pTK159, a multiresistance 40-kilobase (kb) plasmid, was isolated from a clinical strain of Serratia marcescens. pTK159 was nonconjugative and carried determinants for resistance to amikacin, streptomycin/spectinomycin, sulfamethoxazole and ampicillin. A physical and functional map of pTK159 was constructed. By cloning various fragments of pTK159 in pACYC184 or pBR322, genes for resistance to amikacin, streptomycin/spectinomycin, and sulfamethoxazole were found to be located on a 2.0-kb BamHI-HindIII fragment, a 1.4-kb HindIII fragment and a 2.1-kb HindIII fragment, respectively. The map of pTK159 was compared with published maps of amikacin-resistance determinants and transposons.

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Monoclonal antibodies against pigeon and budgerigar strains of Chlamydia psittaci were used to classify the immunotypes of C. psittaci strains by an indirect immunofluorescence antibody (IFA) test. Thirty-three C. psittaci strains from pigeons and 24 from budgerigars were divided into three immunotypes (P-I, P-II, and P-III) and (B-I, B-II, and B-III), respectively. Two strains from human psittacosis patients were identified as P-III and B-I, coinciding with the epidemiological evidence of each human infection. Two strains from psittacine birds, a parrot and a parakeet, were identical to the B-II immunotype. Other mammalian strains were quite distinct from avian strains in their IFA reaction with the monoclonal antibodies.

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The structure of Marek's disease virus (MDV) DNA was investigated by using Southern blot hybridization analysis. A heterogeneous region was observed in the inverted repeats region, IR_S and TR_S, as well as in the TR_L and IR_L. The results of DNA sequencing of the heterogeneous region showed that the heterogeneity of IR_S and TR_S was due to amplification of a 178-bp repeat sequence. Amplification of IR_S and TR_S was found in viral DNA from both pathogenic and nonpathogenic strains. The structure of DNA from the latent MDV genome present in established lymphoblastic cells was also determined. Amplification of the 132-bp repeat sequence in IR_L and TR_L was not found in latent MDV DNA of established lymphoblastic cells, whereas amplification of the 178-bp repeat sequence in IR_S and TR_S was found in the same DNA.

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The toxicity and macrophage stimulating property of Vibrio parahaemolyticus lipid A was studied. The LD₅₀ dose of lipid A in galactosamine-sensitized mice was found to be 0.6μg when injected intraperitoneally. Administration of lipid A resulted in stimulation of peritoneal macrophages as evident by increase in their cellular RNA contents and lysosomal enzyme activities. The treatment also caused enhancement in the phagocytic activity of macrophages.

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BALB/c mice receiving allogeneic C3H/He or C57BL/6 spleen cells via portal venous (p.v.) route or a single administration of cyclophosphamide (Cy) were capable of rejecting the respective allogeneic C3H/He- or C57BL/6-derived tumor cells. In contrast, the combined treatment of p.v. inoculation with allogeneic lymphocytes and Cy administration abrogated the capability of rejecting allogeneic tumor cells. Such abrogation of alloreactivity was alloantigen-specific and associated with the suppression of potentials to generate delayed-type hypersensitivity (DTH) and cytotoxic T lymphocyte (CTL) responses to alloantigens. This was further substantiated by the inhibition of molecular mechanisms underlying anti-allo-DTH and -CTL responses. Thus, the above combined treatment led to the decreased production of lymphokines such as macrophage-activating factor (MAF) and interleukin 2 (IL2) following the stimulation with the relevant alloantigens. These results demonstrate that p.v. inoculation of allogeneic cells followed by a single administration of Cy results in the effective elimination of alloreactivity as verified by the suppression of cellular and molecular mechanisms of alloreactive responses.

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The CD3(T3)/antigen receptor complex appears to function by transducing an antigen signal presented by macrophages into the hydrolysis of phosphatidylinositol 4, 5-bisphosphate [PtdIns(4, 5)P₂]. In order to find out how the CD3/antigen receptor complex regulates the hydrolysis of Ptdlns(4, 5)P₂ to diacylglycerol and inositol trisphosphate, we investigated the possible role played by a guanine nucleotide-binding regulatory protein in PtdIns(4, 5)P₂ hydrolysis in a human T cell leukemia line, JURKAT. JURKAT cells were made permeable to Al³⁺, F^-, GTP, and a nonhydrolyzable GTP analogue, guanosine 5'-O-(3-thiotriphosphate) (GTPγS), by treatment with pseudomonal cytotoxin. In the presence of AlCl₃ NaF stimulated the release of inositol phosphates in the cytotoxin-treated JURKAT cells. NaF plus AlCl₃ induced increases in inositol tris-, bis-, and mono-phosphates and decreases in PtdIns(4, 5)P₂, phosphatidylinositol 4-phosphate, and phosphatidylinositol within 5min after addition to the cytotoxin-treated cells at 37C. GTPγS stimulated, to some extent, polyphosphoinositide hydrolysis in the cytotoxin-treated JURKAT. The cytotoxin-treated JURKAT cells retained the ability to respond to anti-Leu-4 with polyphosphoinositide hydrolysis. It has been shown that Al³⁺ in the presence of F^- modulates the activity of various guanine nucleotide-binding regulatory proteins. Therefore, the results obtained in this study indicate that a guanine nucleotide-binding regulatory protein regulates the polyphosphoinositide breakdown in JURKAT cells by influencing phosphodiesterase activity.

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T cell subsets responsible for clearance of Sendai virus from mouse lungs determined by adoptive transfer of immune spleen cell fractions to infected nude mice. T cells with antiviral activity developed in spleens by 7 days after intranasal infection. Spleen cell fractions depleted of Lyt-2⁺, Lyt-1⁺, or L3T4⁺ cells showed antiviral activity in vivo, although the degree of the activity was lower than that of control whole spleen cells. The antiviral activity of the Lyt-2⁺ cell-depleted fraction was consistently higher than that of L3T4⁺ (Lyt-1⁺)-depleted cells. In vitro cytotoxic activity against Sendai virus-associated, syngeneic lipopolysaccharide-blast cells was detected in stimulated cells from intraperitoneally immunized mice but was lost after depletion of Lyt-2⁺ cells. Multiple injection of anti-Sendai virus antibody into infected nude mice had no effect on lung virus titer. These results indicate that L3T4⁺ (Lyt-1⁺) and Lyt-2⁺ subsets are cooperatively responsible for efficient clearance of Sendai virus from the mouse lung.

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mpo-1 Mutation, which causes the overproduction of at least two membrane and one cytoplasmic proteins, induced high manganese concentration-dependent sporulation in Bacillus subtilis. Sporulation of the mpo-1 mutant was blocked at stage 0-I by a low concentration of manganese.

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By application of the surface-spreading technique, virus particles in infected cells and viremia serum, and precipitates in agar plates of the double immunodiffusion technique of Ouchterlony could easily and clearly be visualized without any purification process.

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