PubMed Health⌕ Search

Biomedical subjects

A Seto

Publications and source records attributed to A Seto.

At least 73 records · Page 4Linked to original sources

The role of Escherichia coli haemolysin in the pathogenic synergy of colonic bacteria in subcutaneous abscess formation in mice.

The growth of nine species of colonic bacteria--Escherichia coli, Enterococcus faecalis, Bacteroides ovatus, Fusobacterium varium, Clostridium perfringens, Klebsiella pneumoniae, Proteus vulgaris, Staphylococcus aureus and Bifidobacterium adolescentis--was examined after concomitant injection to form experimental subcutaneous abscesses in mice. Injection of a mixture of c. 10(5) cfu of each of the first five strains (E. coli, Ent. faecalis, B. ovatis, F. varium and C. perfringens) resulted in abscess formation in all mice tested when the E. coli strain was haemolytic. E. coli and B. ovatus multiplied and reached a maximum population of c. 10(8) cfu/abscess. When non-haemolytic E. coli was used, injection of greater than or equal to 10(7) cfu was required for abscess formation. The inclusion of partially purified E. coli haemolysin (125 HU50) with c. 10(5) cfu of bacteria including non-haemolytic E. coli resulted in abscess formation in most mice tested. These results indicate that E. coli haemolysin is one factor that may potentiate pathogenic synergy among colonic bacteria especially between E. coli and B. ovatus, during abscess formation.

Abscess↗

Protein breakdown in submandibular glands rendered hypertrophic by amputation of lower incisor teeth in rats.

Protein breakdown in submandibular glands rendered hypertrophic by amputation of the lower incisor teeth in rats was investigated. Reduced protein breakdown was observed in the hypertrophic gland tissues, and was found to be inhibited by 20 mM epsilon-amino-n-caproic acid, an inhibitor of serine protease, and 50 microM leupeptin, an inhibitor of trypsin, plasmin, papain and cathepsin B, but not by 2 mM PMSF (phenylmethylsulfonyl fluoride), an inhibitor of serine protease, 10 microM pepstatin, an inhibitor of cathepsin D and 20 microM antipain, an inhibitor of cathepsin A and B. These results suggest that some serine proteases and leupeptin-sensitive proteases (presumably cathepsin B) participate in protein breakdown in hypertrophic gland tissues, and that hypertrophy of the submandibular glands is closely related to the reduced protein breakdown in these tissues.

Aminocaproic Acid↗

IL-2 receptors on rabbit T-cell lines and their transfectants expressing the human IL-2 receptor alpha chain.

Low-affinity (dissociation constant: Kd = 7 nM) and high-affinity (Kd = 27 pM) interleukin-2 receptors (IL-2R) were detected on rabbit T-cell lines by IL-2 binding studies. Chemical cross-linking studies using 125I-labelled IL-2 showed that rabbit low-affinity IL-2R was singly expressed alpha-chain (MW 55,000) and that high-affinity IL-2R was composed of at least alpha- and beta- (MW 75,000) chains, similar to the human and murine counterparts. The existence of an additional chain (MW 25,000) was suggested in the rabbit IL-2R. Rabbit T-cell transfectant lines were established by human IL-2R alpha-chain (IL-2R alpha) cDNA transfection. These transfectant lines possessed not only extremely large numbers of human IL-2R alpha (over 10 times more than endogenous rabbit alpha-chain) but also twice as many high-affinity sites as their parental lines. The number of high-affinity sites on the transfectants significantly decreased when human alpha-chains were blocked, indicating that these transfectants expressed high-affinity receptor consisting of the exogenous human alpha-chain and rabbit beta-chain. This was confirmed by cross-linking experiments. The observation that expression of extremely large numbers of exogenous alpha-chains lead to an increase of the total number of high-affinity sites in the apparent absence of an increase of beta-chain expression raises the possibility that not only the beta-chain but also the alpha-chain may play an important role in regulating the number of high-affinity receptors.

Animals↗

Polyclonal increase of HTLV-I provirus-carrying lymphocytes in HTLV-I-carrier rabbits transplanted with Shope carcinoma cells.

Fifteen HTLV-I carrier rabbits of two inbred strains and their F1 hybrid were inoculated with Shope carcinoma cells. The peripheral blood leukocyte counts in all these rabbits increased to 2-4 times the preinoculation level with a concomitant increase in abnormal lymphocytes. Southern blotting analyses of peripheral blood leukocytes revealed the polyclonal integration of HTLV-I proviral genome in all these animals. However, lymphocytic infiltration without any apparent leukemic infiltration was observed in major organs of these animals; a similar but slight lymphocytic infiltration was also observed in non-carrier control animals inoculated with Shope carcinoma cells. These results are interpreted as indicating that the growth of squamous cell carcinoma in HTLV-I carrier rabbits induced the polyclonal expansion of provirus-carrying cells, which may correspond to the intermediate state between healthy carrier and smouldering ATL.

Animals↗

Induction of leukemic infiltration by allogeneic transfer of HTLV-I-transformed T cells in rabbits.

An HTLV-I-transformed T-cell line from a (B/J x Chbb:HM)F1 rabbit was intravenously inoculated at a dose of 1 x 10(8) cells into B/J and Chbb:HM adult rabbits. All B/J rabbits died or became moribund 6-13 days later, whereas all Chbb:HM rabbits survived without disease symptoms. Marked leukocytosis was observed in Chbb:HM rabbits but not in B/J rabbits, the leukocyte counts in the peripheral blood of the former being 10-30 times the normal level 10 days post-inoculation with most cells being of normal lymphoid appearance. Pathological examination of dead B/J animals revealed leukemic infiltration of abnormal lymphocytes in major organs, the infiltrate being composed of medium-sized lymphoid cells with pan T-cell marker, convoluted vesicular nuclei and frequent mitotic figures. These results indicate that allogeneic transfer of HTLV-I-transformed cells can induce leukemic infiltration under appropriate conditions. Similar leukemic infiltration was observed in major organs of random-bred rabbits 72 h after a similar inoculation of the same cell line. Such adult T-cell leukemia-like disease induced in random-bred rabbits may be useful in studying the mechanism and the prevention of leukemic infiltration.

Animals↗

Seronegative virus carriers in the infection of rabbits with human T lymphotropic virus type I.

Six HTLV-I-transformed T cell lines were prepared from PBL of three rabbits each of B/J and Chbb:HM strains, and were inoculated into newborn rabbits of these two strains, and of their F1 hybrid. None of three B/J cell lines induced anti-HTLV-I antibody response in newborn B/J rabbits, whereas all three Chbb:HM cell lines did induce a response in newborn Chbb:HM rabbits. These B/J cell lines however could induce antibody response in adult B/J as well as newborn Chbb:HM rabbits, and a Chbb:HM cell line could induce a response in a newborn B/J rabbit. Similar unresponsiveness was observed in (B/J x Chbb:HM)F1 hybrids neonatally inoculated with B/J cells. Unresponsiveness was abrogated by reinoculation of some but not other cell lines. Viral antigen-positive cell lines harboring HTLV-I provirus genomes were established from such seronegative B/J and F1 rabbits. Simultaneous inoculation of HTLV-I-transformed cells and SPV resulted in the induction of papilloma and antibody against SPV, but not antibody against HTLV-I. The present findings thus reveal that neonatal infection of HTLV-I could result in immunological tolerance to the virus antigens, thereby leading to a persistent infection without antibody induction.

Animals↗

Adult T cell leukemia-like disease experimentally induced in rabbits.

An HTLV-I-transformed T cell line, obtained from the peripheral blood of a virus-infected (B/J X Chbb:HM) F1 rabbit, was able to kill syngeneic newborn rabbits within 7 days, when inoculated intraperitoneally at a dose of 1 X 10(8) cells. Inoculation of 1 X 10(7) cells killed or rendered moribund 50% of inoculated animals, while surviving animals exhibited cell-mediated cytotoxic activities against the transformed cells. The peripheral blood leukocyte counts increased in all surviving animals, in association with appearance of abnormal lymphocytes with convoluted or lobulated nuclei. Pathological examination of animals that died one week post-inoculation revealed no tumors in the abdominal cavity, but accumulation of ascites containing abnormal lymphocytes. Histological examination showed leukemic infiltration in the liver, lungs, spleen and mesenteric lymph nodes. The same cell line was also able to kill syngeneic adult rabbits in 8-10 days when inoculated intravenously, but not intraperitoneally, at a dose of 1 X 10(8) cells. Leukemic infiltration was observed in the major organs of these animals. Adult animals which were already virus carriers were resistant to this lethal inoculation. This rabbit ATL-like disease may prove to be useful as an experimental model for acute adult T cell leukemia.

Aging↗

Induction of preleukemic stage of adult T cell leukemia-like disease in rabbits.

Two HTLV-I-carrying T cell lines were prepared from peripheral lymphocytes of a virus-infected (B/J X Chbb:HM) F1 rabbit, and these cells were inoculated intraperitoneally into 5 newborn F1 rabbits. These animals were killed 3-5 weeks later. Their leukocyte counts were higher than those in normal control animals, with abnormal lymphocytes amounting to 3-5% of total leukocytes. Histological examination showed leukemic infiltration in liver, spleen, lung and kidneys of all these animals. The peripheral lymphocytes at first lacked HTLV-I antigens, but became antigen-positive after in vitro culture. Southern blot analysis of these cells revealed HTLV-I integration patterns different from those of the inoculated cells.

Animals↗

Induction of antibodies against Newcastle disease virus with syngeneic anti-idiotype antibodies in mice.

Anti-idiotype antibodies were induced by injecting BALB/c mice with syngeneic antibody against the hemagglutinin of Newcastle disease virus (NDV). These anti-idiotype antibodies were purified and injected into syngeneic mice. Anti-anti-idiotype sera thus prepared contained antibodies against the hemagglutinin of NDV. This NDV-mouse experimental system might provide a good experimental model for investigation of basic problems of idiotype vaccine.

Animals↗

[Production of allotype by bone marrow cells transferred to rabbits subjected to suppressor treatment by allotype].

Inbred rabbits of B/J strain were immunized against Salmonella typhi and their bone marrow cells plus LPS were injected into (Chbb: HM X B/J) F1 hybrids at the age of 3-7 weeks, which had received at birth a treatment of the allotype suppression. Antityphoid antibodies bearing the suppressed allotype were found in the serum of the recipients, which showed no signs of the graft versus host reaction.

Animals↗

Autoanti-allotype antibodies and idiotypic network regulating allotype production in rabbits.

Anti-idiotype sera were prepared by immunization of inbred B/J as well as random-bred rabbits with anti-b4 antibodies from a syngeneic rabbit. These antisera inhibited the binding between b4 and anti-b4 from different animals to various degrees. Anti-anti-idiotype sera prepared in syngeneic rabbits also inhibited the binding between anti-b4 and anti-idiotype from different animals, and did not contain anti-b4 antibodies. These results suggest that at least some anti-b4 and anti-idiotype antibodies could carry the same or similar idiotypes, respectively. Treatment of b4b5 F1(B/J X Chbb:HM) hybrids at birth with these anti-idiotype sera from B/J rabbits resulted in a modulated production of the allelic allotypes in the serum. Anti-idiotype serum against anti-b4 induced an elevated production of b4 with little effect on the production of b5 in the same serum. In F1 hybrids born from a doe immunized with anti-idiotype antibodies against anti-b4, there was a decreased production of b4, followed by a gradual recovery to normal levels. Serum b5 levels in F1 offspring of one particular Chbb:HM doe were extremely low, as compared with those in other F1 hybrids and the b4/b5 ratio in the serum was unusually high. Such low b5 levels were no longer observed when offspring of this doe were given normal b5 serum at birth. Anti-b5 activity was not detected in the serum of this doe. These observations strongly suggest the presence in normal rabbits of the autoanti-allotype antibody and of the idiotypic network involving this antibody and regulating allotype production.

Animals↗

Effects of anti-idiotypic immunizations on autoimmune uveitis induced with isologous lens proteins.

Autoimmune uveitis was induced in F1 hybrid rabbits by administering intramuscularly lens proteins in Freund's complete adjuvant. Cellular infiltration in the anterior chamber of the eye appeared in a cyclic manner and anti-lens protein antibody in the serum was mostly of oligoclonal origin, as assessed by isoelectric focusing analysis. Immunizations of such rabbits with autologous or isologous anti-lens protein antibody affected little the appearance of cellular infiltration upon rechallenge with lens proteins, but anti-lens protein antibody was replaced by other antibodies with different isoelectric points. Serum from these rabbits contained antibody which inhibited the antibody activity of certain anti-lens protein antibody.

Animals↗

[Possible existence of autoantibodies against immunoglobulin allotypes in normal rabbits, and their relation to the expression of these allotypes].

The concentration of a3 allotype was increased in the serum of heterozygous a1 a3 rabbits which received antiidiotypic antibodies against anti-a3 antibodies in the perinatal period. This is explained by the normal presence of anti-a3 autoantibodies which control the expression of a3 allotype in heterozygous a1 a3 rabbits under physiological conditions.

Animals↗

Hemopoietic responses of LPS-unresponsive C3H/HeJ mice to salmonella infection.

Effects of Salmonella enteritidis infection on hemopoietic stem cells were examined in LPS-unresponsive C3H/HeJ mice. The salmonella infection increased pluripotent stem cells (CFUs) and granulocyte-macrophage progenitor cells (CFUc) in the spleen and decreased these hemopoietic stem cells in the bone marrow. These responses seemed to be specific to salmonella infection and not due to biological activities of LPS.

Animals↗