Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Macrophages, Peritoneal”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1985

Lysosomal enzyme activity in pulmonary alveolar macrophages, peritoneal macrophages, and blood mononuclear leukocytes in the hypothyroid rat.

Chronic hypothyroidism can result in an increased susceptibility to severe pulmonary or genitourinary tract infections. We postulate that decreased lysosomal activity in the pulmonary alveolar macrophage (PAM), peritoneal macrophage, and mononuclear leukocyte may be a factor which results in the impaired response to infections in hypothyrosis. In this study rats underwent total thyroidectomy and had their PAMs, peritoneal macrophages, and mononuclear leukocytes analyzed after 4, 8, and 12 weeks. The total lysosomal activity (postnuclear homogenate + lysosomal-rich cell fraction) of PAMs was 50% of age-matched controls. Peritoneal macrophage lysosomal enzyme activity was 25-30% of control activity. In separate experiments, rats were administered physiologic replacement of triiodothyronine (T3) 8 weeks after thyroidectomy. This resulted in PAM and peritoneal macrophage lysosomal enzyme activity similar to control activity. Mononuclear leukocyte lysosomal enzyme activity from hypothyroid rats showed decreases in only one of the three enzymes monitored (beta-glucuronidase). Hypothyroidism did result in a decrease in total number of mononuclear leukocytes harvested per animal. Administration of T3 resulted in mononuclear leukocyte beta-glucuronidase activity similar to euthyroid rats (44 +/- 8 U/mg protein vs 42 +/- 3 U/mg protein). In summary, hypothyroidism in the rat results in decreases in subcellular lysosomal enzyme activity in PAMs, peritoneal macrophages, and mononuclear leukocytes.

Animals↗
PubMed1988

Antigen presentation to T cell lines and clones by peritoneal macrophages, peritoneal B cells and antigen-specific B cell hybridomas.

The antigen presenting cell (APC) activity of uninduced, resident peritoneal macrophages and B cells was compared to that of antigen-specific B cell hybridomas by measuring proliferative responses of antigen-specific, MHC-restricted T cell clones. The results demonstrate that peritoneal macrophages and B cells are much more efficient APC than irradiated splenic filler cells, and that unirradiated B cells were as good as, if not better than, macrophages. Both B cells and macrophages can be pulsed with antigen, although pulsed B cells were always found to be more efficient than pulsed macrophages. However, the APC activity of B cells was exquisitely sensitive to irradiation. The relative contribution of macrophages and B cells to the APC activity of mixed populations was easily distinguished by complement dependent lysis with monoclonal antibodies specific for unique differentiation antigens expressed by these cells. Normal peritoneal macrophages and B cells present the synthetic terpolymer of L-glutamic acid60-L-alanine30-L-tyrosine10 (GAT) to GAT-specific T cells clones and beef insulin to insulin-specific T cell lines nonspecifically. The APC activity of antigen-specific B cells was also examined by using novel GAT-specific, nonsecretor B cell hybridomas produced by fusing GAT-primed spleen cells to the HAT sensitive Balb/c lymphoma, M12.4.5. The hybridomas selected for these studies were GAT-specific, sIg+, Ia+ cells. These hybridomas presented GAT to GAT-specific T cells more efficiently than heterogeneous B cells suggesting that interaction with surface Ig receptors facilitated the uptake and/or processing of antigen. GAT-specific B cell hybridomas, like normal B cells, presented soluble beef insulin to an insulin-specific T cell clone nonspecifically. However, after pulsing with antigen overnight, the GAT-specific B cell hybridoma could activate only GAT-specific T cells.

Animals↗
PubMed1996

Changes in the expression of adhesion molecules as peripheral blood monocytes differentiate into peritoneal macrophages.

Peritoneal macrophages, derived from peripheral blood monocytes, are the chief cellular defenders against invasion of the peritoneal cavity by infectious organisms. Monocyte migration into the peritoneal cavity depends upon a coordinated series of adhesive events, utilizing cell surface receptors known as adhesion molecules. In order to better understand the mechanisms of leucocyte infiltration of the peritoneum during peritonitis, we studied the relative expression of adhesion molecules on monocytes and peritoneal macrophages from patients on continuous ambulatory peritoneal dialysis (CAPD). Peripheral blood and spent peritoneal dialysis fluid were obtained from patients undergoing CAPD, and the level of expression of various adhesion molecules on the monocytes/macrophages analysed by flow cytometry using receptor-specific monoclonal antibodies. Monocytes were also purified from the peripheral blood of volunteer donors, cultured in vitro for varying periods, and analysed in the same manner. Consistent differences in expression of certain adhesion molecules were found between monocytes and peritoneal macrophages, and similar changes occurred on monocytes cultured in vitro. Concurrent infection had no clear effect. Several receptors (integrins alpha 4 beta 1, alpha 6 beta 1, alpha L beta 2 and alpha IIb beta 3, and platelet endothelial cell adhesion molecule-1) were significantly decreased on peritoneal macrophages, while only the integrin alpha v beta 5 increased. It is concluded that monocyte differentiation into peritoneal macrophages is accompanied by characteristic alterations in the adhesion molecule repertoire on the cell surface, emphasizing the different adhesive requirements of these two cell types.

Aged↗
PubMed1996

Endotoxin induced expression of tumour necrosis factor, tissue factor and plasminogen activator inhibitor activity by peritoneal macrophages.

Peritoneal fluid was collected aseptically from 30 healthy adult horses and 115 horses with acute gastrointestinal disease and supernatant was separated from cells by centrifugation followed by freezing until assayed for endotoxin and tumour necrosis factor activity. Peritoneal macrophages obtained from healthy horses were incubated in vitro for 3, 6, 12 or 24 h in the absence (media control) or presence of Escherichia coli 055:B5 endotoxin (final concentrations of 1, 10, 100 or 1000 ng/ml). Macrophages obtained from horses with acute gastrointestinal disease were incubated for 12 h in the absence (media control) or presence of 100 ng endotoxin/ml. At the conclusion of the incubation, macrophage supernatants were collected and frozen at -70 degrees C until analysed for tumour necrosis factor activity. Macrophage membranes were lysed and frozen at -70 degrees C until assayed for tissue factor and plasminogen activator inhibitor type 2 activity. Compared to cells incubated with media, incubation of macrophages, obtained from healthy horses, with endotoxin significantly increased tumour necrosis factor, tissue factor and plasminogen activator inhibitor type 2 activity. These increases were dependent on the endotoxin concentration and the duration of incubation. Compared to cells incubated with media alone, incubation of macrophages, obtained from horses with acute gastrointestinal disease with endotoxin, significantly increased tumour necrosis factor and tissue factor activity. Endotoxin induced tumour necrosis factor activity in vitro was significantly less for macrophages from horses with acute gastrointestinal disease, as compared to that produced by similarly treated cells obtained from healthy horses. For those horses with acute gastrointestinal disease, macrophages obtained from horses with either endotoxin or tumour necrosis factor activity in the peritoneal fluid supernatant had significantly less endotoxin induced tumour necrosis factor in vitro, as compared to similarly treated cells obtained from horses without endotoxin or tumour necrosis factor activity in the peritoneal fluid supernatant. The results of this study indicate that exposure of equine peritoneal macrophages to endotoxin results in a significant increase in tumour necrosis factor, tissue factor and plasminogen activator inhibitor type 2 activity. After in vitro exposure to endotoxin, there is significant down-regulation of inflammatory mediator production by peritoneal macrophages obtained from endotoxaemic horses. These results suggest that these macrophages may exhibit early endotoxin tolerance.

Acute Disease↗
PubMed1994

Respiratory burst activity associated with phagocytosis of Ehrlichia risticii by mouse peritoneal macrophages.

Peritoneal macrophages from two strains of mice, BALB/c and C3H/HeN, were analysed by flow cytometry for a respiratory burst associated with the phagocytosis of Ehrlichia risticii. Resident murine peritoneal macrophages failed to respond with a respiratory burst after phagocytosing E risticii. In contrast, mice previously infected with E risticii yielded peritoneal macrophages that did generate a respiratory burst on phagocytosing ehrlichiae.

Animals↗
PubMed1982

Microbicidal capacity and acid hydrolase content of human blood monocytes and peritoneal macrophages.

Peritoneal macrophages and peripheral blood monocytes were collected from healthy women undergoing laparoscopic tubal clipping. Monolayers of adherent cells were examined for protein content, intracellular levels of lysosomal enzymes, and antimicrobial capacity. Compared to blood monocytes, peritoneal macrophages were larger and less glass-adherent and were less capable of intracellular killing of Salmonella typhimurium. Acid hydrolase content, however, was increased in peritoneal macrophages. These data suggest that resting human tissue macrophages may be less active in certain respects than their blood precursors. One should then question whether the enhanced functions observed after long-term in vitro culture of blood monocytes-macrophages accurately reflect the in vivo status of their more differentiated descendants.

Female↗
PubMed1988

Enhancement of host resistance against Listeria infection by Lactobacillus casei: activation of liver macrophages and peritoneal macrophages by Lactobacillus casei.

The functions of liver macrophages and peritoneal macrophages obtained after injection of Lactobacillus casei were examined. Listericidal activity in vivo was enhanced in liver macrophages 13 days after L. casei injection but was somewhat suppressed in the macrophages 2 days after the injection. The listericidal activity in vitro was enhanced in peritoneal macrophages obtained 13 days after L. casei injection but was suppressed in cells obtained 2 days later. The PMA-triggered respiratory burst in the liver macrophages elicited by L. casei was higher than that of resident macrophages. Alkaline phosphodiesterase activity in the liver macrophages was decreased by L. casei injection, as was also the case with peritoneal macrophages. These observations indicate that L. casei augmented cellular functions of both liver and peritoneal macrophages.

Acid Phosphatase↗
PubMed1990

Proteoglycans synthesized in vitro by nude and normal mouse peritoneal macrophages.

Peritoneal macrophages from nude mice were found to be functionally similar to 'activated' macrophages from normal mice. The objective of the present study was to characterize the proteoglycans synthesized and secreted in vitro by peritoneal macrophages isolated from nude and normal Balb/c mice and to investigate the relationship between macrophage 'activation' and changes in the proteoglycan patterns. Macrophages obtained by peritoneal lavage were seeded in Petri dishes. After 2 h incubation at 37 degrees C, the adherent cells (macrophages) were exposed to [35S]sulphate for the biosynthetic labelling of proteoglycans. After incubation, the cell and medium fractions were collected and analysed for proteoglycans and glycosaminoglycans. The glycosaminoglycans were identified and characterized by a combination of agarose gel electrophoresis and enzymatic degradation with specific mucopolysaccharidases. It was shown that 3/4 of the total 35S-labelled glycosaminoglycans were in the extracellular compartment after 24-48 h. The macrophages synthesized dermatan sulphate (68%), chondroitin sulphate (7%) and heparan sulphate (25%). Both cell and medium fractions of normal and nude mouse macrophages contained glycosaminoglycans with the same ratios, although the nude mouse macrophages synthesized 2-fold less glycosaminoglycans than the normal mouse macrophages. Lower levels of 35S-proteoglycans were also obtained from in vitro 'activated' macrophages, but the ratios of dermatan sulphate:chondroitin sulphate: heparan sulphate were altered in these cells as compared to the control. Furthermore, all the 35S-macromolecules found in the extracellular compartment of nude and normal control cells were of proteoglycan nature, in contrast to the medium fractions of 'activated' macrophages, which contain both intact proteoglycans and 'free' glycosaminoglycan chains. These results indicate that, at least as regards the proteoglycans and glycosaminoglycans, the nude mouse macrophages are not identical to the 'activated' macrophages from normal mice.

Animals↗
PubMed2002

[The intervention effects of Angelica sinensis, Salvia miltiorrhiza and ligustrazine on peritoneal macrophages during peritoneal dialysis].

OBJECTIVE: To study the effect of Angelica sinensis, Salvia miltiorrhiza and Ligustrazine on function of peritoneal macrophages during peritoneal dialysis. METHODS: Peritoneal macrophages of mice were cultured in culture medium (control), peritoneal dialysate (PD), drugs contained PD containing Angelica, Salvia and Ligustrazine combined (PD-ASL) or separated (PD-A, PD-S, PD-L) with concentration of 2 micrograms/ml, 10 micrograms/ml and 100 micrograms/ml, separately for 24 hrs. The nitric oxide (NO) content, methyl thiazolyl tetrazolium (MTT) reducing capacity (MTT-RC) and phagocytosis capacity of macrophages were determined and compared. RESULTS: NO content and MTT-RC of macrophages cultured in PD group were significantly lower than those of the control (P < 0.01), as compared with those in drug contained PD groups, the NO content in the PD-L group and the MTT-RC in the PD-ASL group were higher significantly (P < 0.01). The phagocytosis capacity and NO content in the PD-ASL group were raised along with the increased concentration of drug in PD. CONCLUSION: Administering Chinese herbal medicine during peritoneal dialysis has important significance in improving the defense function of peritoneal macrophages, reducing the incidence of peritonitis and enhancing the therapeutic effect of peritoneal dialysis.

Angelica sinensis↗
PubMed2003

In vitro effects of hormones and autacoids on the hydrogen peroxide production and the morphology of endotoxin-activated rat peritoneal macrophages.

Peritoneal macrophages activated in vitro by endotoxin exhibit alterations of their capability to produce hydrogen peroxide after phorbol ester stimulation when certain hormones or autacoids are present in the culture medium. They also show morphological changes, mainly concerning cell size and nuclear appearance. Agents known to increase the intracellular levels of cyclic AMP, e.g. adrenalin and PGE2 reduce the hydrogen peroxide production. Insulin, which is known to decrease cyclic AMP levels, produces opposite results. Agents postulated to act via phospholipase C, e.g. serotonin, augment the production of hydrogen peroxide. We assume that this form of modulation may represent a regulatory mechanism of macrophage activation.

Animals↗
PubMed1993

Effect of ozone on metabolic activities of rat hepatocytes and mouse peritoneal macrophage.

Peritoneal macrophage from mice and isolated hepatocytes from rats were exposed to ozone. Ozone dosages were expressed as 0-5 nmol/10(6) cells. Measurements were made of viability, glucose transport, glutathione, glyceraldehyde-3-phosphate dehydrogenase, Mg-ATPase, Na/K-ATPase, and lipid synthesis. The most sensitive parameter was glyceraldehyde-3-phosphate dehydrogenase in the peritoneal macrophage. In hepatocytes both lipid synthesis and glyceraldehyde-3-phosphate dehydrogenase were sensitive to ozone. Effects on viability, glucose transport, Mg-ATPase, and Na/K-ATPase were small to negligible in both cell types.

Animals↗
PubMed1984

The effect of chemically induced oral carcinomas on peritoneal macrophages.

Peritoneal macrophages derived from normal and 7,12-dimethylbenz(a) anthracene (DMBA) treated, tumor bearing, Syrian hamsters were isolated and characterized. Peritoneal exudate cells from tumor bearing animals as compared to normal controls, showed that there was an increase in the total number of cells in the exudate. Specifically, there was an increase in macrophages as compared to other cell types. In terms of their cytochemical functions, these macrophages demonstrated a reduction in histochemical activity and functional capacity (Fc and C3 receptors), and cytotoxic specific lysis of DMBA squamous cell carcinoma tumor targets. There was also a significant increase in adherence and the number of resident macrophages as opposed to exudate macrophages of the peritoneal macrophages. These results seem to indicate an alteration in functional and cytochemical activity of macrophages derived from a hamster with a growing cheek pouch tumor induced by DMBA.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1985

Infectious-inflammatory changes in cyclic AMP levels and in their regulation by prostaglandins in human peritoneal macrophages.

Peritoneal macrophages of renal patients on continuous ambulatory peritoneal dialysis (CAPD) have been collected when CAPD was without complications, during an intercurrent infectious peritoneal inflammation and after recovery. Levels of cyclic AMP, release of cyclo-oxygenase metabolites, and responsiveness, in terms of cyclic AMP elevation, to either PGE2 or to DC-PGI2 (a stable analogue of PGI2) were examined. Peritoneal inflammation was associated with a sharp drop in cyclic AMP, which was restored after recovery. Production of TXA2, PGI2 and PGE2 parallelled the direction of changes in cyclic AMP levels, except, that release of PGE2 entirely failed to recover. Macrophages during the uncomplicated stage of CAPD proved more responsive to DC-PGI2 than to PGE2. During inflammation the cells displayed a marked increase in sensitivity towards PG stimulation. Improved sensitivity was more pronounced with PGE2 than with DC-PGI2 and so the original difference between responsiveness of the cells to the PGs was abolished. Several findings are compatible with the view that endogenous PGI2 governs the cyclic AMP levels in human non-inflammatory peritoneal macrophages. However, during infectious-inflammation the cells undergo changes which render a reduced production of PGI2 insufficient to explain the drop in cyclic AMP.

6-Ketoprostaglandin F1 alpha↗
PubMedDate not supplied

Androgen metabolism by human peritoneal macrophages.

Peritoneal macrophages (PM) were obtained by peritoneal dialysis from a regularly menstruating woman with renal failure. Macrophages (10(6) cells) were incubated at 37 degrees C for various periods of time (0-4 hr) in the presence of 14C-androstenedione or 3H-androstenedione and various concentrations (0.06-5.06 microM) of nonradiolabeled androstenedione (A). Testosterone (T) formed was purified by column chromatography, thin layer chromatography, acetylation, and recrystalization to constant 3H:14C ratios. The rate of formation of T from A was linear for nearly 2 hr. Conversion of A to T was linear at cell numbers in the incubation up to 1 x 10(6). The formation of T from A followed Michaelis-Menten kinetics at concentrations of A between 0.06 and 5.06 microM. The apparent Km of the enzyme for A was 0.75 microM and the Vmax for T formation from A in these cells was 33.9 pmol x hr-1 x 10(6) cells-1. PM were obtained also from normal patients (n = 6) and patients with endometriosis (n = 5). The rate of T synthesis from A in PM obtained from patients with endometriosis [527 +/- 263 pmol x hr-1 x 10(6) cells-1 (mean +/- SEM, n = 5)] was similar to that observed in PM obtained from normal patients [518 +/- 226 pmol x hr-1 x 10(6) cells-1 (mean +/- SEM, n = 6)]. We observed a near 30-fold variation in the rate of formation of T from A by PM obtained from different individuals (range 54 to 1580 pmol x hr-1 x 10(6) cells-1). Further study is needed to elucidate the physiologic significance of PM androgen metabolism and its relationship to reproductive function.

Adult↗
PubMed1997

Staphylococcal exoproducts down-regulate cyclooxygenase 1 and 2 in peritoneal macrophages.

Peritoneal macrophages (PMOs) are important components of the host defense against microbial infection in patients undergoing continuous ambulatory peritoneal dialysis (CAPD). Incubation of human PMOs with cell-free supernatant (BFS), prepared from Staphylococcus aureus, inhibited prostaglandin E2 (PGE2) and thromboxane B2 (TXB2) production. Slot-blot analysis of cyclooxygenase-1 (Cox-1) and Cox-2 demonstrated a decrease in both Cox-1 (29%) and, to a greater extent, Cox-2 (65%) protein expression after BFS stimulation. When competitive polymerase chain reaction (PCR) was used, the peak levels of Cox-1 and Cox-2 messenger ribonucleic acid (mRNA) in unstimulated PMOs were 0.304+/-0.13 pmol/L and 9.61+/-2.84 pmol/L (mean+/-SEM, n = 3), respectively. After exposure of samples to BFS for 30 minutes, the level of Cox-2 mRNA was reduced to 0.59+/-0.449 pmol/L (16-fold reduction, p < 0.05), and the level of Cox-1 mRNA was reduced to 0.02+/-0.002 pmol/L (15-fold reduction, p < 0.05). In contrast, these same PMOs showed an increased expression of IL-6 mRNA and increased secretion of IL-6 protein. These results indicate that prostaglandin production in PMOs is regulated by alterations in both immunoreactive Cox-1 and Cox-2. The down-regulation of Cox metabolism in these cells is primarily related to the delayed and depressed increase in the Cox-2 gene product.

Adolescent↗
PubMed1985

Divergent expression of cytotoxic and microbicidal functions of rabbit alveolar and peritoneal macrophages: effects of non-specific activation and a natural microbicidal peptide, MCP-1.

Alveolar macrophages from NZW rabbits were intrinsically toxic to 6 xenogeneic cell lines and to Candida albicans in vitro. Macrophage-mediated candidacidal activity, but not cytostasis (inhibition of [3H] thymidine incorporation by target cells) or cytotoxicity (reduction in target cell number), was enhanced by prior injection of rabbits with Freund's complete adjuvant (FCA). Compared with alveolar macrophages, peritoneal macrophages were less candidacidal (median C. albicans killed, 24% versus 16%, p less than 0.01). In contrast to alveolar macrophages, peritoneal macrophages were not consistently cytostatic or cytotoxic. Only candidacidal activity was enhanced in FCA-elicited peritoneal macrophages (median C. albicans killed 28% versus 16% for resident peritoneal macrophages, p less than 0.01). Microbicidal concentrations of a cationic peptide produced by rabbit alveolar macrophages (MCP-1, 25-100 micrograms/ml) did not inhibit growth of 4 murine cell lines in vitro. Macrophage-mediated cytostasis and cytotoxicity were not enhanced by culture with exogenous MCP-1. Macrophage-mediated cytostasis was also unchanged in cultures containing 10(-5) 2' deoxycytidine. We conclude that rabbit macrophage populations are restricted in their expression of cytostatic and cytotoxic functions, that microbicidal activation can occur independently of cytotoxic activation and that in this system mechanisms of macrophage-mediated cytotoxicity to xenogeneic target cells are independent of MCP-1 and thymidine.

Animals↗
PubMed1988

Metabolism of arachidonic acid through the 5-lipoxygenase pathway in normal human peritoneal macrophages.

Peritoneal macrophages (PM), obtained from 39 healthy women with normal laparoscopy findings, were stimulated with the ionophore A23187 or/and arachidonic acid (AA) both in adherence and in suspension. AA lipoxygenase metabolites were determined by reversed-phase HPLC. The major metabolites identified were 5-hydroxyeicosatetraenoic acid (5-HETE), leukotriene (LT)B4 and LTC4. The 20-hydroxy-LTB4, 20-carboxy-LTB4, and 15-HETE were not detected. Incubations of adherent PM with 2 microM A23187 induced the formation of LTB4, 110 +/- 19 pmol/10(6) cells, 5-HETE, 264 +/- 53 pmol/10(6) cells and LTC4, 192 +/- 37 pmol/10(6) cells. When incubated with 30 microM exogenous AA, adherent PM released similar amounts of 5-HETE (217 +/- 67 pmol/10(6) cells), but sevenfold less LTC4 (27 +/- 12 pmol/10(6) cells) (p less than 0.01). In these conditions LTB4 was not detectable. These results indicate that efficient LT synthesis in PM requires activation of the 5-lipoxygenase/LTA4 synthase, as demonstrated previously for blood phagocytes. When stimulated with ionophore, suspensions of Ficoll-Paque-purified PM produced the same lipoxygenase metabolites. The kinetics of accumulation of the 5-lipoxygenase/LTA4 synthase products in A23187-stimulated adherent cells varied for the various metabolites. LTB4 reached a plateau by 5 min, whereas LTC4 levels increased up to 60 min, the longest incubation time studied. Levels of 5-HETE were maximal at 5 min, and then slowly decreased with time. Thus, normal PM, in suspension or adherence, have the capacity to produce significant amounts of 5-HETE, LTB4, and LTC4. The profile of lipoxygenase products formed by the PM and the reactivity of this cell to AA and ionophore A23187 are similar to those of the human blood monocyte, but different from those of the human alveolar macrophage.

Adult↗