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Biomedical subjects

R Gallily

Publications and source records attributed to R Gallily.

At least 73 records · Page 4Linked to original sources
PubMed1984

Studies on the mechanism of macrophage-mediated tumor cell lysis induced by Mycoplasma orale.

Following our previous demonstration that both viable and heat-killed Mycoplasma orale induce selective tumor cell killing by murine peritoneal macrophages, further investigations reported here showed that also macrophages from a continuously proliferating cell line established from long-term cultures of murine bone marrow explants can effectively be induced by the heat-killed mycoplasmas to express cytolysis. The use of single-cell suspensions of M. orale from a 0.45-micron filtrate or following either sonication or treatment with DNase did not significantly affect the level of cytolysis. Minute quantities of M. orale acted synergistically with ineffectively low levels of either lymphokines (LK) or lipopolysaccharide (LPS) to produce killing. The exceptional resistance of M109 lung adenocarcinoma cells to macrophage-mediated killing induced by LK and LPS, as previously reported by us, could not be overcome by the addition of M. orale. These data appear to indicate a mechanism of macrophage activation by M. orale similar to that caused by LPS.

Animals↗
PubMed1984

Wheat germ agglutinin potentiates uptake of bacteria by murine peritoneal macrophages.

Exposure of thioglycollate-elicited murine peritoneal macrophages to wheat germ agglutinin (WGA) increased markedly the uptake of six different bacteria, which have surface receptors for the lectin. Uptake of Staphylococcus aureus H was higher by 3-5-fold, of S. aureus 52A2 by 1.8-fold, of S. aureus 52A5 by 1.7-fold, of S. albus by 2.3-fold, of Shigella flexneri by 6-fold and of Micrococcus luteus by 6.5-fold. Klebsiella pneumoniae, devoid of receptors for WGA, was not phagocytosed following pretreatment of macrophages with the lectin. Pretreatment of the bacteria with the lectin also resulted, in most cases, in an increase in phagocytosis. Interaction of WGA with the macrophages and with the bacteria, as well as the potentiation of phagocytosis, was abolished by tri-N-acetylchitotriose, a saccharide that binds specifically to WGA, but not by monosaccharides which do not interact with this lectin. With non-elicited macrophages, enhancement of phagocytosis by WGA was less pronounced, probably because of the higher number of lectin-binding sites (5-fold) on the elicited cells. Peanut agglutinin and soybean agglutinin, that bind to macrophages but not to the bacteria studied, lack the ability to potentiate phagocytosis. Macrophage surface sugars thus appear to play an important role in phagocytosis by serving as receptors for lectins that form bridges between the macrophages and the microorganisms.

Animals↗
PubMed1983

Induction of macrophage-mediated cytolysis of neoplastic cells by mycoplasmas.

Unexpected cytolysis was encountered when nonactivated murine peritoneal macrophages were cultured with [3H]TdR-prelabeled syngeneic or allogeneic tumor cells at a 10:1 ratio. The level of specific cytolysis reached 70% within 48 hr of cocultivation. Similar killing was observed whether the macrophages were derived from untreated, thioglycollate-treated, or germ-free mice. Cytolytic activity was also demonstrated when bone marrow-derived or peritoneal macrophages from 9- and 5-day in vitro cultures, respectively, were employed rather than freshly harvested peritoneal macrophages. Thus, the macrophage-mediated killing was neither the result of in vivo preactivation nor a consequence of the presence of lymphocytes in the assay. Moreover, macrophages derived from different strains caused similar effects. Our study revealed that the neoplastic target cell cultures susceptible to cytolysis by nonactivated macrophages were contaminated with mycoplasma. A mycoplasma was isolated from the supernatant of a culture of the A9HT fibrosarcoma line, identified as Mycoplasma orale, and cultivated. Addition of viable mycoplasma from that isolate to mixed cultures of thioglycollate-elicited macrophages and [3H]TdR-prelabeled mycoplasma-free target cells resulted in specific cytolysis of transformed A9 cells, but not of normal mouse fibroblasts. The level of macrophage-dependent cytolysis correlated with the number of viable mycoplasma cells added and was higher than that attained by activation with LPS at optimal concentration. Similar specific cytolysis was observed with heat-killed mycoplasmas. Our results demonstrate that mycoplasmas may cause selective macrophage-mediated cytolysis of neoplastic but not of normal target cells, perhaps via activation of the macrophages. It is suggested that undetected infection of experimental systems by mycoplasmas may account for some reports on lysis of neoplastic cells by nonactivated macrophages.

Animals↗
PubMed1983

Mast cell differentiation depends on T cells and granule synthesis on fibroblasts.

Mast cell differentiation was generated in the following three experimental situations: (i) infection of mice with Schistosoma Mansoni or with Nippostrongylus brasiliensis and growth of the lymph node cells in the presence of the corresponding helminth antigen; (ii) immunization with horse serum and growth of blood and lymph node cells in the presence of the horse serum; (iii) exposure of T-cell-depleted suspensions of lymph node cells from unimmunized mice to T-cell factor (TCF) released into medium of the young cultures of (i) and (ii). This differentiation was also obtained when lymph node cells from athymic nude mice were exposed to TCF. The cell suspensions were plated on X-irradiated fibroblast monolayers prepared from embryonic mouse skin. Screening of the suspensions before plating on the fibroblasts in culture revealed no young forms of mast cells, and none were present in culture of nude mice lymph node cells maintained without TCF. Primordial appearance of metachromatic granules generally in the golgi zone was first seen in many 'large lymphoid cells' as early as 18 hr after plating. This was followed by increase in the cytoplasm volume, increase in granule number and mitosis, ending at 10-18 days with homogeneous populations of mature mast cells. When the mesenteric lymph node cells from mice infected with the helminths were grown in the absence of fibroblasts but in the presence of the antigen, homogeneous populations of cells with extended cytoplasm, filled with unstained vacuoles developed during days 7-13. These cells did not contain histamine (or at most 0.2 microgram per 10(6) vacuolated cells). When these cells were plated on fibroblast monolayers clear granule formation in all the vacuoles was seen 2 days later. It increased progressively in size and staining intensity, until the vacuoles transformed into typical mast cell granules. By the fourth day the vacuolated cells attained the typical mast cell morphology and the histamine content greatly increased (from 0.12 microgram per 10(6) vacuolated cells to 3.02 micrograms per 10(6) mast cells). These mast cells were readily degranulated by monoclonal anti-DNP-BSA IgE, and the antigen, releasing 90% of the histamine. The study shows that mucosal mast cells formation from 'large lymphoid-like' cells present in the blood and in the lymph, is stimulated by TCF. The condensation of the metachromatic material and histamine synthesis depends on other cells, presumably fibroblasts which comprise the principal cell in the embryonic skin monolayers. The mechanism of the fibroblast influence is not yet known.

Animals↗
PubMed1983

Recognition and lysis of altered-self cells by macrophages. I. Modification of target cells by 2,4,6-trinitrobenzene sulphonic acid.

Peritoneal exudate macrophages from normal, untreated or thioglycollate-elicited mice, lysed syngeneic fibroblasts and lymphoblasts modified by 2,4,6-trinitrobenzene sulphonic acid (TNBS) in vitro. Optimal lysis of the hapten-modified cells by elicited macrophages was usually seen after 18 hr of co-cultivation at E:T ratios of 10:1-30:1. Cytotoxicity was expressed by macrophages depleted of T cells, and was not potentiated by LPS. Allogeneic TNBS-modified cells were lysed by non-immune, non-activated macrophages to the same extent as syngeneic modified targets, indicating that genetic restriction does not appear to play a role in macrophage-mediated cytolysis of TNBS-modified cells.

Animals↗
PubMed1983

Cultivation, proliferation and characterization of thymic macrophages.

Successful long-term culture of murine thymic macrophages was achieved by plating adherent thymic cells, in the presence of L cell-conditioned medium, on dishes coated with an extracellular matrix. Adherent thymic cells in normal conditions of in-vitro culture do not proliferate. Those maintained on plastic tissue-culture dishes, and exposed to L cell-conditioned medium, proliferate slowly to a limited degree and form very small colonies. In contrast, when cultured in dishes coated with an extracellular matrix formed by corneal endothelial cells, in the presence of L cell-conditioned medium, adherent thymic cells proliferate rapidly and after 12-21 days in culture form large colonies (about 3-5 mm in diameter). The proliferating cells were identified to be mononuclear phagocytes by their morphological appearance, their ability to ingest both bacteria and antibody-coated erythrocytes and by their nonspecific esterase activity. These cells were also shown to exhibit cell surface antigens that are characteristic of differentiated macrophages, e.g. Fc receptors and the specific macrophage cell surface marker F4/80. A high percentage of these cultured cells were found to bear I-A antigens. The adherent thymic mononuclear phagocytes could be trypsinized and passaged while maintaining both their ability to proliferate and their specific macrophage characteristics for a period of 70 days. Thus, monocyte-macrophage stem cells ae present in the thymus, and under appropriate in-vitro conditions, can be made to proliferate and mature to I-A-bearing macrophages.

Animals↗
PubMed1982

Non-immunological recognition and killing of xenogeneic cells by macrophages. III. Destruction of fish cells by murine macrophages.

Non-immune non-activated murine peritoneal macrophage killed in vitro fish (Cyprinus carpio) PHA-induced lymphoblasts. Addition of PHA and WGA to effector-target cell cultures did not potentiate the killing. This killing (xenolysis) was expressed by non-elicited and thioglycollate-elicited macrophages as well as by macrophages depleted of lymphocytes. It is suggested that mammalian macrophages have a xenolytic potential towards phylogenetically distant species which is analogous to the capacity of invertebrate phagocytes to destroy xenografts.

Animals↗
PubMed1981

Mouse macrophage functions under the influence of factors released by spleen cells preincubated with the methanol extraction residue (MER) tubercle bacillus fraction.

Exposure of mouse peritoneal macrophages in vitro to the nonspecific immunomodulator MER (methanol extraction residue fraction of phenol killed, acetone washed tubercle bacilli) failed to heighten their phagocytic and bacteriostatic activities toward Staphylococcus albus, even when amounts of the agent below the threshold of gross toxicity were employed. In contrast, exposure of such macrophages to supernatants of whole splenocyte suspensions that had been obtained from normal donors and were incubated with MER resulted in consistent potentiation of both phagocytosis and bacteriostasis. The findings suggest that the MER effect on macrophages function is mediated, in this system, by soluble lymphocyte product(s).

Animals↗
PubMed1981

Non-immunological recognition and killing of xenogeneic cells by macrophages. I. Repertoire of recognition.

Non-immune non-activated mouse peritoneal macrophages efficiently kill in vitro xenogeneic fibroblasts from various avian species (xenolysis). The killing was less effective for rat and human fibroblasts. Macrophages of all inbred strains tested demonstrated xenolytic activity although they differed in destruction efficiency. Recognition and killing of target fibroblasts were not dependent on the presence of Ca++ and Mg++. Lysis of SPEFAS chicken fibroblasts free of viral antigen expression (gs-chf-) suggests that foreign recognition by macrophages does not involve viruses. Administration of anti-H-2 antiserum and of rabbit anti-macrophage serum (AMS) as well as addition of various carbohydrates or their derivatives to macrophages interacted with fibroblasts, failed either to block or identify foreign recognition sites on macrophages. Morphological studies by scanning electron microscopy showed protrusions of macrophage filopodia unidirected to the target xenogeneic fibroblast.

Animals↗
PubMed1981

Non-immunological recognition and killing of xenogeneic cells by macrophages. II. Mechanism of killing.

Macrophages are cytotoxic to chicken embryonic fibroblasts without either previous activation or lymphocyte assistance. This cytotoxic activity (xenolysis) is expressed by non-activated macrophages from athymic mice as well as by pure macrophage populations. Neither macrophage lysate nor supernatants of macrophages cultivated with fibroblasts cause xenolysis. Unlike macrophage tumoricidal activity, killing of xenogeneic cells is not dependent on specific serum factors and is expressed by macrophages from a lipopolysaccharide (LPS) unresponsive strain (C3H/HeJ). Xenolysis is expressed also by trypsin-treated macrophages and by macrophages from 5-day-old cultures. Killing of chicken fibroblasts by macrophages is not affected by hydrocortisone (100 micrograms/ml) gold salt (1 mg/ml) and colchicine (100 micrograms/ml). On the other hand, cytochalasin B (10 micrograms/ml) completely abolishes the killing, probably by interfering with macrophage mobility and extension of filopodia toward the targets. It is suggested that the xenolytic activity of macrophages represents a primitive trait of phagocytes which assists the body in defence against multicellular parasites.

Animals↗
PubMed1981

Artificial binding of macrophages to syngeneic cells elicits cytostasis but not cytolysis.

Artificial binding of mouse peritoneal macrophages to syngeneic embryonic fibroblasts by means of rabbit anti-mouse anti-macrophage serum or Con-canavalin A inhibited the proliferation of syngeneic target cells without destroying them. It is suggested that an intimate membranal contact between macrophages and target cells triggered cytostasis, whereas cytotoxicity requires an additional step of foreign recognition.

Animals↗
PubMed1980

Effect of colchicine on polymorphonuclear leucocyte chemotaxis in human volunteers.

1 The effect of colchicine on polymorphonuclear leucocyte chemotaxis was assessed in eight healthy volunteers. Four of them received 1.0 mg colchicine and the other four received placebo daily for 8 successive days. 2 Chemotaxis decreased significantly within 24 h of the ingestion of colchicine; the values remained low throughout the 8 days of treatment and returned to normal within 48 h of cessation of medication. 3 There were no significant changes in the placebo treated subjects.

Adult↗
PubMed1980

Monocyte function in rheumatoid arthritis.

Monocytes derived from peripheral blood of patients with rheumatoid arthritis (RA) had a marked defect in their bactericidal activity against Staphylococcus albus and Listeria monocytogenes; whereas the phagocytic capacity of monocytes from RA patients for both Staph. albus and Shigella flexneri was similar to that of monocytes from healthy subjects. There were no significant differences between the patient and control groups with regard to antibody dependent cellular cytotoxicity (ADCC) of monocyte against antibody-coated EL4 leukemia tumor cells. No correlation was observed between the rheumatoid factor (RF) titer in the serum of RA patients and the ADCC capacity of their monocytes. The ADCC of normal monocytes was reduced markedly following their incubation with serum from RA patients. It suggested that the defect in bactericidal activity in monocytes from RA patients may explain, at least in part, the susceptibility of RA patients to infections.

Adolescent↗
PubMed1979

Phagocyte functions in familial Mediterranean fever.

Monocytes derived from peripheral blood of patients with familial Mediterranean fever (F.M.F.) demonstrated lower phagocytic capacity for Shigella flexneri and depressed bactericidal activity against S. albus when compared to monocytes from healthy individuals. Treatment of patients with colchicine did not alter these functions. On the other hand, chemokinesis of PMN of F.M.F. patients was enhanced especially during attacks. Colchicine treatment decreased significantly the PMN chemotactic migration.

Adolescent↗