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Biomedical subjects

S Chouaib

Publications and source records attributed to S Chouaib.

116 records · Page 7Linked to original sources
PubMedDate not supplied

TNF alpha enhancement of NK and LAK cell functions induced by high-dose IL-2 in human peripheral blood mononuclear cells from patients pretreated with alpha IFN + IL-2.

In this study we analyzed the induction of NK and LAK cell functions by TNF alpha, alone or combined with IL-2, in 4 days in vitro culture of PBMC from patients treated with alpha IFN + IL-2. Although the MN cell recovery after 4 days culture was very similar with TNF alpha alone or with IL-2 alone, TNF alpha did not maintain nor induce LAK or NK activities of in vivo preactivated PBMC. When compared to preculture values, TNF alpha alone induced a preferential outgrowth of CD4+ T cells together with a decrease of CD8+ T cells, NK cells and IL-2R (p55)-expressing cells. The combination of TNF alpha (100 ng) and high dose IL-2 (9,000 IUg/ml) did not improve the MN cell recovery after 4 days culture; but increased IL-2-induced NK activities in PBMC from 6/7 patients, and IL-2-induced LAK activities in 4/7 patients. However, these variations were not significant. The combination of TNF alpha and lower doses of IL-2, ranging from 150 IU/ml to 30 IU/ml, did not modify MN cell recovery in culture nor IL-2-induced NK and LAK cell activities. When compared to paired samples cultured with IL-2 alone, the combination of TNF alpha with all doses of IL-2 did not modify the distribution of T and NK cells, but increased the expression of CD8 on NK cells. Furthermore, the combination of TNF alpha and IL-2 increased the expression of IL-2R (p55) on PBMC but the expression of this receptor was restricted to CD4+ T cells and did not appear on NK cells.

Antigens, CD↗
PubMedDate not supplied

Functional and phenotypic modifications induced by IL-4, as single agent or in combination with IL-2, on PBMC preactivated in vivo by alpha-interferon + interleukin-2 therapy.

The effect of human IL-4, used as a single agent or in combination with low or high dose IL-2, upon LAK-cell proliferation and activation has been tested on PBMC from patients treated with alpha 2-IFN and IL-2. Four days in vitro culture with IL-4 did not induce any LAK-cell activation; IL-4 induced the proliferation of CD3+ CD4+ T-cells, but decreased the percentage of NK cells in culture samples. When combined with high dose IL-2, IL-4 improved the recovery of MN cell without modification of T-cell subsets; however, IL-4 had no major effect on IL-2-induced NK or LAK cell activity. The combination of IL-4 and low dose IL-2 still significantly improved the total MN cell recovery but did not modify the distribution of T and NK lymphocytes; IL-4 inhibited low dose IL-2-induced NK and LAK cell activity, and increased the BL-esterase activity induced by high or low dose IL-2. The combination of IL-4 and IL-2 did not induce any large variation in the percentage of IL-2R (p55) expressing cells. In all tested conditions, IL-2R (p55) was mainly expressed on CD4+ T cells; less than 2% of the cells coexpressed the NK cell marker CD56 and IL-2R (p55). The effect of IL-4 upon IL-2-induced LAK cell expansion is thus very different on PBMC pre-activated in vivo by alpha IFN + IL-2 therapy than on PBMC pre-treated in vitro with IL-2.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Lymphokines and cytokines: from clone to clinic.

Cytokines form a complex network of interaction which is crucial in maintaining the homeostasis of the immune and hemopoietic organs and in controlling the balance between different responses of these two systems. The International Congress held in Osaka (17-21 October 1993) was an opportunity to summarize all the information accumulated in the field of cytokines and to evaluate the impact of new approaches and ideas which have invaded laboratories these last two years (the 7th International Congress was held in San Antonio in 1991). In this paper, we will summarize some striking points that were presented in Osaka.

Animals↗
PubMedDate not supplied

Pulmonary edema and shock after high-dose aracytine-C for lymphoma; possible role of TNF-alpha and PAF.

Four out of 23 consecutive patients treated with high-dose Ara-C for lymphomas in our institution developed a strikingly similar syndrome during the perfusion. It was characterized by the onset of fever, diarrhea, shock, pulmonary edema, acute renal failure, metabolic acidosis, weight gain and leukocytosis. Thorough bacteriological screening failed to provide evidence of infection. Sequential biological assays of IL-1, IL-2, TNF and PAF were performed during Ara-C infusion to ten patients, including the four who developed the syndrome. TNF and PAF activity was found in the serum of respectively two and four of the cases, but not in the six controls. As TNF and PAF are thought to be involved in the development of septic shock and adult respiratory distress syndrome, we hypothesize that high-dose Ara-C may be associated with cytokine release.

Acute Kidney Injury↗
PubMedDate not supplied

Phenobarbital prevents the inhibitory effects of tumor necrosis factor on glutathione-S-transferase mu in primary culture rat hepatocytes.

During inflammation and infection, overexpression of the tumor necrosis factor (TNF) is associated with changes in cytochromes P-450 levels in rat and human hepatocytes. The aim of this study was to investigate the effect of TNF on the expression of the glutathione-S-transferases (GSTs) in rat hepatocytes. TNF was added in vitro alone or simultaneously with phenobarbital (PB) into hepatocytes in primary culture or in vivo, before TNF, injected directly to rats. GST activity was assayed by spectrophotometry; protein GSTs alpha, mu and pi were evaluated by immunoblotting. When TNF was added alone to rat hepatocytes in vitro, total GST activity and GST alpha levels were not affected, while GST mu protein levels significantly decreased by 35%. GST pi protein was undetectable in hepatocytes whether treated or not with TNF. When PB was administered in vitro simultaneously to rat hepatocytes with TNF, the decrease observed for GST mu subunit was suppressed while total GST activity and GST alpha content were not affected. When hepatocytes were treated with TNF after PB given in vivo directly to the rat by i.p. injection, GST activity and GSTs subunits were induced by PB, while TNF did not exert any effect. These results indicate that TNF has an inhibitory effect on GST mu and PB abrogates this effect in primary cultured rat hepatocytes. Then, PB could prevent some TNF toxic effects.

Animals↗