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F Ota

Publications and source records attributed to F Ota.

At least 55 records · Page 3Linked to original sources

Epithelioid granuloma induced by muramyl dipeptide in immunologically deficient rats.

When WKA rats were either neonatally thymectomized or injected with anti-rat thymocyte sera, their T-cell functions were effectively suppressed. When neonatally thymectomized plus anti-rat thymocyte serum-treated rats were injected with non-immunogenic muramyl dipeptide in water-in-oil emulsion, they produced massive epithelioid granulomas. Essentially, no morphological difference was noticed between granulomas induced in untreated rats and in thymectomized plus anti-rat thymocyte serum-treated rats. These findings strongly suggest that muramyl dipeptide-induced epithelioid granulomas required no T cells for their formation. In contrast, the induction of adjuvant arthritis appeared to depend on the presence of T cells.

Acetylmuramyl-Alanyl-Isoglutamine↗

Anisotropic inhibition of energy transduction in oxidative phosphorylation in rat liver mitochondria by tetraphenylarsonium.

Tetraphenylarsonium (TPA+) inhibited energy transduction in oxidative phosphorylation in mitochondria but not in submitochondrial particles, which are inside-out relative to the membranes of mitochondria. TPA+ incorporated into the inside of submitochondrial particles inhibited ATP synthesis in the particles. TPA+ also inhibited the reduction of NAD by succinate coupled with oxidation of succinate by O2 and hydrolysis of ATP. Energization of mitochondrial inner membranes with succinate and with ATP induced binding sites on the membranes for TPA+. The amounts of energy-dependent binding sites for TPA+ on mitochondria energized with succinate and with ATP, respectively, were 90 and 13 nmol/mg of protein. TPA+ also caused shrinkage of mitochondria energized with succinate and with ATP in an energy-dependent fashion. The energy-dependent binding of TPA+, TPA+-induced H+-ejection, TPA+-induced shrinkage of mitochondria, and TPA+-induced inhibition of energy transduction occurred in parallel. The present findings show that TPA+ inhibits energy transduction by binding to negative charges created on lipophilic domains near the surface of the outer side (C-side) of the mitochondrial inner membranes, and that it has no inhibitory activity on the inner side (M-side) of the membranes.

Adenosine Triphosphate↗

Preparation of antisera specific for guinea pig B cells.

Heterologous antisera against guinea pig B lymphocytes have been prepared in rabbits. Sera, obtained 1 week after a third injection of cells from a guinea pig leukemic B cell line (L2C), were absorbed with guinea pig and sheep erythrocytes and guinea pig thymocytes. In the presence of complement, selected antisera killed both L2C cells (85%) and B cells from Hartley outbred guinea pigs (85%). Normal rabbit serum kills guinea pig thymocytes and this ability was enhanced in the sera obtained from rabbits immunized with L2C cells. After three absorptions with thymocytes the antisera retained their cytotoxicity for B cells but did not kill guinea pig thymocytes or peripheral T lymphocytes. The antigenic determinants on the L2C cells that simulate anti-B cell activity are unknown but surface membrane immunoglobulins were excluded. The development of methodology for obtaining a potent and specific anti-guinea pig B cell serum should significantly improve the usefulness of guinea pigs as animals for in vitro studies.

Animals↗

Type and strain variation in induction of L forms of Neisseria gonorrhoeae.

Strains of Neisseria gonorrhoeae were inoculated onto brain heart infusion (Difco) agar supplemented with penicillin and polyvinylpyrrolidone (PVP) as a stabilizer and cultivated in a candle extinction jar. L-form colonies became visible after a few days. They continued to grow and were viable for up to 38 days. The extent of inducibility of L forms of N. gonorrhoeae was examined semiquantitatively. It was found to be constant for each type and strain and to depend only slightly on the amount of penicillin added to the medium. None of the types of one strain produced L-form colonies. In another strain, avirulent types (T3, T4) showed more ability to produce L forms than virulent types (T1, T2) and no L forms were produced by the subtypes of T1 and T2-T1a and T2a. In a third strain, only T4 produced L forms. Electron microscopic studies showed that the L forms consisted of a number of membranous vesicles and a variety of cell types such as those completely lacking cell walls and those with only remnants of cell walls. The results indicate the existence of subtypes of T1 and T2 of gonococci and the intrinsic inducibility of gonococcal types and strains to produce L forms.

Culture Media↗

The goat mammary gland as a model infection site for Neisseria gonorrhoeae.

Live and formalin-killed gonococci were instilled into the mammary glands of lactating and nonlactating goats. In lactating goats viable gonococci elicited a limited inflammatory process whereas in non-lactating goats, severe inflammation and swelling appeared and peaked on the 3rd day after instillation and persisted for about 10 days. No viable gonococci were recovered after the first day, but fluorescent antibody staining showed gonococci in the exudate from non-lactating goats up to 7 days after instillation.

Animals↗

Antibody production in milk serum of goats experimentally infected with Neisseria gonorrhoeae.

Instillation of the goat's mammary gland with Neisseria gonorrhoeae colony type T1 has elicited and antibody response in the goat milk serum (GMS). Purification, and characterization of the GMS by gel filtration, electrophoresis, immunodiffusion, analytical ultracentrifugation, and serological analyses demonstrated thtat the active immune component was mainly in the IgA and IgG fractions (F2 and F3) of GMS.

Animals↗

Studies on gonococcal infection. I. Electron microscopic studies on phagocytosis of Neisseria gonorrhoeae by macrophages.

Macrophages from mice were infected with Neisseria gonorrhoeae type 1 cells, and their ultrastructure was studied by electron microscopy. The macrophages showed various stages of engulfment and digestion of gonococci 2 hr after infection. Infected macrophages seemed to develop pseudopodia for phagocytosis, and could engulf more than 30 gonococcal cells. Some engulfed bacteria appeared morphologically intact, while others appeared lysed and some structures resembling the L form of N. gonorrhoeae were also seen. These observations suggest that gonococcal cells may be able to survive intracellularly with normal or altered forms of morphology, and that macrophages containing these bacteria may disseminate gonococcal infection in man.

Animals↗

Studies on gonococcal infection. II. Attachment and fate of gonococci in tissue-culture cells.

Neisseria gonorrhoeae 188, type 1, was cultured with monolayers of Rhesus monkey kidney (RE2) cells. Attachment of gonococci to RE2 cells occurred from about 2 h after inoculation and appeared maximal by 6 h when stained with crystal violet solution and examined under a light microscope. Preferential attachment of gonococci to the perinuclear region of tissue cells could not be demonstrated. Enumeration of the colony-forming units revealed that gonococci became rapidly attached to RE2 cells, increased in number, and after 8 h gradually decreased. The number of cell-free gonococci (not bound to tissue cells) remained constant for the first few hours and then changed in parallel with the cell-bound bacterial number. Gonococci did not multiply in tissue-culture medium. When penicillin was added to the system at intervals, neither cell-free nor cell-bound gonococci were recovered. Electron microscopy of RE2 cells infected with N. gonorrhoeae revealed no intact intracellular organisms, only gonococci attached to tissue cells and imcompletely engulfed or partially digested gonococci. These observations indicate that gonococci only multiply extracellarly in the presence of RE2 cells. Furthermore, some gonococci were engulfed by RE2 cells, but appeared to be digested so rapidly that they could not multiply intracellularly.

Animals↗

Gonococcal growth factors in tissue cultures.

Growth of Neisseria gonorrhoeae in the presence of Rhesus monkey kidney (RE2) cells containing Eagle's minimal essential medium (MEM) 'conditioned' by 18-20 h of contact with RE2 cells began 3-4 h after inoculation and by 16-20 h had reached a maximum. When 'conditioned' medium (CM) was removed from the tissue cells and replaced with fresh medium a 5-6 h lag period occurred before multiplication of gonococci began and by 16 h growth was also near a maximum. CM removed from tissue cells supported the growth of six strains of N. gonorrhoeae. Three strains failed to grow in CM but multiplied when tissue cells were present. None of the strains grew in the presence of tissue cells killed by heating or in tissue-culture medium alone. Of the six strains of N. gonorrhoeae which grew in CM, three kept as their major (90%) population T1 colonies, while the remaining strains produced T1 organisms and T1A, T3, and T4 colonial variants. These results indicate that tissue cells secrete growth factors which support the growth and maintenance of T1 colonial forms of certain strains of N. gonnorhoeae.

Animals↗