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Biomedical subjects

R Snyderman

Publications and source records attributed to R Snyderman.

At least 217 records · Page 12Linked to original sources
PubMed1975

Defective monocyte function in patients with genitourinary carcinoma.

An assay allowing quantitation of monocyte function, i.e., chemotaxis, was used to study the activity of monocytes in patients with neoplasms of the urinary tract. Twenty-four subjects with various stages of renal carcinoma exhibited a mean chemotactic defect of 34% (P less than 0.005) as compared to normal controls and patients hospitalized with nonneoplastic diseases. Twelve persons with transitional cell carcinoma of the bladder had a 29.8% (P less than 0.01) mean chemotactic defect as compared to the controls. There was no correlation between tumor stage and degree of chemotactic defect;--J Natl Cancer Inst 55: 1047-1054, 1975.

Adenocarcinoma↗
PubMed1975

Interaction of complex polysaccharides with the complement system: effect of calcium depletion on terminal component consumption.

Complex polysaccharides and lipopolysaccharides can activate the terminal components of complement by either the classical (antibody, C1, C4, and C2) or alternative complement pathways, but the relative importance of either pathway for terminal component consumption in normal serum is poorly understood. Since classical complement pathway function requires both calcium and magnesium ions, whereas the alternative pathway requires only magnesium ions, selective chelation of calcium ions in serum can be used to block the classical complement pathway while leaving the alternative pathway intact. In these studies, ethyleneglycol-bis-(beta-aminoethyl ether)N, N-tetraacetic acid, a potent chelator or calcium, was used to block the classical complement pathway in normal guinea pig serum. Consumption of the terminal complement components by endotoxin, inulin, and zymosan in such serum was strikingly depressed when compared to serum containing an intact classical complement pathway. These studies demonstrate that in normal serum, both the classical and alternative complement pathways participate in the consumption of the terminal complement components by complex polysaccharides and lipopolysaccharides.

Animals↗
PubMed1975

Quantification of mouse macrophage chemotaxis in vitro: role of C5 for the production of chemotactic activity.

Delineation of the mechanisms of macrophage accumulation at local tissue sites will further our understanding of immunologically mediated host resistance to infectious and neoplastic diseases. Since mice are frequently used for the study of immune function, we developed a method for the quantification of mouse macrophage chemotaxis in vitro. By this method it was found that the fifth component of complement is necessary for the production of chemotactic activity in mouse serum by inflammatory agents such as endotoxin or aggregated gamma globulin. The majority of macrophage chemotactic activity produced by these agents in mouse serum can be attributed to a low-molecular-weight (ca. 15,000) chemotactic factor. The data suggest that this factor is the biologically active cleavage product of the fifth component of complement, C5a.

Animals↗
PubMed1975

Characterization of chemotactic activity produced in vivo by a cell-mediated immune reaction in the guinea pig.

A system that allows repeated sampling of peritoneal fluid at various time intervals has been adapted to study mechanisms of leukocyte accumulation in vivo. Application of this technique in guinea pigs exhibiting delayed hypersensitivity (DH) to horse radish peroxidase (HRPO) has allowed characterization of some events after i.p.challenge with the sensitizing antigen. Within 24 hr of the administration of HRPO i.p. to such animals there is a significant increase in the number of peritoneal macrophages and in the chemotactic activity (CTX) for macrophages in the sampled peritoneal fluid. At 48 and 72 hr the CTX returns to the pre-challenge level and i.p. macrophages appear to be actively phagocytic. Molecular sieve chromatograms of concentrated peritoneal fluid obtained 24 hr after i.p. challenge with HRPO and of supernatants derived from immune spleen cells cultured in the presence of HRPO in the presence of HRPO in vitro revealed that the major portion of CTX for homologous macrophages eluted in the region of the 12,500 dalton protein marker. The partially purified CTX obtained from peritoneal fluid and supernatants of spleen cell cultures was heat stable (56 degrees C for 30 min) and was destroyed by trypsin digestion. These data demonstrate that a chemotactic factor (LDCF) obtained in vitro, is present in vivo at the site of a cell-mediated immune reaction. Moreover, these observations demonstrate the feasibility of studying the kinetics of leukocyte accumulation and the production of mediators of inflammation at the site of well defined immunologic reactions in vivo.

Animals↗
PubMed1974

Production of chemotactic factor and lymphotoxin by human leukocytes stimulated with Herpes simplex virus.

Peripheral blood leukocytes (PBL) of 41 subjects were tested for their ability to be stimulated by herpes simplex virus antigens as measured by [(3)H]thymidine incorporation and lymphokine production (i.e., lymphocyte-derived chemotactic factor and lymphotoxin). The PBL of seronegative subjects failed to respond to viral antigens as measured by stimulation or lymphokine production. In contrast, PBL from seropositive subjects without clinical lesions of herpes labialis were stimulated by herpes simplex virus antigens and produced lymphokines. PBL from seropositive patients with clinical lesions of herpes labialis also produced lymphokines, but [(3)H]thymidine incorporation was slightly depressed. These findings suggest that lymphocytes from patients with a recent herpes simplex virus infection may respond less vigorously to in vitro stimulation by herpes antigens, but our study fails to show any basic defect in the responsiveness of the lymphocytes to account for recurrent herpetic episodes.

Animals↗
PubMed1974

Abnormalities of chemotactic lymphokine synthesis and mononuclear leukocyte chemotaxis in Wiskott-Aldrich syndrome.

Wiskott-Aldrich syndrome is characterized by numerous humoral and cellular immune abnormalities including anergy, defective antibody production, and increased immunoglobulin synthesis. To define better the mechanisms of defective cellular immunity in this disorder, lymphoproliferative responses, lymphokine production, and the chemotactic responsiveness of mononuclear leukocytes (MNL) from patients with Wiskott-Aldrich syndrome were quantitated. Peripheral blood lymphocytes from these patients produced normal amounts of a lymphocyte-derived chemotactic factor (LDCF); however, their lymphoproliferative responses were frequently depressed, particularly to antigenic stimuli. In the absence of exogenous antigens or mitogens, lymphocytes from patients with Wiskott-Aldrich syndrome produced significantly more LDCF than unstimulated normal lymphocytes. In fact, this unstimulated LDCF production frequently approached the level produced by normal cells only after antigen or mitogen stimulation. The chemotactic responsiveness of MNL from Wiskott-Aldrich syndrome patients was impaired, particularly in those patients with the highest rates of unstimulated LDCF production. Furthermore, normal MNL chemotactic responsiveness could be impaired by preincubation of these cells in either LDCF or plasma from Wiskott-Aldrich syndrome patients. These observations suggest that the regulation of LDCF synthesis is abnormal in Wiskott-Aldrich syndrome, and that a humoral chemotactic inhibitor, perhaps LDCF, "deactivates" the circulating MNL of patients with this syndrome.

Antigens↗
PubMed1972

Bone marrow-derived lymphoid cells (B cells): functional depletion with cobra factor and fresh serum.

Treatment of rat spleen cells with cobra factor and fresh rat serum provided a simple, rapid means of functionally eliminating complement receptor lymphocytes. Cells able to differentiate into plaque-forming cells in a syngeneic, irradiated host were diminished, but cells able to induce a graft-versus-host reaction were not diminished. There was no effect on plaque-forming cells from an immune spleen.

Animals↗