Acid resistance is perceived to be an important property of enterohemorrhagic Escherichia coli strains, enabling the organisms to survive passage through the acidic environment of the stomach so that they may colonize the mammalian gastrointestinal tract and cause disease. Accordingly, the organism has developed at least three genetically and physiologically distinct acid resistance systems which provide different levels of protection. The glutamate-dependent acid resistance (GDAR) system utilizes extracellular glutamate to protect cells during extreme acid challenges and is believed to provide the highest protection from stomach acidity. In this study, the GDAR system of 82 pathogenic E. coli isolates from 34 countries and 23 states within the United States was examined. Twenty-nine isolates were found to be defective in inducing GDAR under aerobic growth conditions, while five other isolates were defective in GDAR under aerobic, as well as fermentative, growth conditions. We introduced rpoS on a low-copy-number plasmid into 26 isolates and were able to restore GDAR in 20 acid-sensitive isolates under aerobic growth conditions. Four isolates were found to be defective in the newly discovered LuxR-like regulator GadE (formerly YhiE). Defects in other isolates could be due to a mutation(s) in a gene(s) with an as yet undefined role in acid resistance since GadE and/or RpoS could not restore acid resistance. These results show that in addition to mutant alleles of rpoS, mutations in gadE exist in natural populations of pathogenic E. coli. Such mutations most likely alter the infectivity of individual isolates and may play a significant role in determining the infective dose of enterohemorrhagic E. coli.
e175 was employed to measure the levels of cytokines in the plasma. IL-18 level in the plasma of malarial mice were found to be significantly elevated and positively correlated with the percentage degree of parasitaemia. Inhibition and neutralization of IL-18 production caused significant decrease in the plasma levels of pro-inflammatory cytokines TNF-alpha, IFN-gamma, IL-1 and IL-6. In contrast, the anti-inflammatory cytokine IL-10 was significantly increased. Treatment with rIL-18 on the other hand caused significant increase in pro-inflammatory cytokines plasma levels, whereas the antiinflammatory cytokine level was significantly reduced. Results proved the involvement of IL-18 in malaria infection. Its positive modulatory effects on the release of pro-inflammatory and anti-inflammatory cytokines during the infection may suggest its crucial role(s) in the pathogenesis of the infection. Results also suggest the IL-18 potential as an immunotherapeutic target in malaria therapy.
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