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Biomedical subjects

E Jirillo

Publications and source records attributed to E Jirillo.

At least 199 records · Page 11Linked to original sources
PubMed1982

In vitro modulation of cell-mediated immunity by prostaglandin E2. II. Enhancement of spontaneous plaque-forming cell generation.

The effect of the pretreatment of human peripheral blood lymphocytes by Prostaglandin E2 (dissolved in medium) on the spontaneous Plaque-Forming Cell generation has been evaluated. A significant enhancement of immunoglobulin production, markedly increased by the addition of further PGE2 to the pretreated cells, has been demonstrated. Experiments carried out with indomethacin have shown an inhibition of plaque formation, thus indicating that the content of endogenous prostaglandin E2 may play an important role in the enhancement of antibody synthesis, previously described. Results obtained with populations of rosetting and non-rosetting lymphocytes pointed out that non-rosetting cells are exclusively responsive to prostaglandin treatment.

Dinoprostone↗
PubMed1982

Effects of bacterial lipopolysaccharides (LPS) on leukocytes and platelets. Recent views on the pathophysiological role of LPS in the host.

Some effects of bacterial endotoxin on leukocytes and platelets are reviewed. The release of two mediators, Leukocyte Inhibiting Factor (LIF) and Tissue Factor (TF) from human mononuclear cells are described. These factors may play either beneficial effects (LIF) or noxious activities (TF liberation in certain pathological conditions). Regarding the activities of LPS on platelets the AA. report some personal data about the electrokinetic modification of platelets due to endotoxin. This LPS effect can be performed directly or via a lymphokine release, Platelet Slowing Factor (PSF). In the light of all the mentioned considerations, a scheme of interaction LPS/platelets is suggested.

Animals↗
PubMed1982

[Electrophoretic mobility in acute null cell lymphoblastic leukemia].

The electrophoretic mobility (E.M.) (evaluated by cytopherometer) of human normal lymphocytes, shows a group of cells with a fast mobility, identifiable as T lymphocytes, and a second group with a slow mobility which can be characterized as B lymphocytes. Six cases of Acute Lymphoblastic Leukaemia characterized by negativity of immunological markers and classified as "Null Cells", and ten cases of B cell Chronic Lymphocytic Leukaemia were studied in order to investigate the E.M. behaviour of leukaemic cells and so a comparison with T and B normal lymphocytes migration. The blasts of Acute Lymphoblastic Leukaemia show a E.M. nearly similar to the fast group of normal lymphocytes, while lymphocytes of the B cell Chronic Lymphocytic Leukaemia migrate as the slow component of normal lymphocytes. The possibility of the utilization of cell E.M. in addition to immunological and cytochemical data, into the characterization of Acute Leukaemias is suggested.

Adolescent↗
PubMed1981

Variability of antibody-specific induction and regulation of plaque-forming cells in cultures of normal human peripheral blood lymphocytes.

PFC have been detected in normal human PBL cultures, immunized with sheep red blood cells (SRBC) and supplemented with Concanavalin-A (Con-A) on day 0 (suppressive effect), and on day 2 (helper effect). Five PBL cultures responded punctually on established days, while four cultures failed to reproduce an enhancing effect when Con-A was added on day 2. In one case only no suppression was observed following addition of Con-A on day 0. Furthermore, it should be taken into consideration the dose of Con-A employed that can give suppressive, enhancing and no effects irrespective of the day of its addition in culture. On the basis of these considerations, it has been concluded that such a method is not suitable for clinical purposes, for instance in patients with immunological disorders, since the individual response to Con-A is extremely variable.

Antibody Specificity↗
PubMed1980

Bacterial endotoxin-immunocompetent cells interaction: newer aspects.

Bacterial endotoxin or LPS are constituents of the outer membrane of the cell wall of Gram-negative bacteria. When they invade human or mammalian organisms, they induce many biological effects. Lipid A represents the toxic part of the molecule. In the present communication, the AA. review some of the actions of LPS on immunocompetent cells, with particular reference to mitogenicity, adjuvanticity and tumor regression. Newer aspects of LPS immunobiology are emerging from the collected data. Of particular interest seems to be the relationship among T cells, Macrophages and B cells in LPS-induced adjuvanticity. These cells play a primary role in the potentiation of antibody production and their effects are mostly mediated via LK or MK. About possible mechanisms of tumor regression LPS-dependent, TNF and TNS features are illustrated. Because of the great extent of the present subject, the AA. are not able to include in this context some novel effects of endotoxin on immunocompetent cells as PGs release, SAA protein induction and colony forming activity.

Adjuvants, Immunologic↗
PubMed1978

Leucocyte migration inhibition with Armadillo lepromin in human lymphocytes of healthy donors.

Armadillo lepromin activates human lymphocytes from normal donors to release leucocyte inhibiting factor. The above activity was expressed optimally when leucocytes were incubated with lepromin at 37 degrees C, and only partially when incubation was carried out at 30 degrees C or at 35 degrees C. The possible mechanism of the in vitro production of lymphokine from lymphocytes stimulated by armadillo lepromin is discussed.

Animals↗
PubMed1977

Leukocyte inhibitory factor (LIF) production from lymphocytes stimulated by leucogenenol.

It has been demonstrated that human peripheral lymphocytes incubated in a tissue culture medium containing 0.04, 0.1, or 0.15 microgram/ml of leucogenenol form or release a factor that inhibits the migration of human peripheral PMN leukocyte. The factor is chromatographed of Sephadex G-100 and migrates on electrophoresis as an albumin, thus suggesting that it has the electric charge of an albumin. The factor is stable to neuraminidase and to heating at 56 degrees C for 30 min, but it is inactivated by heating at 80 degrees C for 60 min. Its physical and biological properties suggest that the factor is identical to the LIF reported by Rocklin.

Cell Migration Inhibition↗
PubMed1977

Demonstration of platelet electrophoretic mobility slowing factor (PSF) in supernatants of human lymphocyte cultures stimulated by phytohaemagglutinin (PHA).

It has been demonstrated that human peripheral lymphocytes, stimulated with PHA, form or release a factor that slows platelet electrophoretic mobility (PEM). The factor is chromatographed on Ultrogel AC a 44, has a molecular weight of approximately 45,000, is stable on heating at 56 degrees C for 30 min, but is inactivated by heating at 80 degrees C for 10 min. In addition, it is distinct from leukocyte inhibiting factor, which elutes in the range of BSA (mol. wt. 69,000). The authors conclude, in accordance with previous investigations, that cellular immunity is involved in thrombotic processes.

Blood Platelets↗
PubMed1977

Effects of tilorone hydrochloride on cellular immunity (leukocyte inhibiting factor production from human lymphocyte stimulated by E. coli lipopolysaccharide).

Tilorone hydrochloride, a drug able selectively to affect T-lymphocyte fuction, when incorporated (at three different concentrations 0.1, 0.04, 0.02 microgram/ml) in lymphocyte culture, stimulated by 50 microgram/ml of E. coli LPS (026:B6 W), is able to abolish LIF production, due to endotoxin stimulation. Such effect is, may be, due to an impairment of T-cell activity, since tilorone at the same concentration decreases the number of ARFC and TRFC, which are specific markers for T-cells.

Escherichia coli↗
PubMed1977

Effect of some bacterial products on platelet electrophoretic mobility (PEM).

Bacterial LPS, used in our experiments, are able to decrease PEM at concentration of 100 microgram/ml after incubation with 1 X 10(7) platelets/ml for 30 min at 37 degrees C. Such effect is statistically significant for Bacteroides fragilis LPS, S. enteritidis and S. typhi. E. coli LPS 026:B6 W and E. coli 055:B5 W are not effective at all, S. minnesota (incomplete) LPS 595 and 345 free of 0-polysaccharide and partially lacking core in their molecule did not influence PEM, while S. minnesota LPS (S form) (a complete LPS) strongly decreased PEM. This fact could suggest that 0-polysaccharide is involved in this inhibitory effect on PEM. Klebsiella enterotoxin and B. cereus enterotoxin are able to decrease PEM at concentration of 100 microgram/ml, after incubation with 1 X 10(7) platelets for 30 min at 37 degrees C, while no inhibition of PEM was seen when Shighella enterotoxin and V. parahaemoliticus enterotoxin was used in similar way. The AA. conclude that endotoxin and enterotoxin are able to change the electrokinetic charge (negative) of platelets, thereby, causing a decrease of PEM.

Bacillus cereus↗
PubMed1977

Limulus test, parenteral drugs and biological products: an approach.

The authors report their experience with the LAL test for endotoxin assay. They have examined parenteral drugs, blood products and biological substances employed in immunology. The results were compared with rabbit pyrogen tests. All the data suggest that if correctly performed, the LAL test is a simple, rapid and sensitive test. This assay appears to be very useful for materials employed in immunology in order to test the possible contamination with bacterial endotoxin, since the interference between endotoxin and immunologic response is well known.

Animals↗