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Biomedical subjects

P Toivanen

Publications and source records attributed to P Toivanen.

At least 181 records · Page 10Linked to original sources
PubMed1987

Major histocompatibility complex and cell cooperation.

We have studied the role of major histocompatibility antigens on cell cooperation in the immune response of the chicken. In the 1970's, shortly after the initial discoveries in the mouse, we demonstrated that the T cell-B cell interaction is major histocompatibility complex (MHC)-dependent in the chicken and requires at least one haplotype identity between the collaborating cells. Later, by using MHC-congenic and MHC-recombinant lines, we demonstrated that the T-B cell interaction in antibody response is MHC-restricted, and more precisely, Class II MHC-antigen-restricted. Furthermore, we proved that T-B cell cooperation in splenic germinal center formation is likewise class II MHC antigen-restricted. Recently, we have focused our studies on MHC antigen identity requirements during antigen presentation by macrophages to T cells. In these studies, Class II antigens were found to serve as restriction elements in antigen recognition by T cells. Cytotoxic T cells of the chicken have been shown to be MHC-restricted in their function. Whether Class I or Class II MHC antigens serve as restriction molecules has not yet been determined. In conclusion, it is obvious that the function of the avian immune response is controlled by the polymorphic MHC gene products in the same way as that in the mammalian species.

Animals↗
PubMed1986

Mechanisms of transplantation tolerance in B-cell-chimeric chickens. Impairment of tolerance by T cell growth factor.

Transplantation tolerance was induced in cyclophosphamide-treated, B-cell-depleted chickens by transfer of allogeneic bursal cells. To study the presence of specific suppressor cells in tolerant birds, mitomycin-C-treated peripheral blood lymphocytes (PBL) from tolerant recipients were cocultured in mixed lymphocyte cultures of normal syngeneic responder and allogeneic stimulator cells. No evidence of suppression was detected, since responses in cultures with tolerant cocultured cells were on the same level as the mixed lymphocyte reaction (MLR) of normal responders without cocultured cells. However, responses in cultures with normal cocultured cells were significantly higher. If cocultured cells were not treated with mitomycin C, responses to tolerizing alloantigen were equally high in cultures with tolerant cocultured cells as in cultures with normal cocultured cells. Likewise, when lymphocytes from tolerant chickens were mixed with normal syngeneic cells in graft-versus-host (GVH) splenomegaly assay, no suppression was detected, but the GVH reaction was even stronger than the reaction induced by the mixture of cells from two normal chickens. Furthermore, administration of chicken T cell growth factor (TCGF) into the cultures enhanced considerably the MLR of tolerant cells against the tolerizing alloantigen, but not against syngeneic or third-party stimulator cells. These results indicate that the transplantation tolerance in B-cell-chimeric chickens is due to lack of alloantigen-specific helper cells. When exogenous help is offered to tolerant cells either by normal syngeneic cells or by exogenous TCGF, the reactivity of tolerant cells against the tolerogen is reestablished.

Animals↗
PubMed1986

Inability to transfer immune unresponsiveness of chickens bursectomized at 60 hours of incubation.

Chickens surgically bursectomized (Bx) at 60 hours of incubation have been found unable to produce specific antibodies, in spite of close-to-normal serum immunoglobulin levels. Suppressor cell overactivity as a reason for the impaired antibody production in the Bx chickens has not been ruled out. In the present work, we have studied whether the state of immune unresponsiveness of the Bx chickens can be transferred to normal chickens by transfer of bone marrow cells. Bone marrow cells from 10-week-old Bx or control (Co) chickens were grafted into x-ray-irradiated histocompatible 5-12-day-old normal recipients. After the transplantation the recipients were immunized with a pool of five antigens, and the antibody responses were quantitated by ELISA. The inability of the Bx chickens to produce specific antibodies could not be transferred to normal chickens by transfer of bone marrow cells, as no differences in the antibody responses between the two recipient groups were observed. The results indicate that suppressor cells do not play a role in preventing specific antibody formation in the Bx chickens.

Animals↗
PubMed1986

Reliability of a disk diffusion method using semiconfluent growth in the determination of aminoglycoside resistance.

Susceptibility of 553 blood culture isolates to gentamicin, tobramycin, amikacin, and netilmicin was determined by a routine disk diffusion method with semiconfluent growth (AB Biodisk, Solna, Sweden) and a microtiter-method (Sensititre). The disk diffusion test gave false sensitive results in 9.4-71% of the 9-39 aminoglycoside resistant strains studied. False resistant results occurred in 1.0-7.6% of measurements among the over 500 aminoglycoside sensitive strains. Because of the frequent error rate, the disk method with semiconfluent growth should be replaced with other methods in the determination of aminoglycoside resistance in bacteriological laboratories.

Amikacin↗
PubMed1986

Emergence of trimethoprim resistance in relation to drug consumption in a Finnish hospital from 1971 through 1984.

Emergence of trimethoprim resistance among urinary tract Escherichia coli strains, isolated mostly from long-term patients in the Turku City Hospital, Turku, Finland, was studied from 1971 through 1984. Emergence of resistance to trimethoprim was associated with changes in the consumption of both trimethoprim-sulfamethoxazole and trimethoprim, with occurrence of high-level trimethoprim resistance and sequences homologous to trimethoprim resistance transposon Tn7. Since 1971, resistance of E. coli to trimethoprim-sulfamethoxazole increased from 8 to between 32 and 35% in 1983 and 1984; resistance to sulfamethoxazole varied from 39 to between 40 and 44%. The frequency of DNA sequence homology with our Tn7 probe among trimethoprim-resistant E. coli strains was 42% from 1980 to 1981 and 64% in 1983 (P less than 0.005). Fourteen years after the introduction of trimethoprim therapy in this hospital, resistance has reached the level of resistance to sulfonamide.

Drug Combinations↗
PubMed1985

Trimethoprim resistance of Escherichia coli in outpatients in Finland after ten years' use of plain trimethoprim.

Development of trimethoprim resistance among Escherichia coli collected from urine samples in three areas in Finland was studied in 1978-1984. Three different trends of development of resistance were found: in the Turku area resistance has increased evenly during 1978-1982 from 5.4% to 10.1%, but thereafter a plateau seems to have been reached; in the Helsinki area resistance increased rapidly from 2.9% in 1980 to 11.1% in 1984, possibly due to the spread of a trimethoprim resistance transposon Tn7, which occurred significantly more often among E. coli strains in this area than in the Turku area; in the Rovaniemi area resistance has been at a plateau level, between 3.1 and 5.7%, during the whole study. No clear correlation between the consumption of trimethoprim and the level of resistance was found. The frequency of trimethoprim resistance in E. coli isolated from patients less than 65 years was 5.2% and in those isolated from patients greater than or equal to 65 years 14.7%.

DNA Transposable Elements↗
PubMed1985

Lymphoid cell chimerism and transplantation tolerance induced by bursal and postbursal cells.

Transplantation of allogeneic bursal cells into cyclophosphamide-treated, immunodeficient chickens is a useful experimental model for analyzing the mechanisms of transplantation tolerance, especially because transplanted bursal cells do not produce graft-versus-host disease. In this study we have determined B-lymphoid chimerism in various lymphoid organs after transplantation of allogeneic bursal stem cells or postbursal cells, and used a variety of tests to determine presence of immunological tolerance. Transplanted bursal stem cells induced a state of stable chimerism that could easily be detected in peripheral blood and other lymphoid organs. Chimerism induced by postbursal cells was low in peripheral blood, but clearly observable in other lymphoid organs, especially in spleen and thymus. Both bursal and postbursal cells induced specific unresponsiveness to donor-line alloantigens. Bursal cell recipients accepted donor line skin grafts--and their graft-versus-host reactivity, as assayed by embryonal splenomegaly, and mixed lymphocyte reactivity against donor line alloantigens were significantly decreased. Despite differences in chimerism, a strong transplantation tolerance was readily induced with bursal stem cells and with postbursal cells.

Animals↗
PubMed1985

Natural killer cell activity of human fetal liver cells after allogeneic stimulation.

Cells isolated from the liver of human fetuses were confronted with mitomycin C-treated adult allogeneic cells. After this mixed leukocyte culture (MLC)-type reaction, the cytotoxic activity of fetal cells was tested against K562 cell line in a 4-h 51Cr release assay. Three of the seven fetuses tested (8 to 11 weeks of gestational age) expressed marginal cytotoxic activity before cultivation. Cells from one 8-week-old and one 9-week-old fetus were slightly more cytotoxic when cultured in the presence of allogeneic cells than when cultured in the medium only. Production of gamma interferon (IFN-gamma) was not detected in these cultures. Cells of one 18-week-old fetus expressed strong cytotoxic activity against K562 cells after MLC. Thymocytes from the same fetus were not cytotoxic, either before or after MLC against K562 cells. The results indicate that the 'prethymic' human liver contains cytotoxic cells able to spontaneously kill natural killer (NK)-sensitive target cells. Generation of strong NK-like cytotoxicity from noncytotoxic precursor cells was observed only after the thymus becomes lymphoid, suggesting that thymus-processed cells may regulate the generation of NK-like cytotoxic activity. The results suggest a different ontogeny of spontaneous and MLC-induced NK-like cells in the human fetus.

Cell Division↗
PubMed1985

Emergence of trimethoprim resistance in fecal flora.

The emergence of trimethoprim (TMP) resistance in fecal flora was compared in patients with urinary tract infection treated with TMP or TMP-sulfamethoxazole. No significant differences were found in the occurrence of TMP-resistant fecal aerobic bacteria in the two treatment groups before and after treatment.

Adolescent↗
PubMed1984

Immune capacity of the chicken bursectomized at 60 hr of incubation: cytoplasmic immunoglobulins and histological findings.

Chickens were surgically bursectomized at 60 hr of incubation, before the bursal anlage appears. Completeness of the bursectomy was confirmed at autopsy at 10 weeks of age. These embryonically bursectomized (Bx)3 chickens are known to produce immunoglobulins of IgM, IgG, and IgA classes but so far no specific antibodies have been observed even after heavy immunization. The Bx chickens had mature plasma cells in an almost normal frequency when studied at 10 weeks of age. The amount of germinal center formation in the spleen and cecal tonsils was markedly decreased when compared to the control (Co) chickens. Also, the frequency of cytoplasmic IgA-positive (c-IgA+) cells was severely decreased in the Bx animals, whereas the occurrence of c-IgG+ and c-IgM+ cells was not affected to the same extent. These findings support the hypothesis that heavy-chain class switch may occur without the bursal influence, and that the bursa of Fabricius is essential only for expansion or creation of the antibody repertoire.

Aging↗
PubMed1984

Characterization of trimethoprim resistance by use of probes specific for transposon Tn7.

Transposon Tn7 codes for resistance to trimethoprim and streptomycin. For detection of Tn7 by DNA-DNA hybridization, two recombinant plasmids were constructed. The former contained a 1-kilobase BamHI fragment and the latter contained a 4.3-kilobase EcoRI-BamHI fragment of Tn7. These DNA fragments, which did not include the drug resistance genes, were used as probes for detecting Tn7-like sequences in bacterial strains by colony hybridization. They hybridized strongly to bacterial DNA known to carry Tn7 but not to DNA known to carry transposons other than Tn7. These probes were used to study the occurrence of Tn7 in bacterial strains isolated in the Turku City Hospital in Finland. Transposon Tn7 was present in 47.2% of 199 trimethoprim-resistant enterobacteria (MIC greater than or equal to 8 micrograms/ml). Among the 69 Proteus mirabilis strains studied, 75% contained Tn7, although none of these strains transferred trimethoprim resistance in conjugation tests. The reliability of colony hybridization was further confirmed by Southern hybridization to detect the Tn7-specific 2.6-kilobase HindIII restriction fragment. Colony hybridization proved to be a sensitive and rapid method for detecting Tn7-determined sequences.

Bacteria↗
PubMed1984

Aminoglycoside resistance among blood culture isolates.

A total of 633 blood culture isolates were collected from 1981 to 1982 from seven major Finnish hospitals, including all university central hospitals. Susceptibility of the strains to gentamicin, tobramycin, amikacin, and netilmicin was determined by the Sensititre microtiter procedure. Resistance against any of these agents occurred in 1.3 to 6.5% of all strains studied. In the Turku University Central Hospital, an increased number of tobramycin- and gentamicin-resistant Staphylococcus epidermidis were found; the frequency of strains resistant to tobramycin was 57% and to gentamicin was 29% versus frequencies of 16 and 18%, respectively, which were observed in the other hospitals. An explanation for this might be a change in the use of aminoglycosides in the Turku University Central Hospital; within 3 years, 1979 to 1981, the consumption of tobramycin and amikacin had increased 330 and 290%, respectively, whereas the use of gentamicin had decreased to 24% of that in the beginning of the period. Resistance against tobramycin was mediated by enzymes APH(2")-AAC(6') and ANT(4').

Amikacin↗