Activated macrophages in highly irradiated cercariae-induced immunity toSchistosoma japonicumin rats

Parasitology ◽  
1991 ◽  
Vol 102 (1) ◽  
pp. 65-72
Author(s):  
C. Xu ◽  
S. Xu
Keyword(s):  
Alveolar Macrophages ◽  
Sheep Erythrocyte ◽  
Peritoneal Macrophages ◽  
Rat Serum ◽  
Sheep Erythrocytes ◽  
Proteose Peptone ◽  
Normal Rat ◽  
Induced Immunity

SUMMARYThe results of studies on the schistosomulicidal activity of activated peritoneal and alveolar macrophages (pMø and aMø) from rats immunized with highly irradiated (50 krad.)Schistosoma japonicumcercariae are reported. The authors have examined the activation of these macrophages in terms of spreading, adhesion and ingestion of sheep erythrocytes and pinocytosis of horse-radish peroxidase. Using three criteria, peritoneal macrophages and alveolar macrophages from immunized rats and from rats intraperitoneally injected with BCG were significantly more active than those from normal rats or rats stimulated with 10% proteose-peptone or 1% sodium thioglycolate. A significantly higher percentage of adhesion and ingestion was obtained with the sheep erythrocytes that were co-opsonized by heat-inactivated rat anti-sheep erythrocyte serum and fresh normal rat serum. Schistosomulicidal effects were observed with macrophages from irradiated cercariae-immunized rats in two activation systems:in vitroactivation in the presence of macrophage-activating factor (MAF), andin vivoactivation by the intraperitoneal challenge with sonicated cercarial antigens.

scholarly journals THE FATE OF BACTERIA WITHIN PHAGOCYTIC CELLS

1964 ◽  
Vol 120 (5) ◽  
pp. 869-883 ◽  
Author(s):  
Zanvil A. Cohn
Keyword(s):  
Alveolar Macrophages ◽  
Peritoneal Macrophages ◽  
Immune Serum ◽  
Soluble Form ◽  
Phagocytic Cells ◽  
E Coli ◽  
Heat Stable ◽  
Immune Globulins

The fate of a heat-stable Escherichia coli agglutinogen within three types of rabbit phagocytic cells was examined. A system is described whereby quantitative ingestion of viable E. coli by suspensions of PMN leucocytes, BCG-induced alveolar macrophages, and oil-induced peritoneal macrophages took place in vitro. After various periods of intracellular residence aliquots were injected intraperitoneally into NCS mice and the resulting agglutinins assayed. The loss of immunogenicity within phagocytes was estimated by comparison with a dose-response titration prepared with bacteria alone. Under these conditions no increase in immunogenic mass occurred in vivo or in vitro when viable organisms were employed. PMN leucocytes and alveolar macrophages destroyed the majority of the immunogen within 2 hours of intracellular residence. In contrast, the immunogenicity of E. coli was maintained within peritoneal macrophages for periods up to 5 hours. The use of heat-killed bacilli or specific immune serum did not significantly influence the intracellular fate of the immunogen. Residual immunogenicity was associated with a particle having the same centrifugal properties as the intact organism and essentially none was released in a soluble form. Intracellular residence within phagocytic cells did not influence the resulting temporal sequence of antibody formation nor the proportions of mercaptoethanol-sensitive and resistant immune globulins.

Repair ofHymenolepis diminutaafter complement-mediated damage

Parasitology ◽  
1989 ◽  
Vol 99 (3) ◽  
pp. 437-443 ◽  
Author(s):  
J. Andreassen ◽  
D. Hoole
Keyword(s):  
Neck Region ◽  
Regenerative Process ◽  
Hymenolepis Diminuta ◽  
Embryological Development ◽  
Rat Serum ◽  
Ultrastructural Studies ◽  
Normal Rat ◽  
Electron Lucent

SummarySeven and 56-day-oldHymenolepis diminutawere exposed to complement by incubation in 50% normal rat serum (NRS) in modified Hanks' saline. Ultrastructural studies revealed that the scolex/neck region remained relatively intact whilst in the strobila region microthrix denudation and loss of distal cytoplasm were observed. When complement-mediated damaged worms were incubated in vitro in 50% heat-inactivated normal rat serum (hiNRS) plus M199 or implanted into the duodenum of NMRI mice repair occurred, although destrobilated parasites were only foundin vivo. The regions undergoing repair contained tegumental protrusions, vesicles, large electron-lucent areas and large quantities of lipid. Microtriches were formed parallel to the parasite surface and were raised into a perpendicular position. It is suggested that the regenerative process exhibited after complement-mediated damage does not mimic totally the embryological development of the surface layer.

Rat alveolar macrophages express preprotachykinin gene-I mRNA-encoding tachykinins

1997 ◽  
Vol 273 (5) ◽  
pp. L1073-L1081 ◽  
Author(s):  
Cheryl R. Killingsworth ◽  
Stephanie A. Shore ◽  
Francesca Alessandrini ◽  
Richard D. Dey ◽  
Joseph D. Paulauskis
Keyword(s):  
Alveolar Macrophages ◽  
Peritoneal Macrophages ◽  
Northern Analysis ◽  
Neurokinin A ◽  
Polymerase Chain ◽  
Preprotachykinin Gene ◽  
Lps Treatment

Although the tachykinins substance P (SP) and neurokinin A have been largely localized to neurons, eosinophils have also been shown to express these peptides. Our aim was to determine whether rat alveolar macrophages (AM) express preprotachykinin gene-I (PPT-I) mRNA that encodes these tachykinins and to examine expression during inflammation. PPT-I mRNA was detected by reverse transcription (RT)-polymerase chain reaction (PCR) in AM and brain (control) but not in peritoneal macrophages. Northern analysis showed that PPT-I mRNA was induced two- to fourfold by in vivo treatment of rats with intratracheal lipopolysaccharide (LPS) and in vitro after 4 h of exposure to LPS. This increase was inhibited by dexamethasone. In situ RT-PCR and immunocytochemistry further confirmed that AM express PPT-I mRNA and SP-like immunoreactivity, respectively, which was enhanced by LPS treatment. A 1.3-kb transcript consistent with PPT-I mRNA was detected by Northern analysis of bronchoalveolar lavage neutrophils. Therefore, rat AM express PPT-I mRNA that is upregulated in AM by LPS and is attenuated by dexamethasone. PPT-I mRNA was also detected in lung neutrophils.

scholarly journals Novel Role for Albumin in Innate Immunity: Serum Albumin Inhibits the Growth of Blastomyces dermatitidis Yeast Form In Vitro

2003 ◽  
Vol 71 (11) ◽  
pp. 6648-6652 ◽  
Author(s):  
Steven Giles ◽  
Charles Czuprynski
Keyword(s):  
Molecular Weight ◽  
Inhibitory Activity ◽  
Mammalian Species ◽  
Blastomyces Dermatitidis ◽  
Low Molecular Weight ◽  
Rat Serum ◽  
Yeast Form ◽  
Domain Iii

ABSTRACT In this study we found that serum inhibitory activity against Blastomyces dermatitidis was principally mediated by albumin. This was confirmed in experiments using albumin from several mammalian species. Analbuminemic rat serum did not inhibit B. dermatitidis growth in vivo; however, the addition of albumin restored inhibitory activity. Inhibitory activity does not require albumin domain III and appears to involve binding of a low-molecular-weight yeast-derived growth factor.

scholarly journals MATURATION OF HEMOLYSIN-PRODUCING CELL CLONES

1970 ◽  
Vol 131 (6) ◽  
pp. 1261-1270 ◽  
Author(s):  
George C. Saunders ◽  
Douglas Swartzendruber
Keyword(s):  
Bone Marrow ◽  
Doubling Time ◽  
Sheep Erythrocyte ◽  
Mature Animal ◽  
Cell Clones ◽  
Initial Appearance ◽  
Vitro Data ◽  
In Vitro Data

Cells capable of reacting with sheep erythrocyte (SRBC) antigen to maturate and produce hemolysin appear simultaneously in the bone marrow and spleen of 1-day old Swiss-Webster mice. However, hemolysin-producing cell clones (HPCC) do not result. Complete functional precursor units generally appear in the spleens of mice older than 3 days. In vivo and in vitro data correlate well in this regard. Complete precursor units are not seen in the bone marrow and only very rarely in the thymus. The efficiency of precursor units of neonatal mice when they become functional approximates that of the mature animal when based on the doubling time of plaque-forming cells (PFC). Possible explanations of the initial appearance of incomplete precursor units have been discussed.

scholarly journals Macrophage oxygen-dependent antimicrobial activity. III. Enhanced oxidative metabolism as an expression of macrophage activation.

1980 ◽  
Vol 152 (6) ◽  
pp. 1596-1609 ◽  
Author(s):  
H W Murray ◽  
Z A Cohn
Keyword(s):  
Antimicrobial Activity ◽  
Oxidative Metabolism ◽  
Macrophage Activation ◽  
Systemic Infection ◽  
Peritoneal Macrophages ◽  
H2o2 Production ◽  
Oxygen Intermediates ◽  
Cultivation In Vitro

The capacity of 15 separate populations of mouse peritoneal macrophages to generate and release H2O2 (an index of oxidative metabolism) was compared with their ability to inhibit the intracellular replication of virulent Toxoplasma gondii. Resident macrophages and those elicited by inflammatory agents readily supported toxoplasma multiplication and released 4-20X less H2O2 than macrophages activated in vivo by systemic infection with Bacille Calmette-Guérin or T. gondii, or by immunization with Corynebacterium parvum. Immunologically activated cells consistently displayed both enhanced H2O2 production and antitoxoplasma activity. Exposure to lymphokines generated from cultures of spleen cells from T. gondii immune mice and toxoplasma antigen preserved both the antitoxoplasma activity and the heightened H2O2 release of toxoplasma immune and immune-boosted macrophages, which otherwise were lost after 48-72 h of cultivation. In vitro activation of resident and chemically-elicited cells by 72 h of exposure to mitogen- and antigen-prepared lymphokines, conditions that induce trypanocidal (5) and leishmanicidal activity (14), stimulated O2- and H2O2 release, and enhanced nitroblue tetrazolium reduction in response to toxoplasma ingestion. Such treatment, however, failed to confer any antitoxoplasma activity, indicating that intracellular pathogens may vary in their susceptibility to macrophage microbicidal mechanisms, including specific oxygen intermediates. In contrast, cocultivating normal macrophages with lymphokine plus heart infusion broth for 18H rendered these cells toxoplasmastatic. This in vitro-acquired activity was inhibited by scavengers of O2-, H2O2, OH., and 1O2, demonstrating a role for oxidative metabolites in lymphokine-induced enhancement of macrophage antimicrobial activity. These findings indicate that augmented oxidative metabolism is an consistent marker of macrophage activation, and that oxygen intermediates participate in the resistance of both in vivo- and vitro-activated macrophages toward the intracellular parasite, T. gondii.

IgG modulation in male mice with reproductive failure after prenatal inflammation

Reproduction ◽  
2021 ◽  
Author(s):  
Marina Izvolskaia ◽  
Vasilina Ignatiuk ◽  
Ayshat Ismailova ◽  
Viktoria Sharova ◽  
Liudmila Zakharova
Keyword(s):  
Positive Impact ◽  
Brain Structures ◽  
Peritoneal Macrophages ◽  
The Body ◽  
Male Rats ◽  
Male Mice ◽  
Prenatal Inflammation ◽  
Exposure In Vivo

Sexual performance in adult male rats is highly sensitive to prenatal stress which can affect the functionality of the reproductive system and various brain structures involved in modulating sexual behavior. The immunomodulatory effect of mouse IgG on reproductive maturity in male offspring after LPS exposure in vivo and in vitro was studied. Prenatal IgG injection (20 µg / mouse) had a positive impact on the puberty of male mice whose mothers were exposed to LPS (100 µg / kg) on the 12th day of pregnancy. The number of Sertoli cells were increased, whereas the body weight and the number of symplastic spermatids were decreased in offspring as compared to LPS-treated animals. Besides, IgG had a positive effect on altered hormone levels: reduced estradiol level on the 5th and 14th postnatal days and increased testosterone level on the 30th postnatal day in blood that led to an increased number of mounting attempts in sexually mature males. The cAMP-dependent pathway may be involved in the regulation of the LPS-induced inflammation. IgG reduced the increased level of cAMP in mouse peritoneal macrophages activated by LPS in vitro. IgG is able to modulate inflammation processes, but its exposure time is important.

In situ activation of mouse alveolar macrophages by aerosolized liposomal IFN-gamma and muramyl tripeptide

1996 ◽  
Vol 270 (3) ◽  
pp. L429-L434 ◽  
Author(s):  
P. Goldbach ◽  
S. Dumont ◽  
R. Kessler ◽  
P. Poindron ◽  
A. Stamm
Keyword(s):  
Alveolar Macrophages ◽  
Peritoneal Macrophages ◽  
Target Cells ◽  
Tumoricidal Activity ◽  
Ifn Gamma ◽  
In Situ Activation ◽  
Organ Specific ◽  
Thawing Procedure

Interferon-gamma (IFN-gamma) was entrapped with an efficiency of 30-40% in muramyl tripeptide-containing liposomes by a freeze-thawing procedure. A microcytotoxicity assay was developed to measure the tumoricidal activity of mouse alveolar macrophages (AM) against tumoral target cells with a colorimetric viability test. Free IFN-gamma and liposomal muramyl tripeptide phosphatidylethanolamine (MTP-PE) were found to be only slightly effective to activate in vitro AM, whereas encapsulation of both INF-gamma and MTP-PE within the same liposomes produced higher activation of AM. Aerosolized IFN-gamma and liposomal immunomodulators enhanced antitumor properties of AM recovered in mice 24 h postinhalation. Whereas free IFN-gamma also induced a substantial activation of peritoneal macrophages, liposomal encapsulation significantly reduced the systemic activity of inhaled immunomodulators. This approach provides a useful model for the compartmentalized organ-specific activation of AM in mice.

Measurements of the jejunal unstirred layer in normal subjects and patients with celiac disease

1996 ◽  
Vol 270 (3) ◽  
pp. G487-G491 ◽  
Author(s):  
A. Strocchi ◽  
G. Corazza ◽  
J. Furne ◽  
C. Fine ◽  
A. Di Sario ◽  
...  
Keyword(s):  
Celiac Disease ◽  
Layer Thickness ◽  
Villous Atrophy ◽  
Normal Subjects ◽  
Unstirred Layer ◽  
Maximal Velocity ◽  
Normal Rat ◽  
Kinetics Of

Normal intestinal absorption of nutrients requires efficient luminal mixing to deliver solute to the brush border. Lacking such mixing, the buildup of thick unstirred layers over the mucosa markedly retards absorption of rapidly transported compounds. Using a technique based on the kinetics of maltose hydrolysis, we measured the unstirred layer thickness of the jejunum of normal subjects and patients with celiac disease, as well as that of the normal rat. The jejunum of humans and rats was perfused with varying maltose concentrations, and the apparent Michaelis constant (Km) and maximal velocity (Vmax) of maltose hydrolysis were determined from double-reciprocal plots. The true Km of intestinal maltase was determined on mucosal biopsies. Unstirred layer thickness was calculated from the in vivo Vmax and apparent Km and the in vitro Km of maltase. The average unstirred layer thickness of 11 celiac patients (170 micron) was seven times greater than that of 3 controls (25 micron). The unstirred layer of each celiac exceeded that of the controls. A variety of factors could account for the less efficient luminal stirring observed in celiacs. Although speculative, villous contractility could be an important stirring mechanism that would be absent in celiacs with villous atrophy. This speculation was supported by the finding of a relatively thick unstirred layer (mean: 106 micron) in rats, an animal that lacks villous contractility. Because any increase in unstirred layer slows transport of rapidly absorbed compounds, poor stirring appears to represent a previously unrecognized defect that could contribute to malabsorption in celiac disease and, perhaps, in other intestinal disorders.

Nippostrongylus brasiliensis: further properties of antibody-damaged worms and induction of comparable damage by maintaining worms in vitro

Parasitology ◽  
1975 ◽  
Vol 71 (2) ◽  
pp. 275-283 ◽  
Author(s):  
R. J. Love ◽  
Bridget M. Ogilvie ◽  
Diane J. McLaren
Keyword(s):  
Immune Response ◽  
Isoenzyme Pattern ◽  
Nippostrongylus Brasiliensis ◽  
Ultrastructural Morphology ◽  
Immature Rats ◽  
Normal Rat ◽  
Worm Expulsion ◽  
Anterior Migration

When adult Nippostrongylus brasiliensis were maintained in vitro they became damaged. Using the criteria of ultrastructural morphology, acetylcholinesterase isoenzyme pattern and the behaviour of the worms after transfer to a normal rat, this damage appeared to be similar to that produced by the in vivo action of antibodies.Antibodies were shown to be responsible for the anterior migration of adult worms which occurs during primary infections in mature rats and in the prolonged infections seen in lactating and immature rats.Antibody damaged worms and worms unaffected by antibodies were equally able to stimulate the immune response required for worm expulsion. Apparently antibody damage is not required for the initiation of the second immune component necessary for expulsion of this parasite.

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