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PubMed1983

Effect of penicillin on the adherence of Streptococcus sanguis in vitro and in the rabbit model of endocarditis.

The effect of penicillin treatment of Streptococcus sanguis in vitro, on subsequent bacterial density in the bloodstream and on cardiac valves in the rabbit model of endocarditis was studied. As experimental tools for this study, isogenic pairs of S. sanguis differing in resistance to streptomycin or rifampin were prepared by genetic transformation. Rabbits with traumatized heart valves received an intravenous inoculation of penicillin treated (1 mug/ml) and untreated S. sanguis, each marked by resistance to either streptomycin or rifampin. The number of penicillin-treated and untreated bacteria attached to the valvular surfaces was determined by differential counting on streptomycin or rifampin containing media. Penicillin pretreatment reduced cardiac valve colonization 5 min after inoculation ("adherence ratio" x 10(8) was 4.11 for the control and 3.66 for the penicillin-treated bacteria, P < 0.001). The results were not due to differences in serum killing or bacterial densities in the bloodstream. There was no difference in valvular bacterial densities 24 h after bacterial inoculation (adherence ratio x 10(8), 7.26 untreated vs. 6.34 penicillin-pretreated, P > 0.10). In vitro experiments were performed using platelet-fibrin surfaces to test the possibility that penicillin-induced loss of lipoteichoic acid was responsible for decreased streptococcal adherence. Pretreatment of S. sanguis cultures with inhibitory concentrations of penicillin or with antiserum against lipoteichoic acid and precoating of the platelet-fibrin surfaces with lipoteichoic acid, all caused reduction in bacterial adherence. The findings are interpreted as support for the role of lipoteichoic acid as an adhesin in S. sanguis interactions with particular host tissue surfaces.

Adhesiveness↗

PubMed1996

Biological behavior of Leishmania amazonensis isolated from humans with cutaneous, mucosal, or visceral leishmaniasis in BALB/C mice.

Leishmania amazonensis causes a wide spectrum of disease in humans. In this study, we evaluated BALB/c mice infected with five strains of L. amazonensis isolated from patients with either cutaneous, mucosal, or visceral leishmaniasis. Mice infected with cutaneous and mucosal isolates developed ulcerating footpad lesions with parasite-loaded macrophages and extensive tissue destruction. Skin metastases, early dissemination of parasites to the spleen, and high anti-Leishmania antibody levels were also noted. Mice infected with L. amazonensis strains isolated from patients with visceral disease had a controlled infection, with small footpad lesions with mononuclear cell infiltration, few infected macrophages, and granuloma formation. They had no skin metastases, delayed dissemination of the parasite to the spleen, lower levels of IgG and higher levels of IgG2a against L. amazonensis. These findings demonstrate an unexpected resistance of BALB/c mice to the infection with L. amazonensis isolated from patients with visceral leishmaniasis. This resistance seems to be due to differences in these parasites that may be related to the altered course of the disease in humans and in isogenic BALB/c mice.

Animals↗

PubMed2003

The STT3a subunit isoform of the Arabidopsis oligosaccharyltransferase controls adaptive responses to salt/osmotic stress.

Arabidopsis stt3a-1 and stt3a-2 mutations cause NaCl/osmotic sensitivity that is characterized by reduced cell division in the root meristem. Sequence comparison of the STT3a gene identified a yeast ortholog, STT3, which encodes an essential subunit of the oligosaccharyltransferase complex that is involved in protein N-glycosylation. NaCl induces the unfolded protein response in the endoplasmic reticulum (ER) and cell cycle arrest in root tip cells of stt3a seedlings, as determined by expression profiling of ER stress-responsive chaperone (BiP-GUS) and cell division (CycB1;1-GUS) genes, respectively. Together, these results indicate that plant salt stress adaptation involves ER stress signal regulation of cell cycle progression. Interestingly, a mutation (stt3b-1) in another Arabidopsis STT3 isogene (STT3b) does not cause NaCl sensitivity. However, the stt3a-1 stt3b-1 double mutation is gametophytic lethal. Apparently, STT3a and STT3b have overlapping and essential functions in plant growth and developmental processes, but the pivotal and specific protein glycosylation that is a necessary for recovery from the unfolded protein response and for cell cycle progression during salt/osmotic stress recovery is associated uniquely with the function of the STT3a isoform.

Adaptation, Physiological↗

PubMed1994

The establishment of cytomegalovirus latency in organs is not linked to local virus production during primary infection.

Recovery from primary cytomegalovirus (CMV) infection is associated with resolution of the productive infection without clearance of the virus genome from affected organs. The presence of latent CMV genome in multiple organs provides the molecular basis for recurrence of CMV within multiple organs, and explains the diversity in the organ manifestations of recrudescent CMV disease during states of immunodeficiency. As a part of a unifying concept of multifocal CMV latency and recurrence, previous work has demonstrated the importance of primary virus replication for the overall load of latent CMV in organs and the risk of recurrence. In the present report, the establishment of CMV latency was studied in a murine model in which the course of primary infection in the immunocompromised host after syngeneic bone marrow transplantation was modulated by a CD8+ T cell immunotherapy. The antiviral CD8+ effector cells limited virus replication in all organs and protected the recipients from lethal CMV disease, but after resolution of the productive infection virus DNA remained. Interestingly, the copy number of latent virus DNA in tissue did not quantitatively reflect the preceding virus production in the respective organ. Specifically, in contrast to the case in the lungs and the salivary glands, virus replication in the spleen was suppressed by CD8+ T cells to below the limit of detection; yet, virus DNA was also detected in the spleen during latency and accordingly, virus recurrence in the spleen could be induced. These findings demonstrate that the control of virus replication in a particular organ does not prevent the establishment of latency in that organ.

Animals↗

PubMed1978

Immunity against MOPC 104E plasmacytoma: effects of tumor size and time post therapy on in vivo tumor immunity.

BALB/c mice with the plasmacytoma MOPC 104E were cured of palpable tumors (6-15x10(7) cells) with a single injection of cyclophosphamide (10 mg/kg). Animals cured of tumor showed a considerable increase in their ability to reject secondary challenge with graded numbers of viable tumor cells. Mice with palpable subcutaneous tumors were cured therapeutically and rechallenged 22, 44, or 120 days post therapy. The ability of such animals to reject secondary tumor cell challenge was similar in all groups, which implied that in vivo tumor immunity remained relatively constant for at least 4 months post therapy. A second group of animals was treated therapeutically (10 mg cyclophosphamide/kg) 4, 11, or 20 days post tumor cell injection. These therapeutically treated animals were then rechallenged with various numbers of viable tumor cells 30 days post therapy. Mice given cyclophosphamide 4, 11, or 20 days post tumor injection rejected 6, 60, or 400 times as many tumor cells, respectively, as did control animals. These results implied that, over the range of tumor sizes investigated, exposure to greater amounts of tumor antigen resulted in increasing amounts of residual tumor immunity following cure.

Animals↗

PubMed1976

[Studies on the immunologic specificity of the macrophage-electrophoresis mobility test in mice with syngeneic and allogeneic transplants of mammary carcinoma].

The study was performed to answer the question as to whether the macrophage electrophoretic mobility test (MEM-test) is suitable to detect allogeneic and syngeneic lymphocyte sensitization in the murine mammary tumour host system. Lymph node cells of both CBAf and XVII/Bln mice injected with allogeneic or syngeneic mammary tumour cells reacted specifically to hypertonic KCl extracts from allogeneic or syngeneic mammary tumours. Lymph node cells of nontreated control mice did not react at all. The MEM results reflect lymphocyte sensitizations which are specific with respect to the claim of transplantation and tumour immunology in the system employed.

Animals↗

PubMed1986

Hyperproduction of an intracellular heterologous protein in a sacUh mutant of Bacillus subtilis.

The sacR regulatory region which controls inducible expression of sacB, the gene for extracellular levansucrase, was isolated on a 500-bp fragment of Bacillus subtilis chromosomal DNA. The region was separated into two components: a 325-bp fragment which carries a constitutive promoter and a 175-bp fragment which carries a stem-loop structure presumably involved in the induction process. The constitutive sacR promoter was used to drive expression of the plasmid-borne xylE gene, coding for intracellular catechol 2,3-dioxygenase (C23O), with its Pseudomonas ribosome-binding site, in otherwise isogenic sacU-, sacU+ and sacUh mutant strains of B. subtilis. Mutations at the sacU locus have been previously shown to affect multiple cell functions, particularly production of extracellular enzymes. The presence of the sacUh mutation allowed for hyperproduction of C23O to levels exceeding 25% of total cellular protein. This represents a 50- to 100-fold enhancement over levels observed in sacU- and sacU+ host cells. A 5- to 10-fold improvement of C23O production in sacUh cells was observed when the subtilisin (aprA) promoter was used in place of sacR. In contrast, a bacteriophage T5 synthetic promoter was found to be independent of host strain for high-level synthesis of C23O. Hyperproduction of an intracellular protein in sacUh cells suggests that enhancement of exoenzyme production, previously observed in these mutants, occurs prior to the secretion event. Therefore, hyperproduction is most likely due to elevated transcription or translation of specific nucleotide sequences.

Bacillus subtilis↗

PubMed2002

Photodynamic therapy of human breast cancer xenografts lacking caspase-3.

The human breast cancer cell line MCF-7 is deficient in procaspase-3 and in caspase-3-dependent steps in apoptosis due to deletion of the CASP-3 gene. We previously found that the cells transfected with empty vector (MCF-7v cells) were considerably less sensitive to photodynamic treatment in vitro with the phthalocyanine photosensitizer Pc 4 than were the cells stably transfected with human procaspase-3 cDNA (MCF-7c3 cells); however, overall cell killing, as determined by a clonogenic assay, was not affected by the presence of procaspase-3. The present study was undertaken to determine whether photodynamic therapy (PDT) in vivo was dependent on the ability of the cells to carry out the late steps in apoptosis that are catalyzed by this caspase. Xenografts of MCF-7 cells and the isogenic-derived MCF-7v and MCF-7c3 cells were generated in female athymic nude mice implanted with an estrogen pellet. MCF-7c3 xenografts, but not those of the other two lines, continued to express procaspase-3, as revealed by Western blots of proteins from the cells and the xenografts. When the xenografts reached 50-120 mm(3), some were treated with PDT (1mg/kg Pc 4 i.v. followed 48 h later by 150 J/cm(2) light at 672 nm and 150 mW/cm(2)), while others served as controls (no treatment, light alone, or Pc 4 alone). All Pc 4-PDT-treated tumors and none of the controls exhibited either complete or strong partial responses, and complete responses were durable for the entire observation period of 16 days. The responses were not dependent upon the presence of procaspase-3 in the xenografts. The results indicate that the rapid response of Pc 4-PDT-treated tumors in vivo is not due to their ability to carry out the major caspase-3-mediated late steps in apoptosis.

Animals↗

PubMed1999

Heavy heat shock induced retrotransposon transposition in Drosophila.

The phenomenon of transposition induction by heavy heat shock (HHS) was studied. Males of a Drosophila isogenic line with a mutation in the major gene radius incompletus (ri) were treated by HHS (37 degrees C for 1 h followed by 4 degrees C for 1 h, with the cycle repeated three times) and crossed to untreated females of the same line. The males were crossed 5 d after heat shock, and also 9 d after HHS. Many transpositions were seen in the F1 larvae by in situ hybridization. The rate of induced transposition was at least 2 orders of magnitude greater than that of the control sample, and was estimated to be 0.11 events per transposable element copy per sperm. Two 'hot' subdivisions for transpositions, induced probably during the post-meiotic stage of spermiogenesis, were found: 43B and 97DE. Three-quarters of all transpositions were localized in these positions. In other sites the rates of induced transpositions were (1.3-3.2) x 10(-2) events per occupied segment per sperm, 1 order of magnitude greater than those of the control.

Animals↗

PubMed2005

erbB-2/neu transformed rat cholangiocytes recapitulate key cellular and molecular features of human bile duct cancer.

BACKGROUND & AIMS: Cholangiocarcinomas appear to arise from the malignant transformation of cholangiocytes lining the biliary tract. Because the development of an in vitro model of malignant transformation can provide a powerful new tool for establishing critical events governing the molecular pathogenesis of cholangiocarcinoma, we investigated the potential of achieving malignant transformation of cultured rat cholangiocytes in relation to aberrant overexpression of mutationally activated erbB-2/neu. METHODS: Malignant neoplastic transformation was achieved after infection of the rat cholangiocyte cell line, designated BDE1, with the retrovirus Glu664-neu, containing the transforming rat erbB-2/neu oncogene. RESULTS: Compared with untransformed control cells, malignant transformants carrying the activating erbB-2/neu mutation prominently overexpressed p185neu receptor protein, which was phosphorylated strongly at its major autophosphorylation site at tyrosine 1248. Moreover, erbB-2/neu transformation of BDE1 cells resulted in increased telomerase activity, up-regulation of cyclooxygenase-2 with overproduction of prostaglandin E(2), enhanced phosphorylation of mitogen-activated protein kinase and of serine/threonine kinase Akt/PKB, overexpression of vascular endothelial growth factor, and increased mucin 1 messenger RNA expression. Only erbB-2/neu transformants were tumorigenic when transplanted into isogeneic rats, yielding a 100% incidence of tumors closely resembling human desmoplastic ductal cholangiocarcinomas in their morphology. Malignant cholangiocytes in the tumors were strongly immunoreactive for biliary cytokeratin 19, p185neu, and cyclooxygenase-2. CONCLUSIONS: This unique malignant transformation model recapitulates key molecular features of the human disease and appears to be well suited for testing novel molecular therapeutic strategies against cholangiocarcinoma.

Animals↗

PubMed2000

Evaluation of an isogenic major outer membrane protein-deficient mutant in the human model of Haemophilus ducreyi infection.

Haemophilus ducreyi expresses 2 OmpA homologs, designated MOMP and OmpA2, whose genes are arranged in tandem on the chromosome. Northern blot analysis indicated that momp and ompA2 are transcribed independently. Sequences of the momp open reading frame (ORF) lacking the transcriptional start site were amplified by PCR, and an Omega-Km2 cassette was ligated into the ORF. A plasmid containing this construction was electroporated into H. ducreyi 35000HP, and an isogenic MOMP-deficient mutant (35000HP-SMS2) was generated by allele exchange. In Southern blotting, 35000HP-SMS2 contained one copy of the Omega-Km2 cassette in momp. 35000HP and 35000HP-SMS2 had similar outer membrane protein (OMP) and lipooligosaccharide profiles and growth rates except for up-regulation of a putative porin protein in the mutant. Five subjects were inoculated with three doses of live 35000HP-SMS2 on one arm and two doses of live 35000HP and one dose of a heat-killed control on the other arm in a double-blind escalating dose-response trial. Pustules developed at 7 of 10 sites inoculated with 35000HP and at 6 of 15 sites inoculated with 35000HP-SMS2 (P = 0.14). 35000HP and 35000HP-SMS2 were recovered at similar rates from daily surface cultures and semiquantitative cultures. The data suggest that expression of MOMP is not required for pustule formation by H. ducreyi in the human model of infection.

Adult↗

PubMed1997

N-acyl-homoserine lactone-mediated regulation of phenazine gene expression by Pseudomonas aureofaciens 30-84 in the wheat rhizosphere.

Pseudomonas aureofaciens 30-84 is a soilborne bacterium that colonizes the wheat rhizosphere. This strain produces three phenazine antibiotics which suppress take-all disease of wheat by inhibition of the causative agent Gaeumannomyces graminis var. tritici. Phenazines also enhance survival of 30-84 within the wheat rhizosphere in competition with other organisms. Expression of the phenazine biosynthetic operon is controlled by the phzR/phzI N-acyl-homoserine lactone (AHL) response system (L. S. Pierson III et al., J. Bacterial 176:3966-3974, 1994; D. W. Wood and L. S. Pierson III, Gene 168:49-53, 1996). By using high-pressure liquid chromatography coupled with high-resolution mass spectrometry, the AHL produced by PhzI has now been identified as N-hexanoyl-homoserine lactone (HHL). In addition, the ability of HHL to serve as an interpopulation signal molecule in the wheat rhizosphere has been examined by using isogenic reporter strains. Disruption of phzI reduced expression of the phenazine biosynthetic operon 1,000-fold in the wheat rhizosphere. Coinoculation of an isogenic strain which produced the endogenous HHL signal restored phenazine gene expression in the phzI mutant to wild-type levels in situ. These results demonstrate that HHL is required for phenazine expression in situ and is an effective interpopulation signal molecule in the wheat rhizosphere.

4-Butyrolactone↗

PubMed1999

Modulation of Helicobacter pylori induced interleukin-8 synthesis in gastric epithelial cells mediated by cag PAI encoded VirD4 homologue.

BACKGROUND: Strains of Helicobacter pylori carrying the virulence associated cag pathogenicity island (PAI) induce gastric epithelial synthesis of the chemokine interleukin-8 (IL-8), a neutrophil chemoattractant, and thereby a strong inflammatory response during chronic infection of the human gastric mucosa. Previous mutational analyses have shown that many genes in the cag PAI are needed to elicit IL-8 synthesis in gastric epithelial cells, and also that some genes are not involved. AIM: To test the possibility that certain genes in the cag PAI also downregulate (modulate) the inflammatory response elicited by cag+ H pylori infection. METHODS: Cells of L5F11, a derivative of the Kato-3 gastric epithelial cell line that carries an engineered IL-8 promoter-luciferase reporter gene fusion, were cocultured with H pylori strain 26695 or with an isogenic mutant in which most of the cag PAI ORF 10 gene, an Agrobacterium virD4 homologue, was deleted. Luciferase activity was measured to assess IL-8 gene transcription and secreted IL-8 was measured by enzyme linked immunosorbent assay to assess synthesis and release of IL-8 protein from gastric epithelial cells. RESULTS: Inactivation of ORF10 led to a 2.8-fold increase in IL-8 gene transcription and a 3.6-fold increase in IL-8 synthesis and secretion. CONCLUSIONS: The results suggest that this VirD4 homologue participates in the control of inflammation that H pylori infection elicits by downregulating (modulating) the strong induction of IL-8 synthesis mediated by other cag encoded proteins.

Bacterial Proteins↗

PubMed1999

Inhibition of neointima hyperplasia of mouse vein grafts by locally applied suramin.

BACKGROUND: Saphenous vein grafts are widely used for aortocoronary bypass surgery as treatment for severe atherosclerosis and often are complicated by subsequent occlusion of the graft vessel. METHODS AND RESULTS: We described a mouse model of venous bypass graft arteriosclerosis that can be effectively retarded by locally applied suramin, a growth factor receptor antagonist. Mouse isogeneic vessels of the vena cava veins pretreated with suramin were grafted end to end into the carotid arteries and enveloped with a mixture of suramin (1 mmol/L) and pluronic-127 gel. In the untreated group, vessel wall thickening was observed as early as 1 week after surgery and progressed to 4-fold and 10-fold the original thickness in grafted veins at 4 and 8 weeks, respectively. Pluronic-127 gel alone did not influence neointima formation. Suramin treatment reduced the neointima hyperplasia 50% to 70% compared with untreated controls. Immunohistochemical studies demonstrated that a significant proliferation of vascular smooth muscle cells (SMCs) constituted neointimal lesions between 4 and 8 weeks. The majority of SMCs expressed platelet-derived growth factor (PDGF) receptors-alpha and -beta, which were significantly reduced by suramin treatment. In vitro studies indicated that suramin completely blocked PDGF receptor activation or phosphorylation stimulated by PDGF-AB, inhibited activation of mitogen-activated protein kinase (ERK) kinases (MEK1/2) and ERK1/2, and abrogated transcription factor AP-1 DNA-binding activity. CONCLUSIONS: Suramin inhibited SMC migration and proliferation in vivo and in vitro by blocking PDGF-initiated PDGF receptor and MAPK-AP-1 signaling. These findings indicate that locally applied suramin is effective in a mouse model of venous bypass graft arteriosclerosis.

Animals↗

PubMed2000

The effect of vincristine on the biodistribution of technetium-99m DTPA, GHA, and DMSA in Balb/c female mice.

OBJECTIVE: Vincristine has been widely used in various chemotherapeutic protocols in oncology. The purpose of this study was to evaluate the effect of vincristine on the biodistribution of 99mTc-DMSA, 99mTc-GHA, and 99mTc-DTPA in Balb/c female mice. METHODS: Vincristine (0.03 mg, 0.3 mL) was injected into female isogenic Balb/c mice (n = 15), in 3 doses over an interval of 96 h. The 99mTc-DMSA, 99mTc-GHA, or 99mTc-DTPA (7.4 MBq) was administered after the last dose of vincristine. After 0.5 h the animals were killed rapidly. The organs (pancreas, thyroid, brain, thymus, ovary, uterus, spleen, kidney, heart, stomach, lung, liver, bone, and lymph nodes) were isolated and the radioactivity in each organ was counted in a NaI(Tl) well counter. The percentage of radioactivity (%) in each was calculated and compared with the control group. Statistical analysis was performed by Wilcoxon test (P < 0.05). RESULTS: The percentage of 99mTc-DMSA was increased in the lung, pancreas, heart, thyroid, brain, bone, and lymph nodes (inguinal and mesenteric). The percentage of 99mTc-GHA was decreased in the uterus, ovary, spleen, thymus, lymph nodes (inguinal and mesenteric), kidney, and heart. The percentage of 99mTc-DTPAwas increased in thymus, lymph nodes (inguinal and mesenteric), ovary, uterus, spleen, kidney, heart, stomach, lung, liver, and bone. CONCLUSION: The results could be explained by the metabolization, toxic effect, therapeutic, or immunosupressive action of the studied chemotherapeutic drug.

Animals↗

PubMed2004

Intestinal colonisation-inhibition and virulence of Salmonella phoP, rpoS and ompC deletion mutants in chickens.

Administration of live Salmonella strains to day-old chicks provides profound protection against superinfection with a related strain within a matter of hours by a colonisation-inhibition mechanism, which is primarily a bacterial physiological process. Although currently available, commercial, live attenuated Salmonella vaccines induce protection by adaptive immunity, none of them is able to induce protection against Salmonella organisms by colonisation-inhibition and, therefore, they are unable to protect newly-hatched birds immediately after oral vaccination. In this study, mutants of Salmonella Typhimurium and Enteritidis with deletions in phoP and rpoS, either alone or in combination with ompC, were characterised and tested for their level of attenuation and their ability to inhibit the intestinal colonisation of the isogenic parent strains in chickens. Mutants with deletions only in rpoS demonstrated an unaffected potential to inhibit the intestinal colonisation of the challenge strain but were still fully virulent for the chickens. Mutants with deletions in phoP, either alone or in combination with rpoS, resulted in a high level of attenuation, unimpaired ability to colonise the gut and a nearly unaffected potential to inhibit the challenge strain from caecal colonisation. Mutants with an additional deletion in ompC revealed a reduced capacity of intestinal colonisation-inhibition when compared to the control strains and both the single rpoS and the phoP deletion mutants. Mutations in phoP- or phoP-regulated genes may therefore be used for the development of live attenuated Salmonella vaccines possessing these novel characteristics.

Animals↗

PubMed2002

Morbidity and mortality of chronic GVHD after hematopoietic stem cell transplantation from HLA-identical siblings for patients with aplastic or refractory anemias.

We analyzed effects of successive changes in prevention and treatment of chronic GVHD in 405 patients with aplastic anemia and refractory anemia given HLA-matched hematopoietic stem cell transplantation (HSCT) from 1970-1997. For analysis, patients were divided into group I, transplantations from 1970-1976; group II, 1977-1983; group III, 1984-1990; and group IV, 1991-1997. The overall incidence of chronic GVHD was 28%. Incidences of chronic GVHD for groups I through IV were 20%, 46%, 41%, and 22%, respectively, reflecting added buffy coat infusions in groups II and III. Five-year survival rates of patients with chronic GVHD for groups I through IV were 58%, 74%, 82%, and 76%, respectively (NS). Among group I patients, 50% were alive off immunosuppression, none were alive on immunosuppression, and 50% died. These figures were 76%, 0%, and 24% in group II; 80%, 10%, and 10% in group III; and 64%, 21%, and 14% in group IV patients. More serious infections and skin contractures were seen in group I than in groups II, III, and IV (P = .0001, .02, .01 and P =.0003, .001, .05, respectively). Lung complications, aseptic necroses, depression, and Karnofsky scores were comparable among groups. Gastrointestinal complications seemed less frequent among groups II through IV. Diabetes mellitus was more frequent in group IV than in groups I through III (P = .008). Secondary malignancies occurred in 33%, 6%, 3%, and 0% of patients in the 4 groups, respectively. In conclusion, over 28 years, chronic GVHD has remained challenging, with only slight improvements in quality of life. Decisive improvements in therapy and survival will have to await both a better understanding of the immunological events underlying chronic GVHD and better infection prevention and control.

Adolescent↗

PubMed1994

Transplantation of fetal adrenal glands in syngeneic rat strains.

In a syngeneic rat model we investigated the feasibility of fetal adrenal gland transplantation into adult recipient animals. We determined the optimal site of graft implantation by morphological criteria. Transplantation into the omentum majus proved superior to transplantation underneath the fascia of the rectus abdominis muscle possibly due to superior access to vascular supply. We assessed transplant function by sequential determinations of serum corticosterone, aldosterone, sodium and body weight. We compared rats which received syngeneic fetal adrenal transplants and underwent excision of their own adrenal glands four weeks thereafter to control animals without adrenalectomy or transplantation and to adrenalectomized animals without prior transplantation. The total study period was 16 weeks. Whereas all adrenalectomized rats without prior transplantation died within 2 weeks, all the animals which had received fetal adrenal grafts survived. Their serum sodium remained within normal limits. Weight gain and serum corticosterone levels were decreased when compared to control animals. Aldosterone levels dropped intermittently but had normalized by 16 weeks. We conclude that fetal adrenal grafts may be able to substitute for the animals' own adrenal glands in the syngeneic model.

Adrenal Glands↗