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Biomedical subjects

M Zembala

Publications and source records attributed to M Zembala.

At least 73 records · Page 4Linked to original sources
PubMed1996

[Most common laryngological diseases in patients after heart transplantation].

Based on our own material containing 78 patients after heart transplantation the analysis of the most common laryngological diseases in postoperative period was performed. The attention was paid on the character, location of the diseases and the time of appearance after operation. The effort to find the correlation between kind and dose immunosuppression and frequency of infections was made. The necessity of careful and permanent laryngological control of patients after heart transplantation was emphasized due to the serious complications avoidance.

Adolescent↗
PubMed1995

Interaction of HIV-1 gp120 molecule fragments with human monocytes: different requirements for tumor necrosis factor-alpha and IL-6 production.

The HIV-1 gp120 recombinant protein fragment encompassing aa residues 410-511, that contains the CD4 binding region (rp120cd), and fragment aa 446-511, which lacks the sequence responsible for CD4 binding (rp120), were synthesized to study their ability to induce TNF synthesis in human monocytes. The rp120cd stimulated TNF alpha secretion by monocytes while the rp120 and full-length recombinant protein (FL gp120), used as control, failed to do so. However, FL gp120 stimulated peripheral blood mononuclear cells (PBMC) and lymphocytes for TNF production and this was inhibited by anti-CD4 MAb. The rp120cd also caused TNF secretion by PBMC that was not blocked by this antibody. Furthermore, FL gp120 but not rp120cd inhibited anti-CD4 mAb binding to CEM cells. Hence, FL gp120 may cause TNF release from lymphocytes by binding to CD4, while rp120cd interacts with monocytes but not lymphocytes and induces TNF production by a mechanism not involving CD4 binding. Unexpectedly, FL gp120 but not rp120cd stimulated IL-6 secretion and IL-6 mRNA synthesis in monocytes. The FL gp120-induced production of IL-6 by monocytes was inhibited by anti-CD4 monoclonal antibody (MAb). Thus, there may be different requirements for TNF induction in lymphocytes and monocytes stimulated with various preparations of gp120 and for the selective induction of cytokines in monocytes. The enhanced production of TNF in HIV infection and AIDS may involve distinct cellular sources and different mechanisms.

Antibodies, Monoclonal↗
PubMed1995

MHC class I and class II determinants and some adhesion molecules are engaged in the regulation of nitric oxide production in vitro by human monocytes stimulated with colon carcinoma cells.

Surface molecules that are involved in tumor-monocyte interactions were studied. The in vitro system in which human blood monocytes are stimulated with human colon carcinoma cells for nitric oxide (NO) production was used. Monoclonal antibodies (mAbs) against various adhesion molecules (LFA-1, ICAM-1, VNR) were unable to block NO production in coculture of monocytes with carcinoma cells. However, anti-CD44, -LFA-3, and -VLA beta 1 chain mAbs effectively blocked NO production. Also mAbs against MHC class I and HLA-DR molecules inhibited, in a dose-dependent manner, No release. It was concluded that some adhesion molecules and MHC class I and/or class II determinants of monocytes may be involved in tumor-monocyte interactions leading to signal transduction for NO production.

Antibodies, Monoclonal↗
PubMed1995

Isotype-specific regulation of MHC class II gene expression in human monocytes by exogenous and endogenous tumor necrosis factor.

The control of expression of MHC class II molecules on antigen-presenting cells is important for the induction of immunity, while aberrant expression of these molecules plays a role in the immunopathology of autoimmune diseases. This study explored the role of tumor necrosis factor alpha (TNF) in controlling the level of HLA class II mRNA in human monocytes. Exposure of monocytes to exogenous recombinant TNF (rTNF) selectively up-regulated DR alpha-mRNA but not DP or DQ alpha-mRNA. Inhibitors of TNF synthesis, pentoxifylline (PTX) and thalidomide, inhibited TNF mRNA accumulation in LPS-activated monocytes and down-regulated DR mRNA but not DP or DQ mRNA. The inhibitory effect of anti-TNF monoclonal antibody (MAb) indicated that endogenously generated TNF acted extracellularly. Anti-p75 TNF-R2 receptor and to a lesser extent anti-p55 TNF-R1 MAbs inhibited TNF-mediated up-regulation of DR mRNA and TNF mRNA. Taken together, this implies that endogenously generated TNF plays a role in controlling isotype-specific MHC class II gene expression in human monocytes/macrophages. These results may have some implications for anti-tumor response and autoimmunity.

Antibodies, Monoclonal↗
PubMed1995

Modulation of monocyte antigen-presenting capacity by tumour necrosis factor-alpha (TNF): opposing effects of exogenous TNF before and after an antigen pulse and the role of TNF gene activation in monocytes.

We have previously shown that exogenous human recombinant tumour necrosis factor-alpha (rTNF), added before an antigen pulse, enhanced antigen presentation by human blood monocytes. The present study shows that, surprisingly, rTNF added after an antigen (PPD) pulse inhibited, while anti-TNF monoclonal antibody (mAb) enhanced, antigen presentation. mAbs htr-9 against p55 TNF receptor type I (TNF-RI) abrogated rTNF enhancing effect on PPD presentation and decreased presenting activity of untreated monocytes while utr-1 mAb, against p75 TNF receptor type II (TNF-RII), reversed the inhibitory effect of rTNF given after antigen pulse. PPD and rTNF when added singly induced TNF-mRNA accumulation in monocytes. Pretreatment of monocytes with rTNF followed by a PPD pulse caused an enhancement of TNF-mRNA accumulation. However, when post-treatment with rTNF was applied to PPD-pulsed monocytes, then inhibition of TNF gene expression was seen. This may point to the role of endogenously generated TNF in regulation of antigen-presenting capacity of monocytes. These studies indicate that TNF is an important regulator of monocyte antigen-presenting capacity and that the level of TNF gene activation in monocytes may be associated with their ability to present nominal antigen.

Antibodies, Monoclonal↗
PubMed1995

Elimination of monocytes from cultures activated with recall antigens.

Recent data provide evidence that antigen-specific CD4+ T-cell clones or antigen-activated T-cell lines can kill antigen-presenting cells (APC). We focused our studies on monocytes acting as APC in cultures of T cells freshly isolated from peripheral blood. The presence of monocytes in culture was monitored by their ability to emit light during phagocytosis of latex particles (latex-induced chemiluminescence). Using this approach as well as flow cytometry, evidence is presented that monocytes are eliminated from cultures with T cells activated with recall antigens (PPD or TT). The mechanism of monocyte elimination involved apoptosis as judged from in situ detection of DNA strand breaks by the terminal deoxynucleotidyl transferase assay. The antigen- but not lectin-dependent monocyte elimination was MHC-restricted and mediated by CD4+ T lymphocytes. This finding supports the hypothesis that elimination of APC is a general phenomenon during T-cell activation and may represent an important immunoregulatory mechanism.

Antigen-Presenting Cells↗
PubMed1995

Monocyte-mediated regulation of antigen-driven IFN gamma production by T cells. The role of endogenously produced TNF.

The question was asked whether tumour necrosis factor alpha (TNF) is involved in regulation of interferon gamma (IFN gamma) production by T cells. Monocytes were exposed to exogenous TNF or to TNF synthesis inhibitors (pentoxifylline, PTX and adriamycin, ADR) and then used as antigen (PPD) presenting cells for autologous T cells. The ability of T lymphocytes to release IFN gamma was assessed after 3 days of culture. Preincubation of monocytes with rTNF enhanced their ability to induce IFN gamma production while TNF synthesis inhibitors decreased it. Anti-TNF and anti-TNF-R2 monoclonal antibodies (mAbs) inhibited monocyte ability to present PPD for IFN gamma production which suggested that endogenously produced TNF by monocytes had to be released and acted on TNF-R2 on the monocyte surface. The enhancing effect of exogenous TNF was also abrogated by anti-TNF-R2 mAb. Pretreatment of monocytes with rTNF enhanced, while pretreatment with PTX decreased, PPD-induced IL-6 production. An increased production of IL-4 was found in cultures of PTX-treated, PPD-pulsed monocytes with T cells. This may indicate that in the relative absence of monocyte costimulatory signal(s), probably IL-6, Th2 cells are stimulated. These results indicate that TNF is involved in control of monocyte-mediated regulation of cytokine production by T cells.

Antibodies, Monoclonal↗
PubMed1995

Characterization of human pancreatic adenocarcinoma cell line with high metastatic potential in SCID mice.

The CD44 molecule and CD44 isoforms are expressed on some malignant tumours and it has been suggested that their expression may correlate with tumour spread. Human pancreatic carcinoma cell line (HPC-4) expressing CD44 was established from a patient with adenocarcinoma of pancreas. This line showed a rapid growth in vitro, several chromosome abnormalities and surface expression of some adhesion molecules (ICAM-1, LFA-3, beta 1-chain of VLA integrins, VNR). Xenotransplanted HPC-4 cells were able to grow rapidly in SCID mice as subcutaneous tumour, leading to 100% mortality within 3-5 weeks when 1 x 10(5)-1 x 10(7) cells were inoculated. Spontaneous metastases in the liver, lung, spleen and kidney of SCID mice were observed. Interestingly enough, HPC-4 cells in vivo and ex vivo also expressed HLA-DR molecules, but these were rapidly lost upon culture in vitro. It is suggested that the appearance of HLA-DR may be the result of interaction of the tumour with a local environment of the host, while CD44 expression may explain the rapid growth and occurrence of distant metastases in SCID mice. The ability of HPC-4 cells to form spontaneous metastases in SCID mice may prove to be a potentially interesting model of human carcinoma for testing new treatment modalities.

Adenocarcinoma↗
PubMed1995

[Uremic autonomic neuropathy--pathogenesis, diagnostic methods].

Autonomic impairment is associated with poor prognosis in many diseases. The pathogenesis of the uremic autonomic neuropathy has not been convincingly established, so the article reviews available information on factors involved in its development, furthermore the authors put forward their own hypothetical scheme of the pathogenesis. The last section outlines the methods most commonly used for its diagnosis and finally the authors discuss symptoms suggestive of this neuropathy in clinical setting.

Autonomic Nervous System Diseases↗
PubMed1995

[Prevention and treatment of uremic autonomic neuropathy].

The autonomic impairment, which is the frequent complication of end-stage renal failure, may eventually trigger numerous crippling consequences. It is doubtful if standard dialysis techniques may effectively treat once developed autonomic lesions. Renal transplantation seems to be much more efficient. The article points out the discrepancies in symptoms attributable to autonomic impairment and results of autonomic testing, discusses also differences between somatic and autonomic nervous system involvement in uremic patients. The one of the most important part of the article describes the practical approach to the patient with severely symptomatic uremic autonomic neuropathy. Finally the authors articulate their proposals for further research on uremic autonomic neuropathy.

Autonomic Nervous System Diseases↗
PubMed1995

Preactivation and phenotype of monocytes have no influence on their elimination from culture by activated T lymphocytes.

T lymphocytes can kill antigen-presenting cells (APC) in the presence of antigen or lectin. The subject of this study was to investigate whether the state of activation or phenotype of monocytes, influence their susceptibility to killing by T cells activated with pokeweed mitogen (PWM) or anti-CD3 monoclonal antibody. The data are presented which show that monocytes activation with cytokines (IFN-gamma, IL-4, or IL-2), PPD, phorbol ester or phagocytic stimulus, have no influence on monocyte susceptibility to killing by T lymphocytes. Furthermore, flow cytometry data suggest that monocytes eliminated from culture have no characteristic phenotype. In conclusion, our data indicate that elimination of monocytes by activated T lymphocytes does not depend on the state of activation of monocytes.

Cell Death↗