The production and roles of endogenous gamma interferon (IFN-␥), tumor necrosis factor (TNF), and interleukin-6 (IL-6) in both lethal and nonlethal infections of Staphylococcus aureus were investigated in mice. In the case of nonlethal infection, although no bacteria were detected in the bloodstreams, bacteria that colonized and proliferated persistently for 3 weeks were found in the kidneys. All mice given lethal injections died within 7 days, and large numbers of bacteria were detected in the bloodstreams, spleens, and kidneys. The first peaks of IFN-␥, TNF, and IL-6 were observed in the bloodstreams and spleens of the mice with nonlethal and lethal infections within 24 h. Thereafter, in the nonlethal cases, IFN-␥, TNF, and IL-6 peaked again in the spleens and kidneys during the period of maximum growth of bacteria in the kidneys, although only IL-6 was detected in the sera. In contrast, in the case of lethal infection, the titers of IFN-␥ and IL-6 in the sera and TNF in the kidneys peaked before death. Effects of in vivo administration of monoclonal antibodies (MAbs) against IFN-␥ and TNF on the fates of S. aureus-infected mice were studied. In the nonlethal infections, anti-TNF alpha (anti-TNF-␣) MAb-treated mice, but not anti-IFN-␥ MAb-treated mice, died as a result of worsening infection, suggesting that endogenous TNF plays a protective role in host resistance to S. aureus infection. In the mice that received lethal doses, injection of anti-TNF-␣ MAb accelerated death. However, although injection of anti-IFN-␥ MAb inhibited host resistance of the infected mice early in infection, most of the animals survived the lethal infection by injection of anti-IFN-␥ MAb, suggesting that endogenous IFN-␥ plays a detrimental role in S. aureus infection. Thus, this study demonstrated that IFN-␥ and TNF play different roles in S. aureus infection.
Protonic ceramic fuel cells (PCFCs) have limited application below 500 °C owing to their high ohmic and polarization resistances. Hence, efforts are ongoing to develop advanced fuel cells based on semiconductor device science as well as material interfacial engineering. Here, we demonstrate that hydrogen-permeable metal-supported fuel cells (HMFCs) exhibit improved energy conversion efficiency at relatively lower temperatures due to the retardation of secondary conduction (that of the oxide ions) at the oxide/metal heterointerface. The electrolyte membrane in HMFCs is forced to gain extra protons to compensate for the charge from the oxide ions accumulating via blocking, resulting in extremely high proton conductivity. Simultaneously, the heavily hydrated membrane pumps protons out of the cathode side during cell operation. This significantly promotes interfacial proton diffusion for cathode reactions. Hence, HMFCs can operate at high efficiency even at temperatures lower than the operational temperature of PCFCs and will help improve the power generation performance of protonic oxide fuel cells at temperatures lower than 500 °C.
The capability to utilize different forms of nitrogen (N) by sorghum (Sorghum bicolor), rice (Oryza sativa), maize (Zea mays), and pearl millet (Pennisetum glaucum) was determined in pot experiments. Seedlings were grown for 21 d without N, or with 500 mg N kg(-1) soil applied as ammonium nitrate, rice bran or a mixture of rice bran and straw. No treatment-dependent changes of root length, surface area, and fractal dimension were observed. Shoot growth and N uptake in maize and pearl millet correlated with the inorganic N (ammonium and nitrate) concentration in the soil, suggesting that these species depend upon inorganic N uptake. On the other hand, shoot growth and N uptake patterns in sorghum and rice indicated that these two species could compensate low inorganic N levels in the organic material treatments by taking up organic N (proteins). Analysis of N uptake rates in solution culture experiments confirmed that sorghum and rice roots have higher capabilities to absorb protein N than maize and pearl millet.
Immunosuppressive properties of seminal plasma inhibit the recovery of infectious HIV from semen, and led to the view early in the pandemic that semen HIV was transmitted principally by infected semen cells. More recent studies have revealed significant titers of HIV RNA in seminal plasma, however, even from men receiving successful antiviral therapy. Thus, studies of infectious HIV in seminal plasma are important to understanding sexual transmission and response to therapy. The present studies were undertaken to determine whether seminal plasma immunosuppression is mediated by the induction of programmed cell death (PCD). Peripheral blood mononuclear cells (PBMCs) were cultured without or with phytohemagglutinin and seminal plasma from normal donors, or men postvasectomy, or seminal vesicle protein collected at surgery. PBMC survival was measured at 3, 6, and 18 hr of culture; cells were examined for evidence of PCD by uptake of the fluorescent dye YO-PRO, and for fragmented nuclear DNA by the TUNEL assay. Approximately 90% of PBMCs cultured with seminal plasma from intact or vasectomized men were lost during 18 hr of culture; seminal vesicle protein did not induce cell loss. PCD assays were positive for PBMCs exposed to the seminal plasma, and negative for PBMCs cultured with seminal vesicle protein. Serum was not required for PCD induction. A 3-hr pulse with seminal plasma was sufficient to initiate PCD. These findings indicate that PCD induction accounts for the cytotoxic properties of semen, that the PCD is not the result of semen amine oxidases, and either that substances produced by seminal vesicles only at ejaculation, or by the prostate, are responsible for PCD induction.
Suckling and adult mice were infected intragastrically with different doses of viable Listeria monocytogenes. The 50% lethal dose for the intragastric infection was 10(3.7) CFU for suckling mice, while adult mice were highly resistant and the 50% lethal dose was more than 10(9.3) CFU. When adult mice were infected intragastrically with 5 x 10(8) CFU of L. monocytogenes, no mice died. However, 35% of adult mice died when they were treated with cyclosporin A 1 day before infection. Although mice did not die when treated with an L. monocytogenes-resistant broad-spectrum cephalosporin, sodium cefbuperazone, before and during infection, the number of L. monocytogenes bacteria increased in the feces. The sodium cefbuperazone treatment of mice resulted in superinfection, i.e., a marked decrease of Escherichia coli and an increase of Enterococcus spp. in the intestines. Furthermore, host resistance against the intragastric infection markedly decreased when the mice were treated with both drugs. The growth of L. monocytogenes was augmented in the spleens, mesenteric lymph nodes, Peyer's patches, and feces, and the mortality of the mice was 65%. These results suggest that both cellular immunity and the intestinal bacterial flora are required for host resistance against oral L. monocytogenes infection.
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