased and correlated well with the blunted lymphocyte proliferation induced by anti-CD3 mAb; (2) these findings were associated with diminished binding capacity of IL-1 beta and IL-6 to their receptors (IL-1R, IL-6R) on helper-inducer T cells, whereas (3) the IL-2 receptor (IL-2R) and molecule expression of CD4 and lymphocyte function antigen-1 (LFA-1) were increased, and (4) uremic monocytes displayed a decreased density of intercellular adhesion molecule-1 (ICAM-1) expression, which interacts as receptor-ligand pair with LFA-1. The incubation of uremic and control peripheral blood mononuclear cells with uremic serum enhanced these above-mentioned changes in the expression of examined receptors and molecules. These data might also support the hypothesis that the blunted T-cell response to antigen in uremia is due to downregulation of the TCR/CD3 receptor complex by uremic milieu.

Adult↗
PubMed1991

Immunodeficiency in ESRD-patients is linked to altered IL-2 receptor density on T cell subsets.

The interdependence of blunted T cell proliferation induced by anti-CD3 monoclonal antibodies (mAb) and the preactivation of T lymphocytes (CD25+) in ESRD patients was investigated in this study. We focused on the density of IL-2 (CD25) receptors [IL-2R] on the lymphocyte surface rather than enumeration of IL-2R positive cells. The effect of exogenous IL-2 on these parameters was also tested. Blunted T lymphocyte proliferation induced by anti-CD3 mAb is only partially corrected by addition of exogenous IL-2 after 24 hrs. Freshly isolated uremic CD4 T cells show higher percentage of IL-2 positive cells and a higher IL-2R density on the cell surface compared to controls. However, after anti-CD3 mAb stimulation the number of IL-2R positive cells and IL-2R density in CD4 T subset was significantly lower than in samples from normal donors. Exogenous IL-2 had no influence on IL-2R expression on CD4 cells in uremic patients. On the other hand, following anti-CD3 mAb stimulation uremic CD8 cells reveal more IL-2R positive cells with higher IL-2R density than in controls. Moreover, exogenous IL-2 enhance IL-2R expression and density on uremic CD8 cells more than in controls. Our results suggest that the blunted T cell proliferation in ESRD patients might result from (a) preactivation of CD4 T cells, (b) diminished response of uremic CD4 T cells to IL-2, and (c) higher suppressor cells activity.

Adult↗
PubMed1991

Does uremic environment down-regulate T cell activation via TCR/CD3 antigen receptor complex?

TCR/CD3 receptor complex plays a central role in antigen recognition and T cell activation. Therefore, the present study investigates TCR alpha/beta (TCR-1) and CD3 receptor density (RD, number of receptors per cell) on uremic CD4 T lymphocytes in relation to T cell proliferative response induced by anti-CD3 monoclonal antibodies (mAb). The influence of uremic serum on TCR/CD3 receptor expression of normal and uremic CD4 T lymphocytes was evaluated as well. We found, that: a) percentage of TCR-1 and CD3 positive cells of freshly isolated CD4 T lymphocytes is the same in controls and ESRD-patients, but the TCR/CD3 RD is lower on uremic CD4 T lymphocytes, b) Incubation for 24 h with uremic serum lowers TCR/CD3 RD on normal and uremic CD4 T cells, c) There is positive correlation between TCR/CD3 RD and anti-CD3 induced lymphocyte proliferation. These data might also support the hypothesis that blunted T-cell response to antigen in uremia is due to down-regulation of the TCR/CD3 receptor complex by uremic milieu.

Adult↗
PubMed1991

Activity of B-cell lineage system in the cord blood of newborns.

To evaluate the B cell lineage system in newborns we estimated IL-4 (BCGF/BSF-1) production by lymphocytes isolated from the cord blood and its influence on antibody synthesis. Undertaken experiments were performed in two groups of newborns: stressed newborns mainly with perinatal infection and full-term healthy neonates, comparing to peripheral blood of adults as control. Results revealed 1) the significantly higher percentage of mature B cells (B1) in cord blood of stressed newborns, 2) the significantly higher IL-4 production comparing to full-term neonates, 3) diminished IgG and IgA synthesis in vitro by allogenic activated B cell blasts in the presence of supernatants from cultures of PHA-stimulated lymphocytes isolated from cord blood of stressed newborns. Induction of IgM synthesis by these active supernatants was significantly higher in stressed newborns than in the other examined groups. We suggest that immunoregulatory mechanisms, which control the production of IL-6 (BCDF/BSF-2) are still not completely mature at birth.

B-Lymphocytes↗
PubMed1991

Immunopathology of hepatitis B mediated membranous glomerulonephritis.

The study was undertaken to establish the clinical and immunological aspects of HBV-mediated membranous glomerulonephritis in children. Out of 54 children with membranous GN treated in the Children's Memorial Hospital 51 children (94.4%) had the disease related to HBV infection. The inhibitory effect of immune complexes: HBsAg-IgG and HBeAg-IgG, isolated from sera of these children on lymphocyte proliferation of blood donors was observed. This may partly explain the status of immune tolerance towards HBV in the infected children.

Adolescent↗
PubMed1990

Influence of immune complexes containing HBsAg and HBeAg on IL-2 dependent human lymphocyte proliferation.

Studies were undertaken to evaluate the effect of hepatitis B virus (HBV) immune complexes (HBV-IC) on IL-2 dependent human lymphocyte proliferation. The following parameters were studied: 1) Effect of HBV-IC (HBsAg-IgG or HBeAg-IgG) on PHA-mediated lymphocyte proliferation; 2) Influence of HBV-IC on the ability of PHA-stimulated peripheral blood lymphocytes (PBL) for IL-2 production and IL-2 receptor expression. HBV-IC induced a dose dependent and antigenic dependent suppression of PHA stimulated lymphocytes. The suppressor effect exerted by HBsAg-IgG was irreversible. In contrast, the suppression mediated by HBeAg-IgG was reversible: lymphocytes preincubated with this preparation washed and activated with PHA responded well to mitogen. The presence of HBV-IC in the cultures of PHA-activated PBL decreased their ability to produce IL-2: HBeAg-IgG exerted a stronger suppressor effect. This effect was partially reversible: removal of HBV-IC from the culture by washing and subsequent stimulation of PBL with PHA increased the capacity of lymphocytes to produce IL-2. This was particularly evident with HBeAg-IgG. Decreased activity of IL-2 observed in the cultures, was also partially dependent on the ability of HBV-IC to bind IL-2 present in the culture medium. Experiments performed using ultracentrifugation indicated that HBV-IC, especially HBsAg-IgG, may bind to IL-2 and inactivate it. HBV-IC had also an effect on IL-2 receptor expression: 1) their presence in the cultures of PHA-stimulated PBL decreased the number of Tac positive cells; 2) the response of HTCL to exogenous IL-2 was decreased by HBV-IC present in the culture medium. This was especially observed in the case of HBsAg-IgG. We suggest that the observed inhibition of PHA-induced lymphocyte proliferation exerted by immune complexes containing HBsAg-IgG or HBeAg-IgG may be caused mainly by their influence on IL-2 dependent mechanism of lymphoproliferation.

Antigen-Antibody Complex↗
PubMed1989

Effect of Pseudomonas aeruginosa exotoxin a on PHA-induced lymphocyte proliferation.

P. aeruginosa Exotoxin A induced a dose dependent suppression of PHA-stimulated human lymphocyte proliferation. The suppressor effect was not reversed by interleukin 2 (IL-2) added to the culture medium. Expression of IL-2 receptors (IL-2R) on PHA-blasts a well as their ability for IL-2 binding were decreased by Exotoxin A. Kinetic studies of IL-2 production showed that IL-2 activity was still present in cultures of lymphocytes activated for 72 hours with PHA and Exotoxin A. In contrast, supernatants of lymphocyte cultures activated with PHA and Exotoxin A for 18 hours had low activity of IL-2. Hence, Exotoxin A probably could decrease the utilization of IL-2 due to either inhibition of IL-2R expression or suppression of their ability for IL-2 binding.

ADP Ribose Transferases↗
PubMed1989

Effect of HBV antigens and their immune complexes on the PHA induced lymphocyte proliferation. Modulatory influence on interleukin-2 activity.

Studies were undertaken to evaluate immunomodulating properties of Hepatitis B virus (HBV) preparations: HBsAg, HBeAg and their complexes: HBsAg-IgG and HBeAg-IgG, on PHA-induced lymphocyte proliferation. Cells were obtained from blood of healthy individuals, serologically negative for HBV markers. HBV preparations were purified from sera of children with HBV-mediated glomerulonephritis. Suppression of lymphocyte proliferation observed in the presence of HBsAg and HBsAg-IgG complexes was irreversible. However, the suppressive effect of HBeAg and HBeAg-IgG was abolished when these preparations were removed from the culture. Addition of exogenous interleukin-2/IL-2/reversed only the suppressive effect of HBeAg-IgG which was constantly present in the culture. The inhibition of lymphocyte proliferation correlated well with the decreased level of IL-2 activity in cultures with HBV-preparations. Experiments performed using ultracentrifugation indicated that HBV preparations, especially HBsAg and HBsAg-IgG, may bind to IL-2 and inactivate it in supernatants. The experiments indicate that HBV antigens, as well as other viral products, can inhibit lymphocyte proliferative response to the mitogen. Furthermore, we suggest that this inhibition may occur via suppression of IL-2 synthesis.

Antigen-Antibody Complex↗