摘要:

Ia+ cells of bone marrow origin were studied in the thymus of normal and bone marrow‐reconstituted radiation chimeras of rats and characterized on morphology and acid phosphatase (APh)‐ and la‐staining pattern in‐vivo and in‐ vitro, In‐vivo, the majority of the bone marrow‐derived la+ ceils were present in the medulla. They were large, had cell processes extending between surrounding thymocytes, and frequently weak APh activity. In‐vitro, the la staining was demonstrated on the cell surface in variable intensity, la + cells showed a frayed outline with cell processes between adherent thymocytes and had weak cytoplasmic APh activity, frequently in a central spot. They had an elongated, usually invaginated, nucleus and a rather pale cytoplasm, in which Birbeck granules sometimes were observed. The characteristics of the bone marrow‐ derived la + cells demonstrate these cells are an equivalent of the interdigitating cells present in thymus medulla. They distinguish themselves from a population of la‐, strongly APh+ macrophages predominantly localized in the cortex, and from the la +, APh ‐ thymic reticular epithelial cells.

ISSN:0741-5400    

DOI:10.1002/jlb.36.5.561

出版商:Wiley    

年代:1984

数据来源: WILEY

摘要:

The degradation of soluble immune complexes (ICx) and stable soluble immunoglobulin aggregates was studied in vitro. To obtain insight into the capacity of phagocytes from different organs to degrade soluble ICx we studied monocytes, peritoneal macrophages, and Kupffer cells. Peritoneal macrophages and Kupffer cells degrade similar amounts of aggregated guinea pig lgG2 (AlgG) and ICx per cell. Monocytes were at least ten times less effective than peritoneal macrophages and Kupffer cells. The presence of normal guinea pig serum as a source of complement enhanced the degradation of ICx and AlgG by peritoneal macrophages and monocytes. There was, however, a diminished degradation of ICx and AlgG by freshly isolated Kupffer cells in the presence of complement. After culturing of the Kupffer cells for 40 hours, there was an increase in the density of C3b receptors and a concomitant reversal of inhibition of AlgG degradation in the presence of complement. It can be concluded from the present experiments that the capacities of peritoneal macrophages and Kupffer cells to degrade soluble ICx and AlgG are comparable and that monocytes are much less active than peritoneal macrophages and Kupffer cells.

ISSN:0741-5400    

DOI:10.1002/jlb.36.5.569

出版商:Wiley    

年代:1984

数据来源: WILEY

摘要:

In previous studies, macrophages have been shown to influence in vitro colony formation by erythroid progenitors (CFU‐E). To determine whether the origin of the macrophages influences their effects on in vitro erythropoiesis, plasma clot cultures of CFU‐E were grown over adherent monolayers of macrophages from various strains of mice. Macrophages were separated from the plasma clot cultures by an intermediary layer of agar. Normal resident macrophages from BALB/c mice and several other inbred strains had no effect on CFU‐E colony formation. In contrast, macrophages from a strain of mice termed BWF, which were originally identified as BALB/c but subsequently shown to be a hybrid of BALB/c and outbred CFW mice, strongly inhibited erythroid colony formation. Resident macrophages from the parental outbred CFW mice inhibited CFU‐E in 50% of the animals tested. Inhibition was obtained in both homologous and autologous macrophage‐CFU‐E combinations and was therefore not due to histoincompatibility effects, nor was inhibition related to prostaglandin production by the macrophages or to effects on erythropoietin levels in the assay system. The results demonstrate that normal resident macrophages influence in vitro erythropoiesis and that the effects observed are dependent on the genotype of the mice from which the cells are derived.

ISSN:0741-5400    

DOI:10.1002/jlb.36.5.581

出版商:Wiley    

年代:1984

数据来源: WILEY

摘要:

Various substances, including lysosomal enzymes, are produced by Kupffer cells and other macrophages; their release has been implicated in the toxic response to endotoxins. C3H/HeJ mice exhibit little or no response to doses of endotoxin that are lethal in syngeneic C3HeB/FeJ mice. To explore the nature of this deficient response, the Kupffer cells of these mice were studied using in vivo microscopic as well as histochemical and electron microscopical methods. In vivo, the rate of phagocytosis of single 0.8μm latex particles was measured in individual Kupffer cells as was the number of phagocytic cells per microscopic field. Frozen sections of livers were stained for a variety of lysosomal enzymes and liver specimens also were processed for electron microscopy. In comparison to the endotoxin‐sensitive C3HeB/FeJ mice, the livers of the C3H/HeJ mice contained 60% fewer Kupffer cells that phagocytosed latex. However, the rate of phagocytosis by these cells was not statistically different and ranged from 19–26 sec. The volume density of acid‐phosphatase‐positive Kupffer cells was 40% less in the C3H/HeJ mice. Similar differences were observed with other lysosomal enzymes including cathepsins B and H and dipeptidyl peptidases I and II. However, light and electron microscopy revealed a relatively normal number of Kupffer cells in livers stained for peroxidase, a nonlysosomal enzyme. The results suggest that the insensitivity of C3H/HeJ mice to endotoxin may be related in part to a lysosomal enzyme deficiency and a paucity of phagocytic Kupffer cells in these animals.

ISSN:0741-5400    

DOI:10.1002/jlb.36.5.591

出版商:Wiley    

年代:1984

数据来源: WILEY

摘要:

The prominent role of plasma fibronectin (pFN) in the host defense system as an opsonin for gelatin (collagen)‐coated colloids has been established. In the present study we investigated the interaction of pFN and membrane isolates from cells devoid of collagen, as well as several tissues. In a liver slice assay system it was shown that subcellular membrane fractions from lung macrophages, peritoneal exudate cells, spleen, testes, and liver were able to competitively inhibit the pFN‐mediated uptake of125l‐gelatin coated latex beads (gLtx*) at low concentrations. Endocytosis of125l‐labeled membrane isolates by macrophage monolayers was also promoted by addition of pFN. In an attempt to characterize the membrane component(s) interacting with pFN, it was found that mild extraction procedure with 1 M KBr could release a significant amount of this inhibitory activity. Further studies demonstrated that the agent(s) responsible for inhibition of gLtx* uptake was heat sensitive, not altered by trypsin treatment, and did not contain actin, a protein known to interact with pFN. This work indicates that pFN interacts specifically with an as yet unknown membrane component(s) and that such interaction will promote clearance of cellular debris by macrophages. This suggests that pFN may be an important opsonin for the reticuloendothelial system in clearance of collagenous and noncollagenous cellular debris once they are exposed to interact

ISSN:0741-5400    

DOI:10.1002/jlb.36.5.601

出版商:Wiley    

年代:1984

数据来源: WILEY

摘要:

Exposure of lymphocytes from guinea pigs sensitized to keyhole limpet hemo‐ cyanin and of macrophages from nonsensitized animals to noncytotoxic doses of lidocaine (10−4to 10−6M) resulted in the inhibition of the production of macrophage migration inhibitory factor and of macrophage motility. The inhibition of both processes was related to the concentration of lidocaine in the medium. The effects of lidocaine, a membrane‐stabilizing drug, were apparently related to its ability to interact with the cell surface and cause changes in the surface ionic configuration of the cells, as determined by cell electrophoresis. The drug conferred permanent changes in the surface of lymphocytes at all concentrations tested, but the changes in the surface of macrophages induced in the presence of 10−5and 10−6M of the drug were reversible. The presence of noncytotoxic doses of lidocaine in the cellular environment resulted in significant changes in cellular functions that appeared to be related to the ability of the drug to interact with cell membranes in a manner determined by the specific surface properties of the cell.

ISSN:0741-5400    

DOI:10.1002/jlb.36.5.621

出版商:Wiley    

年代:1984

数据来源: WILEY

摘要:

The encapsulated coagulase‐negative strain of Staphylococcus simulans (strain 76) was inoculated into the mammary glands of lactating mice. In contrast to the coagulase‐positive encapsulated Staphylococcus aureus (strain M), which elicited a neutrophil response within 18 hr, strain 76 organisms multiplied in the glands but failed to elicit a neutrophil response for 3 days; they were then eliminated from the gland by 8 days. When strain 76 was inoculated into mice whose offspring had been removed 3 days earlier, a neutrophil response was induced within 18 hr and, although phagocytic ingestion was resisted for at least 42 hr, the organisms were eliminated from most glands within 5 days. Inoculation of a naturally occurring double‐stranded RNA (BRL 5907) into the mammary gland induced a macrophage infiltration of the alveolar lumen that was qualitatively similar to 3 days involution. Intramammary inoculation of strain 76 18 hr after BRL 5907 resulted in a neutrophil infiltration within 6 hr. In vitro, strain 76 stimulated the release of chemotactic factors for neutrophils from bovine mammary gland macrophages. The results suggest that the recruitment of neutrophils by strain 76 in the mammary gland of the mouse is mediated by macrophages.

ISSN:0741-5400    

DOI:10.1002/jlb.36.5.633

出版商:Wiley    

年代:1984

数据来源: WILEY

摘要:

The half‐life of an intravenously injected bolus of intralipid 20% was measured in normal rats in order to asess its relationship to reticuloendothelial system (RES) activity. Groups of animals were studied following various treatments, and the results compared to measurement of carbon clearance in similar groups. The RES effects of silica and C parvum were confirmed by the carbon clearance test, but no effect was seen on the half‐life of intralipid. Intralipid clearance was shortened by fasting and the administration of intravenous heparin, neither of which affected carbon clearance. It is concluded that the intravenous intralipid test has no place in the asessment of RES function.

ISSN:0741-5400    

DOI:10.1002/jlb.36.5.647

出版商:Wiley    

年代:1984

数据来源: WILEY

ISSN:0741-5400    

DOI:10.1002/jlb.36.5.651

出版商:Wiley    

年代:1984

数据来源: WILEY

摘要:

The Reticuloendothelial Society and the Biological Response Modifiers Program of the National Cancer Institute have organized and co‐sponsored this workshop.

ISSN:0741-5400    

DOI:10.1002/jlb.36.5.659

出版商:Wiley    

年代:1984

数据来源: WILEY