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At least 19 recordsLinked to original sources
PubMed1972

Bacteriological and pathological study of animals given Freund adjuvant.

Freund complete adjuvant, with allegedly "killed and dried" Mycobacterium butyricum added (intramuscularly in rabbits and intraperitoneally in mice), produced a local granulomatous lesion and frequently a similar lesion in the viscera. Acid-fast bacilli were present in these lesions, and in some animals M. butyricum was obtained in culture. When this culture was inoculated in mice, a similar lesion developed. Pathological lesions with similar acid-fast organisms also were observed by us in rabbits given Freund complete adjuvant by two other investigators.

Animals↗
PubMedDate not supplied

[Alterations in diurnal sleep structure, electrical activity, and neurochemical parameters of the rat brain induced by systemic injection of complete Freund adjuvant and immunization by bovine serum albumin with complete Freund adjuvant].

Investigations of the effects of animal immunization with immunogenesis stimulator Freund's adjuvant complete (alone or in combination with bovine serum albumin often used in control experiments) on brain electrical activity, sleep, and neurochemical parameters were carried out in male Wistar rats. It was shown that both injection of Freund's adjuvant complete alone (0.25 ml) and immunization with bovine serum albumin (2 mg/kg in 0.25 ml of saline) mixed with Freund's adjuvant complete (0.25 ml) led to an increase in the slow-wave and REM sleep. After injection of Freund's adjuvant alone, development of sleepiness was gradual and reached its maximum within 3-5 weeks, while after the combined treatment the alterations in the sleep structure became pronounced already 1 week after the first antigen injection and persisted at least for 5 weeks. Neurochemical analysis revealed no significant changes in the noradrenaline, dopamine, and serotonin content in striatum and frontal neocortex after the injection of Freund's adjuvant. After the combined treatment, the serotonin content in these structures decreased. After the Freund's adjuvant injection, the dynamics of changes in power spectra of the brain electrical activity of different brain structure in the state of quiet wakefulness was complicated. Increase in the slow-wave activity in the delta 1 range (1-2 Hz) in caudate putamen, basomedial nucleus of amygdala, and sensorimotor cortex was observed in the animals immunized with bovine serum albumin mixed with Freund's adjuvant complete 1 week after the antigen injection and later on during the whole observation period. This was probably associated with an adaptive increase in the functional activity of serotoninergic system.

Animals↗
PubMed1984

Effect of pertussigen on inflammation caused by Freund adjuvant.

Pertussigen, one of the toxins from Bordetella pertussis, greatly increased the inflammatory response produced by complete Freund adjuvant in the footpads of mice. This effect was not produced by pertussigen when the emulsion was made with saline and incomplete Freund adjuvant, but if an antigen was included in incomplete Freund adjuvant, the strong potentiating effect was again demonstrated. As little as 100 ng of pertussigen given intravenously was effective, but 400 ng proved better, and this latter dose was used routinely. The most striking action occurred when pertussigen was injected on the same day or 3 days after complete Freund adjuvant, but an effect was demonstrated when given from 3 days before to 6 days after complete Freund adjuvant. The action of pertussigen was not apparent until about 6 to 8 days after complete Freund adjuvant. The footpad swelling reached its maximum by day 14 and remained undiminished until day 29. Forty days later, a significant effect was still present. Histologically, the cellular infiltrate in the feet of mice injected with complete Freund adjuvant was more intense in animal treated with pertussigen. Nude BALB/c mice receiving an emulsion of complete Freund adjuvant in the footpads did not respond with an increased inflammation after receiving pertussigen, suggesting the possible involvement of T cells in this phenomenon. The intense and prolonged inflammatory response produced in pertussigen-treated mice by Freund adjuvant containing antigenic substances may serve as a useful model to study chronic inflammation.

Animals↗
PubMedDate not supplied

Diethylaminoethanol action in the arthritis with Freund adjuvant, in rats.

The authors have studied the action of diethylaminoethanol on Freund adjuvant arthritis, induced in female Lewis rats. They worked on 3 groups, each one including 14 rats, weighing 110-130 g: group I = control; group II = rats injected intracutaneous with 0.1 ml Freund adjuvant; group III = rats injected with Freund adjuvant and treated with diethylaminoethanol i.m. (10 mg/kg body weight), and gel application (2.5%) on paws and tail, daily. During the experiment clinical observations and measurements were made and when the animals were killed, blood was sampled for haematological and immunological assays (CD4, CD8, CD25 T cells and NK cells, antinuclear autoantibody and immune complexes). While in all the rats from group II (without treatment) inflammatory processes developed at the level of the peripheral joints, in group III (diethylaminoethanol treated), these ones were present in only 64% of the rats and by much more reduced forms, followed by a short period of involution. The paw volume, measured with an electronic plethysmometer, was more reduced in the treated rats (7.1-14.2%) than in the non treated ones (27.7-29.3%). The haematologic examination showed an increased number of neutrophiles in both groups with FA injecting. The immunological investigations revealed: a decrease of CD4 cells and an increase of CD8 T cells and NK cells in both groups, a much more decreased level (13.2%) of circulatory immune complexes in treated rats, as compared to the non-treated ones (71.7%). No differences were found regarding the CD25 cells and antinuclear antibodies. The histo-pathological examination showed that the intensity and the extension area of the joint lesions (granulation tissue with fibrous change, cartilage invasion and dilaceration, bone atrophy) were much more reduced in the treated rats. The authors put forward the hypothesis that these effects might be due to diethylaminoethanol antiinflammatory properties.

Animals↗
PubMed2003

Freund adjuvant induces TLR2 but not TLR4 expression in the liver of mice.

Freund adjuvants are used extensively to establish experimental animal models of autoimmune diseases and to produce antibodies. However, studies on their mechanisms of action have been largely neglected, particularly their effects on liver, the primary target organ for host-microbe interaction. Here we show that treatment with either complete (CFA) or incomplete (IFA) Freund adjuvant induced a 5-10-fold increase in toll-like receptor (TLR) 2 mRNA but not TLR4 mRNA in livers of mice. Since CFA is essentially made of killed Mycobacterium tuberculosis bacilli (Mtb) dissolved in IFA, it is the solvent in CFA that induced an increase in TLR2 expression. As TLR2 is the receptor activated by killed Mtb, this solvent-mediated increase in TLR2 expression will result in enhanced recognition of killed Mtb by hepatocytes during CFA administration. We propose that the potency of Freund adjuvant in eliciting an immune response lies in their ability to induce expression of the appropriate TLR, TLR2, for the active ingredient, killed Mtb, in CFA.

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PubMed2001

Freunds adjuvant alone is antiatherogenic in apoE-deficient mice and specific immunization against TNFalpha confers no additional benefit.

TNFalpha participates in the pathogenesis of atherosclerosis. The effect of immunization against TNFalpha on development of advanced vascular lesions in atherosclerosis-susceptible apoE-deficient mice was investigated. At 5-7 weeks of age, animals received immunization with either Freunds adjuvant and a recombinant antigenic TNFalpha molecule (TNF106), Freunds adjuvant alone, or no immunization. All mice received a Western-type high-fat diet for 12 weeks. Aortic sinus lesion area was determined by microscopic morphometry, the total aortic arch cholesterol content was determined by gas chromatography, and antibodies against TNFalpha, malondialdehyde-modified low density lipoprotein, or heat shock protein 60, were assessed by ELISAs. Immunization with TNF106 induced high-titered circulating antibodies against TNFalpha (n=23), and these antibodies were not detected in mice immunized with Freunds adjuvant alone (n=22), or in non-immunized control animals (n=25). After 12 weeks, the atherosclerotic lesion size was significantly reduced in immunized animals, whether they had been immunized with TNF106 or Freunds adjuvant alone, and the total lesional cholesterol content was decreased in mice immunized with TNF106. There were no correlations between circulating antibody titers and plaque size, total aortic arch cholesterol content, or plasma lipid levels, respectively. Administration of Freunds adjuvant alone can thus reduce formation of mature atherosclerotic lesions in apoE-deficient mice and this response is not modified by specific immunization against TNFalpha.

Animals↗
PubMed1994

Prevaccination with diluted Freund adjuvant prevents the development of chronic pain and transient release of cerebrospinal fluid substance P in adjuvant-induced arthritis in rats.

Parallel time courses of preclinical and behavioural pain-related parameters and levels of substance P-like immunoreactivity in plasma (plasma-SPLI) and cerebrospinal fluid (CSF-SPLI) were studied in 2 groups of rats injected with an arthritogenic solution (concentrated Freund adjuvant) over a 9-week post-infection (PI) period; 1 group was pretreated with saline (control) and 1 pretreated with diluted Freund adjuvant (immunized). In control rats all symptoms of adjuvant-induced arthritis (AIA) developed while in immunized rats AIA symptoms were significantly reduced or did not appear. A significant increase in plasma-SPLI was obvious as early as the 2nd week PI and remained at this level in both groups of animals until the end of the 9-week PI observation period, but with a significantly higher increase in control versus immunized group at all stages. In contrast, CSF-SPLI transiently peaked only in the control group at 3 weeks PI whereas CSF-SPLI values did not differ from one week to another in both groups of rats. These results suggest that successive injections of diluted Freund adjuvant impairs the development of chronic inflammation and pain in AIA in rats, as well as the transient increase in SP release in CSF at 3 weeks PI, but not the long-lasting increased SP release in plasma. Since there is a clear dissociation between our biochemical and preclinical and behavioral data, this study does not provide evidence for the role of substance P as a possible biologic marker of chronic pain either in plasma or in CSF.(ABSTRACT TRUNCATED AT 250 WORDS)

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PubMed1981

Increased content of microbicidal cationic peptides in rabbit alveolar macrophages elicited by complete Freund adjuvant.

We measured the microbicidal peptides MCP-1 and MCP-2 in rabbit alveolar macrophages (AM), comparing rabbits pretreated with complete Freund adjuvant with untreated control animals. Levels of MCP-1 increased from 4.7 +/- 0.6 microgram/10(7) resident AM to 13.2 +/- 0.1 microgram/10(7) complete Freund adjuvant-elicited AM. MCP-2 levels rose from 1.8 +/- 0.1 microgram/10(7) resident AM to 7.3 +/- 0.4 microgram/10(7) complete Freund adjuvant-elicited AM. The activities of five lysosomal hydrolases (beta-D-glucuronidase, beta-D-galactosidase, acid phosphatase, N-acetyl-beta-D-galactosaminidase, and N-acetyl-beta-D-glucosaminidase) were 44 to 96% higher in complete Freund adjuvant-elicited AM, and lysozyme activity was three- to fourfold higher. As MCP-1 and MCP-2 are major constituents of rabbit AM and exhibit potent antibacterial and antifungal properties, they may contribute to the expression of microbicidal activity in both resident and activated states.

Animals↗
PubMed1982

Tissue localization of complement component 3 receptor-bearing cells in lymphoid tissue after injection with complete Freund adjuvant.

Localizations of complement component 3 (C3) receptor (C3R)-bearing cells in lymph nodes obtained from normal guinea pigs or from guinea pigs inoculated with complete Freund adjuvant were examined by staining with fluorescein-labeled anti-guinea pig C3 antibody after treatment with aggregated rabbit immunoglobulin M bound with guinea pig complement. In normal lymph nodes, a small number of C3R-positive cells were observed in the cortical and medullary areas. Non-granulomatous lymph nodes from complete Freund adjuvant-inoculated animals showed a number of C3R-positive lymphocytes in a mantle zone of the secondary follicles between the follicles and medullary cords, whereas in the paracortical areas and germinal centers, only a few positive cells were scattered. Long-lasting existence of positive cells was seen in the epithelioid cell granuloma, although the staining patterns were different from those of the lymphocytes. The appearance of a number of C3R-bearing lymphocytes in lymph nodes from complete Freund adjuvant-inoculated animals might be an expression of adjuvant activity.

Animals↗
PubMed1980

[Experimental carcinogenesis in the urinary bladder against a background of Freund adjuvant and levamisole administration].

Administration of complete Freund's adjuvant (CFA) to rats before carcinogenesis and in its early period was associated with an increase (not less than 2-fold) in the number of spindle-shaped dark cells that permeated the hyperplastic urothelium and, judging the ultrastructure, had a macrophage nature. These animals demonstrated a relationship between the increased number of dark cells and delayed development of the subsequent stage of carcinogenesis--papillomatous hyperplasia. CFA administration to the animals with a developed cancer of the urinary bladder did not affect it noticeably. It did not produce any effect on subcutaneous transplantation of cancer that had taken in 100% of cases. No morphological features of carcinogenesis were recorded either after levamisol administration. However, none of the tumours withdrawn from the rats given levamisol took under the skin of the recipients.

Animals↗
PubMedDate not supplied

The effect of complete Freund--adjuvant on chronic proliferating inflammation in an experimental granuloma model.

Histometric, biochemical, radiochemical and autoradiographic studies were undertaken to investigate the influence of complete Freund-adjuvant (CFA) on a defined chronic proliferating inflammation of a granuloma model in two different experimental situations. Where as the percentage fraction of the fibroblasts, 3H-thymidine marking index of the fibroblasts and the impulse rate of the fibroblasts and endothelial cells do not differ from the values found for the control animals, both the protein and DNA content of the implanted sponges, as well as the DNA content of the individual fibroblasts in the implants increased, independent of the stage of the chronic proliferating inflammation at which the CFA was administered. Surprisingly the quantity of the fibroblast specific synthetic product, collagen, did not increase in proportion to the absolute number of fibroblasts, but remained either constant or even significantly decreased. A possible inhibition of collagen synthesis after CFA administration during chronic proliferating inflammation is discussed.

Animals↗
PubMed1988

Pulmonary gallium uptake in rats with granulomatosis induced by complete Freund adjuvant.

To investigate the mechanism of gallium-67 uptake in lung granulomatosis, we studied 13 rats in which lung granulomatosis was induced by injection of complete Freund adjuvant (CFA) and 14 controls. Gallium uptake was assessed in bronchoalveolar lavage fluid and lavaged lung. The cells responsible for gallium uptake were identified by latent image activation autoradiography. Gallium activity in both lavaged lungs and bronchoalveolar cells (BAC) was higher in CFA-treated animals than in controls [172,205 +/- 134,783 DPM versus 44,456 +/- 14,486 DPM +/- SD (p less than 0.05) and 40,083 +/- 16,350 DPM versus 9100 +/- 4114 DPM (p less than 0.05), respectively]. In control rats, about two-thirds of total lung gallium was located in the interstitium, whereas in CFA-treated rats it was found in the mononuclear cells of lung granulomas. Gallium tracks were more numerous in the alveolar macrophages (AM) of CFA-treated rats than in control AM (28.4 +/- 10.0/field versus 8.4 +/- 3.8/field, p less than 0.001) but the number of tracks was proportional to the number of AM (52.4 +/- 18.7 versus 12.2 +/- 4.3, respectively; p less than 0.001). It is concluded that in rats with CFA-induced lung granulomatosis 1) pulmonary gallium uptake increases, 2) mononuclear cells are responsible for this uptake in both granulomas and AM, and 3) the increased uptake is due to the increased number of mononuclear cells.

Animals↗
PubMed1975

Relationship between the response to complete freund adjuvant, phytohemagglutinin, and subsequent tumor growth in mice.

Groups of inbred C3H mice selected on the basis of strong or weak PPD reactions after sensitization with complete Freund adjuvant had significantly different reactions to PHA. The growth rate of a methylcholanthrene-induced tumor, previously shown to elicit a cell-mediated immune response, was significantly different in these two groups of mice. The basis for the marked variation observed between members of an inbred mouse strain in response to CFA is not understood but may bear an important potential relationship to tumor growth.

Animals↗
PubMed1990

Nonspecific immunopotentiators and pregnancy loss: complete Freund adjuvant reverses high fetal resorption rate in CBA x DBA/2 mouse combination.

CBA/J female mice mated with DBA/2J males show a high incidence of fetal resorptions. This paper presents data demonstrating that nonspecific immunopotentiation by complete Freund adjuvant (CFA) reversed pregnancy loss in CBA/J mothers. Immunization of more than 70 CBA/J females mated with DBA/2J males with CFA reduced the incidence of fetal resorption from 27.3 +/- 1.9 to 7.9 +/- 1.5%. The injection of Thymus Humoral Factor known to be a potent T cell stimulator did not reduce the number of fetal resorptions. The route of CFA distribution was found to be important--only foot pad injections were effective in fetal protection, whereas i.p. treatment did not reduce fetal resorptions. Fetal protection could be transferred by splenocytes of CFA-injected CBA/J mothers (9.6 +/- 5.0% fetal resorptions). Sera from treated CBA/J mice could not cause such an effect (17.6 +/- 4.6 vs. 21.3 +/- 6.1 in control animals). Thus, stimulation of the maternal immune system by nonspecific immunopotentiators can improve reproductive performance of this mouse combination which has an increased rate of pregnancy loss. Possible mechanisms of this fetal protection are discussed.

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PubMed1994

c-Fos expression in the spinal cord and pain-related symptoms induced by chronic arthritis in the rat are prevented by pretreatment with Freund adjuvant.

We previously showed that pathological adjuvant-induced arthritis (AIA), a chronic pain model, is associated with an increase in the number of Fos-like immunoreactivity (Fos-LI) in lumbar spinal cord neurons; maximal Fos-LI corresponds to the peak of pathological and behavioral signs of the disease. On the other hand, AIA is prevented in rats that have previously been injected with diluted complete Freund adjuvant (CFA). Here, the effects of pretreatment with CFA were studied in parallel on both pathological parameters and pain-related tests, and on Fos-LI, 3 weeks after the inoculation of the arthritogenic solution during the acute phase of the disease, that is, when hyperalgesia is maximal. One group of rats (vaccinated group) was pretreated with diluted CFA, 3 weeks and 1 week before inoculation (AIA) (with the concentrated arthritogenic solution), while a second group (arthritic group) was pretreated with the vehicle for the CFA solution and then inoculated with the concentrated arthritogenic solution. Control groups consisted of rats treated with various combinations of either saline or vehicle solutions during the pretreatment periods or at the time of inoculation. The arthritic group developed all pathological symptoms of AIA (i.e., loss of weight, difficulties in walking, increases in paw diameter, and decreases in the vocalization thresholds to mechanical pressure of the hindpaw, and finally an increase in the vocalization response to flexion and extension). In contrast, the vaccinated group did not develop AIA symptoms.(ABSTRACT TRUNCATED AT 250 WORDS)

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PubMed2005

Immunization with myelin oligodendrocyte glycoprotein and complete Freund adjuvant partially protects dopaminergic neurons from 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced damage in mouse model of Parkinson's disease.

The concept of neuroprotective immunity identifies a new role of autoimmune cells in the CNS pathology. Specifically, immune cells infiltrating the CNS during an injury may help in a regeneration process and prevent the secondary degeneration of neurons. The objectives of our study were to determine the role of autoimmune and peripheral immune enhancement in neurodegeneration process, and to compare the results between young adult and aging animals. C57Bl mice were immunized with either myelin oligodendrocyte glycoprotein (MOG) 35-55 combined with complete Freund adjuvant (CFA), or CFA alone. Following 6 days, the animals were injected with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine to produce a damage of the nigrostriatal dopaminergic system. Although immunization with MOG 35-55 combined with CFA resulted in autoimmune encephalomyelosis, it substantially enhanced neuronal survival after the toxic insult. The immunization with CFA alone was also effective in preventing neuronal cell death, but the magnitude of the neuroprotective effect was smaller. Interestingly, the neuroprotective effect of MOG 35-55 and CFA was more pronounced in aging (i.e. 10-month-old) compared with young (i.e. 2-month-old) mice. Our results indicate that an increased immune activation may be beneficial for neurodegenerative processes following the CNS injury, but the mechanisms of such immune neuroprotection and of age differences need further investigation.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗