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M Zembala

Publications and source records attributed to M Zembala.

At least 217 records · Page 12Linked to original sources
PubMed1970

Contact sensitivity in the mouse. IV. The role of lymphocytes and macrophages in passive transfer and the mechanism of their interaction.

Contact sensitivity skin reactions were produced in mice by immunization with 2-phenyl-4-ethoxymethylene oxazolone (oxazolone) and detected by the increase in ear thickness after challenging the ears with 2% oxazolone. These skin reactions can be transferred from immunized donors to irradiated recipients by peritoneal exudate cells induced by thioglycollate. The peritoneal exudate cells were separated into purified macrophage and purified lymphocyte populations. Both cell populations transferred skin reactions. However, their time course was different. The reactions produced by lymphocytes were greater at 24 hr than at 12 hr while the reactions produced by macrophages declined slightly between 12 and 24 hr. The working hypothesis was formed that the peritoneal lymphocytes conveyed a factor (presumptive cytophilic antibody) to peritoneal macrophages which enabled them to transfer ear reactions. Experiment showed that peritoneal and lymph node lymphocytes from sensitized donors within a Millipore chamber conveyed a factor to macrophages outside the chamber which enabled them to transfer ear reactions. In contrast, peritoneal macrophages (from sensitized donors) within the chamber and peritoneal lymphocytes outside the chamber were inactive. These findings suggested that there are three modes of immunological tissue damage: hypersensitivity mediated by lymphocytes (classical delayed hypersensitivity), hypersensitivity mediated by circulating antibody (classical immediate type hypersensitivity), and hypersensitivity mediated by macrophages which have passively acquired a factor (macrophage-mediated hypersensitivity).

Animals↗
PubMedDate not supplied

Nuclear mean gray level and chromatin distribution changes in cardiomyocytes of heart transplant recipients suffering from acute cellular rejection.

BACKGROUND: Distribution and staining of the nuclear chromatin are sensitive indicators of changes in physiology and pathology of cells. However, their use in heart transplant recipients is rare. The aim of this study was to compare cardiomyocyte status in heart transplant recipients suffering from moderate acute cellular rejection and subjects without signs of active cellular rejection. MATERIALS AND METHODS: One hundred twenty-nine endomyocardial biopsy samples from 43 heart transplant recipients (no later than 6 months after surgery) were evaluated. Overall, 3235 cardiomyocytic nuclei were analyzed using the Quantimet image analysis system to assess the mean gray level: 1584 nuclei were found in biopsies without signs of rejection or with nonsignificant rejection (ISHLT grades 0, 1A, and 1B), whereas the remaining 1651 nuclei were measured from biopsies showing ISHLT grade 3A (significant rejection). Additionally, the chromatin distribution was assessed in all eligible nuclei. RESULTS: The mean gray level was markedly increased in nuclei from biopsy samples with significant rejection (182.6 vs 112.5, P < .001, Mann-Whitney U test). Moreover, the analysis of chromatin distribution revealed significantly more frequent chromatin marginalization and irregular distribution in rejecting subjects (P < .001, chi-square test). CONCLUSION: Inflammatory stimulation of cardiomyocytes during acute cellular rejection of the transplanted heart influences the chromatin distribution in the nuclei, which may have an additional value, when assessing the severity of rejection.

Acute Disease↗
PubMedDate not supplied

General considerations in the interpretation of I-J genetic restrictions: evidence that the antigen-binding chain of antigen-specific T-suppressor factor has two recognition sites for members of the I-J hierarchy.

(CBA X B10)F1 [(H-2k X H-2b)] mice produce two types of antigen-specific T-suppressor factor (TsF), which can be separated by affinity chromatography on anti-I-J monoclonal antibody. After reduction and alkylation, both chains of F1 TsF are required for biological activity. However, the antigen-binding chain (AgBC) of F1 TgFk (AgBCk) is only complemented by I-Jk and likewise for F1 TsFb. In other words, interchain complementation shows the same genetic restriction in interchain complementation in parental and F1 mice. F1 TsF bearing, for example, I-Jk (TsFk), interacts with haptenized 'antigen-presenting cells' ('APC') and parental I-Jk chains interacts with haptenized 'APC' of both parental haplotypes (dual reactivity). In contrast, the combination of parental AgBCb and F1 I-Jb shows single reactivity and only interacts with haptenized 'APCb'. It was inferred that the antigen-binding chain is responsible for the dual reactivity and, hence, for the interaction with a member of the I-J hierarchy on the 'APC'. It was concluded that the antigen-binding chain of TsF has two recognition sites for members of the I-J hierarchy--one for interchain complementation and the other for interaction with the haptenized 'antigen-presenting cell'. The term member of the I-J hierarchy is used instead of I-J because it is not clear whether the AgBC interacts with I-J or a receptor for I-J, or indeed a receptor for that receptor.

Animals↗
PubMedDate not supplied

Gastric mucosal damage and adaptive protection by ammonia and ammonium ion in rats.

Helicobacter pylori (Hp) is considered as the major pathogen in Hp-associated gastritis but the mechanism of its action has not been fully explained. We investigated both the damaging and protective effects of intragastric (i.g.) application of ammonia (NH4OH) and ammonium ion (NH4Cl), the major products of Hp-derived urease, on the rat stomach with intact and capsaicin-deactivated sensory nerves or suppressed prostaglandin (PG) and nitric oxide (NO) synthesis. NH4OH given i.g. resulted in a concentration-dependent mucosal damage starting at 30 mM and reaching maximum at 250 mM (pH 11), the extent of damage being similar to that obtained with 100% ethanol. NaOH solution (1 mM) at pH 11 given i.g. did not affect mucosal integrity. The damage caused by NH4OH was accompanied by the fall in gastric blood flow (GBF) reaching at 250 mM NH4OH about 30% of the vehicle control value. The NH4OH-induced gastric damage was augmented by capsaicin-induced deactivation of sensory nerves, the suppression of nitric oxide (NO) synthase with L-NAME or the decrease of i.g. acidity by ranitidine. The pretreatment with scavengers of reactive oxidants significantly reduced the area of NH4OH-induced gastric lesions. When the mucosa was first exposed to a low 15-mM concentration of NH4OH and then insulted with large 250 mM NH4OH or with 100% ethanol, the lesion area was markedly reduced as compared to that obtained with 250 mM NH4OH or 100% ethanol alone. This adaptive protection by 'mild' concentration of NH4OH against strong irritants (250 mM NH4OH or 100% ethanol) was reversed, in part, by pretreatment with L-NAME and indomethacin. NH4Cl (60-500 mM) given i.g. alone failed to affect the mucosal integrity but when applied before 100% ethanol it produced a concentration-dependent fall in the mucosal damage by these irritants. We conclude that; (1) ammonia at higher concentrations damages the gastric mucosa, while ammonium ion exerts the protective activity; (2) the ammonia-induced gastric damage may involve the formation of reactive oxidants; (3) ammonia at lower concentration acts like a mild irritant via the activation of sensory nerves, NO-arginine pathway and PG.

Adaptation, Physiological↗
PubMedDate not supplied

Lectin-activated CD4+CD45RA+ T-lymphocytes have no ability to kill monocytes.

Monocytes are eliminated from cell culture by antigen or mitogen activated cytotoxic CD4+ T-lymphocytes. In this report we asked the question whether CD4+CD45RA+ and CD4+CD45RO+ subpopulations differ in the ability to kill monocytes in pokeweed mitogen (PWM)-activated cultures. Data are presented that although CD4+CD45RA+ vigorously proliferate in the presence of PWM, they do not kill monocytes or secrete IFN gamma.

Antigen-Presenting Cells↗
PubMedDate not supplied

Heart retrieval for cardiac homograft.

BACKGROUND: The use of homograft tissue instead of various artificial materials in contemporary cardiovascular surgery, although limited by the constant shortage of donor organs, has become the clinically preferable procedure. The proper technique of heart retrieval, with strict donor qualification criteria and sterility procedures, is one of the key points in the successful preparation of allografts to be used later in a selected group of patients undergoing cardiac surgery, especially in the repair of pediatric congenital heart defects. MATERIAL AND METHODS: The article presents the most popular surgical technique to use for retrieving a heart for cardiac homograft in multiorgan procurement and routine autopsy, including the immediate preliminary preparation and transport, as recommended by the majority of tissue bank institutions. The qualification criteria for tissue donation, delicate preparation techniques, and sterility protocols are also important issues for successful cardiac homograft retrieval. Recently a tendency towards a growing number of pediatric donors can be observed. The techniques presented in this article should also be applied in cases of homograft retrieval from pediatric donors. RESULTS: This article analyzes our seven-year-long experience, involving a total number of 608 hearts retrieved for cardiac homografts, with special attention to the main reasons for disqualification of the organs delivered to the tissue bank. CONCLUSIONS: 1. The procedures for the sterility of tissue retrieval, especially in autopsies with heart retrieval, although they may sometimes be difficult for the surgeon or pathologist, are necessary to provide maximum benefit from harvested tissues. 2. The proper technique for pediatric homograft retrieval is twice as important in tissue delivery protocols.

Autopsy↗