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Biomedical subjects

D P Fine

Publications and source records attributed to D P Fine.

At least 37 records · Page 2Linked to original sources
PubMed1983

Chronic relapsing colitis due to Strongyloides stercoralis.

The small intestine is the usual site of chronic infection with Strongyloides stercoralis. Colonic involvement has generally been seen in the hyperinfection syndrome in immunosuppressed individuals. We describe an immunologically competent female who underwent multiple abdominal operations over a 5-year period for hematochezia and diffuse abdominal pain of obscure etiology. Eosinophilia had been present but never investigated until 1981, at which time stool examination revealed S. stercoralis larvae. Pathological specimens from operations in 1977 and 1981 demonstrated extensive colonic wall invasion with filariform larvae consistent with S. stercoralis. Involvement of other organs was never documented. We believe this case is consistent with chronic colitis due to strongyloidiasis. This entity has not been previously described, and expands the spectrum of this disease.

Adolescent↗
PubMed1981

Local heat urticaria/angioedema: evidence for histamine release without complement activation.

A 42-yr-old white woman reported onset in 1976 of local pruritus, burning, erythema, and edema within minutes after exposure in heat. With more extensive exposure, she occasionally had transient headaches and nausea. In order to investigate the etiology of this condition, her forearm was exposed to water at 44 degree C for 4 min. Within a few minutes, a lesion identical to her spontaneously induced ones developed only at the area exposed to heat. Samples of venous blood from this extremity demonstrated a transient rise in plasma histamine levels without any significant change in serum hemolytic complement activity or in C3, C4, or factor B. These findings suggest that this rare syndrome involves local activation of mediator release from mast cells, without participation of the complement system.

Adult↗
PubMed1981

Opsonization of pneumococci. II. Metabolic effects of a "third" human serum activity that mediates intracellular killing.

We investigated the mechanisms by which a serum activity, neither complement nor immunoglobulin, mediates killing of pneumococci by polymorphonuclear leukocytes (PMN). Electron microscopy revealed type 25 pneumococci to be within PMN when incubated in normal serum, in serum absorbed twice at 0 degrees C with type 25 pneumococci, or in absorbed plus heat-inactivated serum. Uptake of radiolabeled bacteria, and activation of oxygen consumption and of the hexose monophosphate shunt by PMN with pneumococci, were similar in normal serum, absorbed serum, or the combination of absorbed and heat-activated serum. Reduction of nitroblue tetrazolium (NBT) and of cytochrome c by PMN in the presence of type 25 pneumococci and absorbed serum, with or without heat-inactivated serum were one-third and one-half, respectively, of those in normal serum. Likewise, protein iodination was one-half that in normal serum. Reduction of cytochrome c by cytochalasin B-treated PMN was the same in normal, absorbed, or absorbed plus heat-inactivated serum. Furthermore, release of beta-glucuronidase from PMN after ingestion of pneumococci in 10% normal, absorbed, or absorbed plus heat-inactivated serum was identical. These data indicate that the "third" serum activity is not necessary for attachment of pneumococci to or ingestion by PMN, nor is it necessary for stimulation of the plasma membrane oxidase. Rather, it functions somehow in intracellular killing.

Absorption↗
PubMed1981

Trypan blue inhibition of complement receptor function on various cells.

Trypan blue has previously been shown to inhibit complement-mediated phagocytosis by interaction with the C3 receptor but not with the Fc receptor. In studies reported here, trypan blue inhibited EAC3 rosette formation with human polymorphonuclear leucocytes (PMN) and mononuclear cells, rabbit alveolar macrophages (AM) and peritoneal PMN, and guinea-pig spleen cells. Trypan blue also inhibited C3-mediated bacterial adherence to the same receptor-bearing cells and to human glomerular cells. EAC3bi rosette formation was also inhibited, but EAC3d rosettes were not detected in our assay system. Although the precise molecular nature of C3b fragments deposited on antibody-sensitized erythrocytes has not been fully determined, trypan blue probably inhibits all C3 receptors from different species and may prove useful in vivo and in vitro for the definition of C3-receptor function in various aspects of the immune response.

Animals↗
PubMed1980

The role of opsonins in recovery from experimental pneumococcal pneumonia.

The opsonization of type 1 and type 25 pneumococci in the rabbit lung early in the course of experimental pneumonia was studied. Bacteria washed from the lungs of animals with type 1 pneumonia were coated with IgG, IgA, and complement within 24 hr of infection; these bacteria were not phagocytized. Both type 1 and type 25 pneumococci, when incubatd in concentrates of nonimmune bronchopulmonary washings (BPC), adsorbed IgG, IgA, and C3, but neither type of pneumococci was opsonized. Killing of pneumococci by surface phagocytosis, with or without the use of nonimmune BPC, was not demonstrated. When nonimmune serum was used, opsonization of type 25 pneumococci depended on the presence of heat-labile adsorbable factors, and when immune serum and immune BPC were used, opsonization was dependent on adsorbable factors. Depletion of serum complement with cobra venom factor before infection with type 25 pneumococci resulted in severe bacteremic pneumonia in the rabbit, but immunization before complement depletion allowed animals to clear type 25 pneumococci from the blood and lungs within 24 hr. Thus, opsonization is required for efficient clearance of pneumococci from the lung, and in the nonimmune animal, complement is also required for clearance.

Animals↗
PubMed1980

Complement-independent adherence of Escherichia coli to complement receptors in vitro.

We studied adherence to human cells by a strain of Escherichia coli. Adherence to erythrocytes was assessed directly by phase-contrast microscopy and indirectly by hemagglutination; adherence to peripheral blood leukocytes, using radiolabeled bacteria and subsequent determination of leukocyte-associated radioactivity; and adherence to renal glomeruli, by microscopy of fluoresceinated bacteria and of Gram-stained nonfluoresceinated bacteria. In serum-free systems, E. coli of this strain adhered to human erythrocytes, which have surface receptors for the third component of complement (C3), but not to erythrocytes from species lacking this receptor. 1 mM trypan blue, a reagent that inhibits complement receptor function, inhibited adherence to human erythrocytes, as well as adherence to leukocytes and glomeruli. Preincubation of erythrocytes and leukocytes with complement-coated zymosan particles partially blocked subsequent bacterial adherence. Incubation of human erythrocytes with aging human serum, with trypsin-cleaved C3, or with C3 cleaved by the classical pathway convertase (EAC142)-all of which treatments deposited C3 on the erythrocyte surface, presumably at C3 receptors-inhibited subsequent E. coli adherence. Finally, incubation of E. coli with rabbit antiserum to human C3 blocked adherence to erythrocytes.Bacterial hemagglutination and erythrocyte adherence were not inhibited by mannose in concentrations up to 2.5%. And this strain of E. coli did not adhere to or agglutinate guinea pig erythrocytes, the usual test particle used for demonstration of common pili. Finally, electron microscopy of adherent bacteria showed only rare surface pili. In contrast, adherence to and agglutination of guinea pig erythrocytes by a stock piliated E. coli was inhibited by mannose but not by trypan blue. We conclude that organisms of this strain of E. coli adhere to human erythrocytes, leukocytes, and glomeruli at complement receptors. Complement is not required for this interaction. Adherence apparently involves a C3-like structure on the bacterial surface, but bacterial surface pili play no role. The physiological or pathological role of this adherence is not apparent, but study of this phenomenon may elucidate functions of complement receptors on various cells.

Animals↗
PubMed1978

Evidence for quantitative variability of bacterial opsonic requirements.

We studied human serum opsonins by using combinations of heat inactivation and chelation to inhibit complement, adsorption to remove antibody, and trypan blue to inactivate the C3 receptor of human polymorphonuclear leukocytes. Streptococcus pneumoniae, serotype 25, required both complement and immunoglobulin for opsonization, even though that strain activated the alternative complement pathway. Both strains of Escherichia coli required antibody and complement, but varied in the degree of dependence on the C3 opsonin, since trypan blue moderately inhibited the killing of E. coli-1 and markedly inhibited the killing of E. coli-2. Serratia marcescens was opsonized in heat-inactivated serum (limited complement) or serum absorbed at 0 degrees C with S. marcescens (limited antibody), but depended on the C3 receptor in absorbed serum. S. marcescens activated the alternative pathway. Thus, opsonic requirements varied with the availability of opsonins. Requirements for bacterial opsonization vary with species and strains within species, perhaps reflecting quantitative relationships among alternative and classical pathway activation of C3, efficiency of adsorption of C3 or immunoglobulin G to bacterial surfaces, and efficiency of attachment of these ligands to polymorphonuclear leukocyte receptors. Furthermore, although not always sufficient for opsonization, the C3 opsonin (activated through either the classical or alternative pathway) appears necessary for effective phagocytosis and killing of all strains studied.

Antibodies, Bacterial↗
PubMed1978

Trypan blue inhibits complement-mediated phagocytosis by human polymorphonuclear leukocytes.

Trypan blue completely inhibited attachment of human polymorphonuclear leukocytes (PMN) to Sepharose beads coated with C3 ant to sheep erythrocytes coated with IgM plus C3, but it did not inhibit attachment to erythrocytes coated with IgG. These results suggested that trypan blue inhibited C-mediated attachment to PMN membranes. Corroborative studies were performed with a strain of Staphylococcus aureus that requires C but not antibody, for opsonization and that activates the alternative pathway. Trypan blue was not toxic to PMN or bacteria, did nto interfere with immunoglobulin or C interactions, and did not affect attachment of opsonins to bacteria. However, the dye impaired PMN killing of S. aureus in normal nonimmune serum by inhibiting bacterial attachment to and ingestion by PMN. Further evidence that the inhibition was at the C3 receptor level came from the observations that, 1) once staphylococci were attached to PMN at either 37 degrees C or 0 degrees C, addition of trypan blue did not inhibit killing; and 2) trypan blue inhibited killing of bacteria opsonized with serum sufficient in C but previously absorbed at 0 degrees C with the same strain of organism to deplete specific antibody. Further studies with this agent may elucidate the roles of opsonic receptors on human phagocytes.

Cell Adhesion↗
PubMed1977

Studies of the coagulation and complement systems during experimental Rocky Mountain spotted fever in rhesus monkeys.

We studied the coagulation and complement systems during Rocky Mountain spotted fever in Macaca mulatta experimentally infected with Rickettsia rickettsii. Ninety-one percent of monkeys infected intravenously with a high dose (10(6) plaque-forming units [pfu]) and 56% of monkeys infected with low doses (10(-1)-10(2) pfu) of R. rickettsii died after two to four days of illness. With the onset of fever and rickettsemia, animals developed hyperfibrinogenemia, mild thrombocytopenia, prolonged prothrombin and activated thromboplastin times, and increased serum fibrin/fibrinogen degradation products (FDP). Rickettsemia, thrombocytopenia, and FDP were greater in fatally ill monkeys than in survivors. Hemolytic titers of the second and third components of complement were not depressed except in a single surviving monkey that developed peripheral gangrenous ecchymoses at a time when both rickettsemia and agglutinating antibody were present. Thus, although activation and consumption of complement may occur during Rocky Mountain spotted fever, the hemostatic disturbances in fulminant infections seem to be a direct effect of the infectious vasculitis.

Animals↗
PubMed1977

Comparison of ethyleneglycoltetraacetic acid and its magnesium salt as reagents for studying alternative complement pathway function.

The divalent cation chelators, ethyleneglycoltetraacetic acid (EGTA) and its magnesium salt, MgEGTA, were compared in studies of alternative complement pathway function. EGTA (0.01 M) inhibited both the rate and the amount of complement activation by zymosan whether compared to nonchelated serum or to serum chelated with MgEGTA (0.01 M). The rate of alternative pathway activation by zymosan was slightly slower in MgEGTA-chelated serum than in nonchelated serum, but the overall amount of complement consumed by a given amount of zymosan was not decreased. MgEGTA chelation spontaneously activated the alternative pathway, as reflected by lysis of erythrocytes from a patient with paroxysmal nocturnal hemoglobinuria. No evidence could be found that MgEGTA either spontaneously activated C2 or facilitated zymosan activation of C2. Suggested guidelines for the use of these chelators are advanced.

Adult↗
PubMed1977

Disseminated intravascular coagulopathy during experimental pneumococcal sepsis: studies in normal and asplenic rhesus monkeys.

Disseminated intravascular coagulation (DIC) was induced in both normal and asplenic rhesus monkeys by intravenous challenge with Streptococcus pneumoniae. Our observations in the infected monkeys have led us to conclude that (1) pneumococcal capsular polysaccharide (PCP), immune complexes and complement may not have primary roles in the initiation of DIC; (2) intact pneumococci may be catalysts for the development of DIC; (3) the initial event in DIC may be activation of Hageman factor; and (4) evidence of activation of Hageman factor-dependent systems is present regardless of severity of infection.

Animals↗
PubMed1976

Functional and morphologic changes during experimental Rocky Mountain spotted fever in guinea pigs.

Experimental Rocky Mountain spotted fever was studied in guinea pigs following intraperitoneal inoculation of 10(7) Rickettsia rickettsii. After a 2-day incubation period, animals developed fever, progressive emaciation, and scrotal swelling with necrosis. Vasculitis, with increased small vessel permeability for colloidal carbon, was evident in cremaster muscles as early as 1 day after inoculation. Inflammatory changes in vessels became progressively more severe as numbers of circulating rickettsiae increased. Thrombosis and vascular occlusion were first evident on day 4. Mild thrombocytopenia developed, coinciding with the development of vasculitis, and preceding the appearance of either fibrin-split products in blood or thrombi in vessels. Rickettsiae were first detected in blood on day 2; peak rickettsemia occurred on days 5 to 8. Rickettsiae were demonstrated in inflamed vessels on day 5 and later, but not at earlier stages. Serum lysozyme concentration was moderately elevated and hemolytic complement was moderately depressed throughout the illness. Agglutinating antibody was present in low titers on days 3 to 10. Antibody titers increased on days 12 to 16 after the rickettsiae were cleared from blood. These studies indicate that vasculitis seen early in the course of Rocky Mountain spotted fever is the result of rickettsial infection, but is not dependent on the presence of rickettsiae in endothelial cells or other blood vessel components.

Agglutination Tests↗
PubMed1975

Pneumococcal type-associated variability in alternate complement pathway activation.

Opsonization of Streptococcus pneumoniae may be mediated by the alternate complement pathway. To study the importance of this interaction to human disease, complement consumption by pneumococci of various serotypes was measured in humwn serum chelated with ethyleneglycoltraacetic acid, a substance that blocks the classic but not the alternate complement pathwway. Serotype I, in contrast to all other types studied, lacked ability to consume complement in this system. The ability for serotypes III, IV, and VIII to activate the alternate pathway could be eliminated by prior serum absorption at O C with they type in question, a condition that would remove antibody but not complement. Types VII, XII, XIV, and XXV readily activated the alternate pathway in unabsorbed and absorbed sera. Differences could not be related to properties of the capsules. It was concluded that types I, III, IV, and VIII lack intrinsic ability to activate and thus be opsonized by the alternate complement pathway, although types III, IV, and VIII can do so in concert with specific antibody. The fact that these same types are especially prominent in human disease suggests that the ability to evade opsonization by the alternate complement pathway in pre-antibody phases of infection may be a virulence factor in pneumococci.

Antigen-Antibody Complex↗
PubMed1973

Schistosoma mansoni infection in mice depleted of thymus-dependent lymphocytes. I. Eosinophilia and immunologic responses to a schistosomal egg preparation.

Chronic murine schistosomiasis is characterized by a host cell-mediated immune response to schistosomal egg antigens. This response is manifested in vitro by lymphocyte blastogenic reactivity to a soluble schistosomal egg antigen preparation (SEA) and in vivo by delayed dermal hypersensitivity to SEA. In addition, mice develop reaginic, agglutinating, and early dermal reactive antibodies to SEA and a characteristic pattern of peripheral blood eosinophilia. In this study, depletion of thymus-dependent lymphocytes abolished the anti-SEA lymphocyte blastogenic response and delayed dermal reactivity, reaginic antibody response and the major peak of peripheral blood eosinophilia, which in normal mice occurs at the same time as SEA-induced blastogenesis. Antibodies mediating the early dermal reaction to SEA and agglutinins for SEA-coated particles were not inhibited by T-lymphocyte depletion. The experimental group did not develop the normally observed granulomatous response, but rather suffered focal hepatic and mucosal liquefactive necrosis, bacteremia and accelerated mortality.

Agglutination↗
PubMed1973

Schistosoma mansoni infection in mice depleted of thymus-dependent lymphocytes. II. Pathology and altered pathogenesis.

Murine schistosomiasis mansoni is a more rapidly fatal disease in hosts deprived of their cell-mediated immune capabilities. Analysis of the histopathology of the disease under these circumstances indicates that rather than the hepatic granulomata characteristic of the normal infection, the host develops zones of liquefactive necrosis in the liver and intestinal mucosa. These lesions are associated with severe parenchymal cell destruction. Such hepatic and mucosal damage, with subsequent toxemia and septicemia, is presumed central to the altered course of the disease.

Animals↗