PubMed HealthSearch

Biomedical subjects

S Becker

Publications and source records attributed to S Becker.

At least 91 records · Page 5Linked to original sources

Colony-stimulating factor-induced monocyte survival and differentiation into macrophages in serum-free cultures.

The role of mononuclear phagocyte-specific colony-stimulating factor (CSF-1) in human monocyte to macrophage differentiation was investigated. The addition of 1000 U/ml of CSF-1 to serum-free monocyte cultures resulted in monocyte survival comparable to that in cultures containing 5% AB serum, whereas cells in serum- and CSF-1-free medium lost their viability in 3 to 5 days. The requirement for CSF-1 coincided with the time (40 to 64 hr of culture) when the major changes in morphology and biochemical function took place in monocytes undergoing differentiation into macrophages. If CSF-1 was removed from the cultures before this time, death of the monocytes resulted. In cultures containing CSF-1, as in serum containing cultures, the lysosomal enzyme acid phosphatase was enhanced 10- to 20-fold by day 4 to 5. Superoxide production in response to phorbol myristic acetate was maintained in CSF-1 cultured monocytes, but declined with time in monocytes cultured in serum. The expression of monocyte-macrophage antigens p150.95 (LeuM5), OKM1, LeuM3, Fc receptors (32.2), and HLA-DR had increased in CSF-1 containing cultures at day 4. When antigen expression was analyzed at day 2 to 3, when cell size and 90 degrees scatter characteristics were still identical to control serum-free cultures, only p150.95, HLA-DR and FcR expression were enhanced by CSF-1. Low amounts of lipopolysaccharide (0.1 ng/ml) were found to enhance monocyte survival in the absence of added CSF-1. Lipopolysaccharide-containing cultures were found to produce CSF-1 (up to 450 U/ml, as detected by radioimmunoassay). Lipopolysaccharide (1 microgram/ml), however, did not induce enhanced expression of the maturation-related antigens. Based on these observations we conclude that CSF-1 is enhancing human monocyte survival and is involved in the events leading to the differentiation of monocytes into macrophages.

Acid Phosphatase

[Does a single oral dose of famotidine influence the blood alcohol level?].

Six healthy volunteer medical students (three men and three women) on four separate occasions drank 500 ml of beer or 250 ml of white wine 30 min after having taken 40 mg of famotidine or a placebo (after 48 hours of abstinence and six hours of fasting). Administration of drug or placebo followed a double-blind, randomized protocol. There was no demonstrable effect of famotidine on the serum level of alcohol (maximal values 0.29-0.67 mg/dl) or on the time until maximal serum concentrations of alcohol were reached.

Adult

Altered maturation and function of peritoneal macrophages: possible role in pathogenesis of endometriosis.

Human peritoneal macrophages from healthy women and patients with endometriosis were analyzed with flow cytometry for size distribution, cell membrane antigen expression, and membrane function. Endometriosis was associated with a significantly increased number of peritoneal macrophages and a higher proportion of large macrophages with increased expression of three antigen markers. Peritoneal macrophages from normal patients exhibited diminished cell membrane capping function as compared with that of endometriosis-related macrophages or blood monocytes. On the basis of these findings, a hypothesis is formulated suggesting that endometriosis is associated with an increased influx of macrophages that are allowed to undergo further maturation-activation. The resultant population of large macrophages may contribute to the maintenance of the disease or associated infertility.

Ascitic Fluid

Growth inhibition of Cryptococcus neoformans by human alveolar macrophages.

Macrophage cytotoxicity for Cryptococcus neoformans was investigated by culturing human alveolar macrophage (AM) with a thin-capsuled clone of C. neoformans in a polypropylene culture tube assay system. Yeast replication was quantitated by electronic particle counting after detergent lysis of AM and viability by quantitative plate counts. Under appropriate conditions, fungal replication was inhibited in the presence of human AM. This effect persisted over the 48-h time course that was evaluated. During this period, organisms in medium alone proliferated rapidly, doubling their number every 4 h. Human AM did not require endotoxin, fetal calf serum, or specific rabbit anticryptococcal antibody for fungistasis. Under these conditions, microscopic evaluation of a cytocentrifuge preparation of AM-yeast cocultures, stained by a modified Giemsa technique, revealed all the fungi to be extracellular. In the presence of 10% fresh human serum, AM phagocytized C. neoformans and exhibited fungicidal activity. Tumor necrosis factor did not affect the replication rate of the yeast. These findings suggest that there may be at least 2 mechanisms by which human AM protect against C. neoformans. One is serum-independent and extracellular and results in fungistasis, and the other is dependent on a serum factor and leads to intracellular inhibition of growth and possibly killing of the organism.

Blood

[Pseudolinitis plastica of breast origin].

The most common type of gastric metastases secondary to carcinoma of the breast is the one showing a linitis plastica appearance. The roentgenologic aspect when performing an upper gastrointestinal examination with barium contrast is typical and allows the differential diagnosis with the primitive linitis. The linitis plastica type of metastatic breast carcinoma results from transmural infiltration of the stomach wall with initial deposit of tumor cells in the submucosal or subserosal regions. CT provide valuable information concerning the metastatic spread.

Adenocarcinoma, Scirrhous

Interleukin-1 production and antigen presentation by normal human peritoneal macrophages.

Human peritoneal macrophages from healthy females have been investigated for their capability to produce interleukin-1 (IL-1), their expression of HLA-DR and -DQ, and for their antigen-presenting capacity in concanavalin A, tetanus toxoid (TT), and autologous T-cell proliferative responses. Fifteen out of thirty macrophage populations produced IL-1 but the activity was 1/5 to 1/10 that of peripheral blood mononuclear cells stimulated under similar conditions. High levels of HLA-DR were expressed on all macrophages while lower and more variable levels of DQ were found. All macrophages induced mitogen-dependent T-cell proliferation while the ability to induce a proliferative response to TT was variable, 12/23 tests were positive. In five samples stimulatory capacity of macrophages in the absence of TT was as strong as in the presence of the stimulus, suggesting that in vivo processed immunogen could be responsible for the proliferative response. The surface density of HLA-D-region-determined antigens was not indicative of the macrophages' ability to induce antigen-specific proliferation. IL-1 production, however, correlated with this function. Antigen presentation was not confined exclusively to peritoneal populations consisting of recently immigrant monocyte-like cells, nor were all young macrophages able to present antigen. This may reflect on the diversion of macrophage function by the local environment.

Antigen-Presenting Cells

Antitumor immune response to colorectal cancer antigen detected by the leukocyte adherence inhibition test (LAI) in groups at high risk for colorectal cancer.

Colorectal cancer is the second leading cause of cancer death in western populations. As treatment outcome is highly correlated with stage at diagnosis, early detection is a very important task. Three high-risk groups for colorectal cancer (first-degree relatives of colorectal cancer patients; individuals with past history of colorectal neoplasms, polyps, or carcinoma; and patients with ulcerative colitis) were screened for colonic neoplasms. The study program included the leukocyte adherence inhibition test (LAI), a specific immune response test for colorectal cancer antigen; fiberoptic sigmoidoscopy or colonoscopy; and guaiac impregnated slide test. The main finding was the detection of 92 positive LAI tests out of 451 high-risk individuals tested (20%), compared to eight positive tests out of 194 (4.1%) in a control group. Fifty-six colonic neoplasms were found out of 344 (16%) colonoscopies performed, most of them adenomatous polyps and a few carcinomas. Our findings, compared with the expected 2-3% neoplasms in low-risk groups, would prove that the screenees were indeed at high risk. However, only 11/56 (19%) of the polyps identified were LAI positive. The number of polyps found among LAI positive individuals were, so far, 11/92 (11%). The guaiac impregnated slide test for occult blood in the stool was performed in 221 screenees. Of these only 10 were positive (4.5%) compared with the average of 1% positive tests in low-risk groups.

Antigens, Neoplasm

Phagocytosis by receptors for C3b (CR1), iC3b (CR3), and IgG (Fc) on human peritoneal macrophages.

Human peritoneal macrophages (HPM) obtained via laparoscopy were examined for the presence and functional capacity of complement and Fc receptors. Between 5 and 20 ml of peritoneal fluid containing 1-2 X 10(6) macrophages/ml was available for each study. Macrophages made up 80-95% of the cells in the fluid. Fc and C3 receptors on HPM were characterized by rosette formation with, and phagocytosis of, IgG- and C3-coated sheep erythrocytes (E). ElgG were bound by 82% and ingested by 63% of HPM, with 4-15 E ingested/HPM. The HPM formed rosettes with EC3b (56%) and EC3bi (71%) but not EC3d,g or EC3d. Antibodies to complement receptors type 1 (CR1) and type 3 (CR3) inhibited rosette formation with EC3b and EC3bi, respectively, indicating that HPM possessed separate and distinct receptors for the C3b and iC3b ligands. In 60% of the samples studied, HPM demonstrated the ability to ingest both EC3b and EC3bi, as well as ElgG. Because of the heterogeneous nature of the cells obtained in peritoneal fluid, due to their progressive change from monocytelike cells into mature macrophages, HPM were separated by 1 g velocity sedimentation into fractions of increasing maturity. They were then examined for phagocytosis via Fc and complement receptors. Fc receptor mediated phagocytosis occurred throughout the monocyte-to-macrophage maturation sequence, while the ability of HPM to ingest via CR1 and CR3 was maturation dependent, with ingestion via CR3 occurring before CR1, in a manner analogous to in vitro differentiation of monocyte-derived macrophages.

Erythrocytes