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Biomedical subjects

S Sone

Publications and source records attributed to S Sone.

At least 397 records · Page 22Linked to original sources
PubMed1985

Synergism between human recombinant gamma-interferon and muramyl dipeptide encapsulated in liposomes for activation of antitumor properties in human blood monocytes.

Highly purified human blood monocytes, isolated by centrifugal elutriation under endotoxin-free conditions, were activated in vitro by combining subthreshold amounts of human recombinant gamma-interferon (r-IFN-gamma) and muramyl dipeptide (MDP) to become tumor cytotoxic against allogeneic A375 melanoma cells. Only intact r-IFN-gamma and MDP produced synergism for human monocyte activation. Neither pH 2-treated r-IFN-gamma and intact MDP nor heat-treated IFN-gamma and intact MDP, nor intact IFN-gamma and the biologically inactive stereoisomer of MDP, N-acetylmuramyl-D-alanyl-D-isoglutamine, produced activation of blood monocytes. The encapsulation of intact r-IFN-gamma and MDP within the same preparation of multilamellar liposomes was synergistic for monocyte activation. These data show that synergism for monocyte activation can be produced by human r-IFN-gamma and MDP produced synthetically can be simultaneously delivered to monocytes. Because both r-IFN-gamma and MDP can now be produced in large standardized quantities their synergism for activation of tumoricidal properties in human monocytes could be of clinical significance.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1985

[Induction of human monocyte-mediated tumor cell killing by alpha or beta interferon].

Human blood monocytes, separated on a continuous percoll gradient, were not cytotoxic to allogeneic A375 melanoma cells. The monocyte monolayers were activated to become tumoricidal by incubation for 24 hr with interferon (IFN)-alpha or beta at concentrations of more than 1,000 IU/ml. Significant and reproducible activation of the monocytes was achieved by incubating them with 10,000 IU/ml of IFN-alpha or IFN-beta for 24 hr. Similarly, suspended, but not plated, monocytes were activated to a tumoricidal state by interaction with IFN-alpha or IFN-beta. Monocytes that had lost tumoricidal activity during culture, were reactivated by a second exposure to IFN-alpha. Fluorescence analysis showed that the monocyte-rich adherent monolayers were contaminated with up 2.0% of natural killer (NK) cells. Pretreatment of isolated monocyte preparations with anti-NK cell monoclonal antibody (Leu-11b) to deplete them of NK cell activity did not inhibit the monocyte-mediated cytotoxicity. These results indicate that human monocytes are rendered tumoricidal by direct interaction with IFN-alpha or IFN-beta, although more than 1,000 IU/ml of IFN-alpha or IFN-beta is required for maximal expression of monocyte activation.

Cell Line↗
PubMed1985

Induction by interferon-alpha of tumoricidal activity of adherent mononuclear cells from human blood: monocytes as responder and effector cells.

Human blood monocytes, separated on a Percoll gradient, were not cytotoxic to allogeneic melanoma (A375) cells. Fluorescent analysis showed that the monocytes were contaminated with up to 2.0% natural killer (NK) cells. The monocytes became tumoricidal on incubation for 24 h with greater than or equal to 1,000 IU/ml interferon-alpha (IFN-alpha) derived from human lymphoblastic leukemia cells. Anti-IFN-alpha antibody abolished the ability of IFN-alpha to render the monocytes tumoricidal, whereas anti-IFN-beta antibody had no effect. Pretreatment of isolated monocyte preparations with anti-NK cell monoclonal antibodies (Leu-7 and Leu-11b), to inhibit NK cell activity, did not affect the cytotoxicity of IFN-alpha-activated monocytes on tumor cells. Full expression of cytotoxicity on tumor cells required the interaction of monocytes with IFN-alpha for 24 h. These results indicate that IFN-alpha directly activates human monocytes to become tumoricidal, although greater than or equal to 1,000 IU/ml IFN-alpha is required for maximal activation.

Cell Line↗
PubMed1985

Activation of tumoricidal properties in macrophages and inhibition of experimentally-induced murine metastases by a new synthetic acyltripeptide, FK-565.

The effect of FK-565, a novel low molecular weight (MW) acyltripeptide, on tumoricidal properties of murine macrophages is reported here. Peritoneal macrophages (PMs) harvested from C57BL/6 mice and beige mice were rendered cytotoxic to syngeneic B16 melanoma cells following their interaction in vitro with FK-565. Maximal and reproducible activation of tumoricidal properties in PM were obtained by interaction in vitro with 25 micrograms/ml of FK-565 for a 24 h period, and as little as 0.5 microgram/ml of FK-565 was sufficient to induce significant cytotoxicity. Murine PMs activated by FK-565 in vitro were cytotoxic to syngeneic and xenogeneic tumor cells, but did not affect allogeneic nontumor cells. The PMs were also activated to kill B16 melanoma cells by intraperitoneal injections of FK-565 (10 mg/kg). Multiple injections of FK-565 into mice also slightly but significantly inhibited lung metastases. These results suggest that FK-565 has potential as an effective immunopotentiator in immunotherapy.

Adjuvants, Immunologic↗
PubMed1984

Activation by a new synthetic acyltripeptide and its analogs entrapped in liposomes of rat alveolar macrophages to the tumor cytotoxic state.

FK-565 (heptanoyl-gamma-D-Glu-(L-meso-a, epsilon-A2pm (L)-D-AlaOH) is a synthetic acyltripeptide closely resembling cell wall peptidoglycan peptides of Streptomyces in structure. Alveolar macrophages (AM) lavaged from lungs of F344 rats were activated by in vitro treatment with FK-565 and its derivatives at concentrations of 1-50 micrograms/ml medium, and the activated AM killed syngeneic mammary adenocarcinoma cells. When FK-565 and related compounds were encapsulated in multilamellar (MLV) liposomes composed of phosphatidylcholine and phosphatidylserine, dose-response experiments showed that they were about 800 times more effective than the free compounds in activating AM. Liposome-encapsulated FK-565 and its analogs caused significant activation of AM within 4 h. These data indicated that acyltripeptide and its analogs encapsulated in liposomes are more efficient than the free compounds in rendering AM tumoricidal.

Adenocarcinoma↗
PubMed1984

Stimulatory effect of vitamin A on tumoricidal activity of rat alveolar macrophages.

F344 rats were given saline, vitamin A placebo or vitamin A analogues orally for 4 consecutive days. The following day they were killed and their alveolar macrophages (AM phi) were harvested by lavage. The functional integrity of the AM phi was determined by their capacity to phagocytize opsonized SRBC and to kill syngeneic adenocarcinoma cell lines nonspecifically. Results showed that 4 days treatment with greater than 100 IU of vitamin A as retinyl palmitate per gram body weight rendered the AM phi tumoricidal against syngeneic mammary adenocarcinoma cell lines (MADB-100 and MADB-200) and that AM phi activated with retinyl palmitate showed increased ability to phagocytize opsonized SRBC. Other retinoids, such as retinoic acid and retinol, had the same effect of inducing tumoricidal activity in rat AM phi. AM phi harvested from normal rats were also rendered tumoricidal by direct interaction with greater than 10(3) IU ml-1 of retinyl palmitate for 24 h in vitro. Thus, vitamin A at high doses can increase the phagocytic and tumoricidal activities of rat AM phi.

Adenocarcinoma↗
PubMed1984

Sonographically guided needle biopsy for diagnosis of thoracic lesions.

Fluoroscopically guided percutaneous biopsy of thoracic lesions is widely accepted. However, some lesions are not sufficiently visible on fluoroscopy. When this is the case, sonographic guidance may be helpful. Real-time sonographically guided needle biopsy was performed in 38 such cases, including 27 pulmonary nodules adjacent to the chest wall, three mediastial tumors, five chest wall masses, and three pleural lesions. Definitive diagnoses were made in 30 cases (78.9%), including 21 (91.3%) of 23 malignancies and nine (60%) of 15 benign lesions. Sonographically guided needle biopsy could be performed safely and easily, taking advantage of the real-time monitoring of needle position for the pulmonary masses located adjacent to the chest wall, even when fluoroscopic or CT guidance was not effective. It is suitable for biopsying chest wall tumors, pleural lesions, and anterior mediastinal masses. It is particularly suited to biopsying small pulmonary nodules adjacent to the chest wall, nodules in the apical or juxtadiaphragmatic regions, and those obscured by pleural effusion.

Adult↗
PubMed1984

Carcinoembryonic antigen (CEA) levels in pleural effusions and sera of lung cancer patients.

For determining the value of carcinoembryonic antigen (CEA) levels in diagnosis of malignant tumors of the lung, the CEA levels in 187 specimens of pleural fluid and sera obtained simultaneously from patients with pleural fluid were measured. In all 70 patients with benign diseases, the CEA levels in the effusions were less than the cut-off value of 5 ng/ml (mean +/- SD: 1.44 +/- 1.01 ng/ml). In contrast, in 88 of 117 patients (75.2%) with malignant diseases, the CEA levels in the effusions were over 5 ng/ml (25.3 +/- 24.5 ng/ml) and in 58 of the 117 patients (50.4%), the CEA levels in the serum were values of 5 ng/ml or more (11.9 +/- 18.4 ng/ml). There was a significant correlation between the CEA levels in the effusions and in the sera. The CEA levels in effusions in patients with malignant lung tumors were usually much higher than those in their sera. The incidence of CEA levels of 5 ng/ml or more in both the serum and effusion was highest in the patients with adenocarcinoma. These data indicate that determination of the CEA level in effusions, when done in combination with cytological examinations, may have additional value in diagnosis of lung cancer.

Adenocarcinoma↗
PubMed1984

Functions of multinucleated giant cells formed by fusing rat alveolar macrophages with lymphokines containing macrophage fusion factor.

Rat alveolar macrophages (AM) fused and formed multinucleated giant cells (MGC) when incubated with lymphokines released from mitogen-stimulated syngeneic lymphocytes. Several functions of these MGC populations were evaluated in vitro. MGC populations phagocytized opsonized sheep red blood cells to a lesser degree than unfused AM. The tumoricidal activity of MGC populations was compared with that of unfused AM after both populations had been treated with lipopolysaccharide (LPS) or lymphokines devoid of fusion factor activity. Results showed that MGC populations lost tumoricidal properties more rapidly than unfused AM. Treatment of MGC with LPS enhanced the production and release of lymphocyte-activating factor(s) (IL-1, interleukin 1) that augmented the blastogenic response of lymphocytes to phytohemagglutinin. These studies suggest that one possible function of MGC that lack phagocytic and tumoricidal properties may be in maintenance of granuloma formation by IL-1 production.

Animals↗