Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A major aim in many areas of microbiology is to ensure sterility, and even where this is impossible, to reduce the number of viable organisms occurring in particular environments to an absolute minimum. This applies in the aquatic environment, where e.g. water treatment must ensure as complete absence of viable microbes as possible. It is also crucial in food processing and production; many food constituents contain appreciable numbers of viable organisms, even potential pathogens, and the number must be greatly reduced and in many situations, the presence of viable organisms totally abolished. Cleaning of food production components and surfaces must also kill associated microbes. In domestic, hospital and commercial situations, similar disinfection is critical. Ultimately, the aim is to ensure, if possible, sterility, with the assurance that microbial problems cannot occur if organisms are absent. Additionally, however, it has been implicitly assumed that killed organisms and even killed cultures cannot (except in minor and trivial ways) influence the behaviour of living organisms that later enter the environment. The work reviewed here challenges that view and in fact disproves it. The findings described show that killed enterobacterial cultures, which prior to killing had phenotypically gained the ability to resist potentially lethal stresses, can pass on such ability to living organisms that later enter their environment i.e. that such killed cultures can convey a baleful legacy to living ones. This phenomenon is so widespread that it is clear that it has significance for enterobacterial survival in natural waters, in foods and in food production, in the domestic, commercial and hospital situation, and in the animal and human body. In fact, in this last area, the likely effect of killed cultures appears to be of appreciable public health importance. Here, the ability of appropriate killed cultures to transfer tolerance to acidity, alkalinity and thermal stress is described, as well as their ability to pass on sensitisation to acid and alkali. Other work reviewed suggests that killed cultures can almost certainly transfer the ability to tolerate hydrogen peroxide, ultraviolet irradiation and metal ions. The serious implications of this phenomenon are further emphasised by the fact that numerous killing methods produce cultures effective in tolerance response transfer. All the evidence suggests that it is extracellular components (extracellular sensing components, ESCs, and extracellular induction components, EICs), in the killed cultures which are involved in stress response transfer, and that the actual stress response induction process depends on interaction of living organisms with EICs from the killed cultures. It is of note that ESCs and EICs survive in killed cultures because of their extreme resistance to irreversible inactivation by lethal levels of stressing agents and conditions. This is in contrast to the fact that EC activation, namely the conversion of ESC to EIC occurs on exposure to very low levels of stressors. Not only is this the case, but in fact high levels of stressors (e.g. those that kill organisms) generally fail to convert ESC to EIC.
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PMID:How killed enterobacterial cultures can activate living organisms to resist lethal agents or conditions. 1507 95

Several striking findings, related to biological effects of external acidity, are reviewed here. The first of these relates to the role of PhoE in the penetration of H+ and protonated metabolites into the cell. PhoE is an anion pore and would not be expected to take up protons. The work reviewed here, however, shows that the loss or repression of PhoE leads to poor H+ passage through the outer membrane (OM), whilst derepression of PhoE leads to facilitated passage. It is now believed that H+ crosses through the PhoE pore in association possibly with oligopeptides, and that other protonated molecules, such as the acid tolerance EIC, use the same means to cross the OM. Additionally, several processes that form early warning systems against acidity are reviewed here. First, the properties of the acid tolerance EIC alarmones allow them to diffuse to regions not yet facing acid stress, and there give early warning and induce sensitive organisms to tolerance. Second, some agents, such as glucose, induce acid tolerance in organisms, long before these organisms are exposed to catabolically-produced acidity, preparing them, in advance, to resist this impending acid challenge. Third, the occurrence of multiple forms of ESCs (i.e. of varisensors) ensures that where organisms have been grown under conditions that sensitise them to acid stress, the ESCs formed are modified so as to be activated at much higher pH values, ensuring that lethality by acid is reduced or abolished. Fourthly, normally only EICs induce tolerance. Strikingly, however, pH 8.5 or 9.0-grown cells are induced to tolerance by ESC formed at pH 6.5. This is believed to provide another early warning system, protecting alkali-grown cells against sudden acidification of media. Two other finding reviewed here should be emphasised. First, the hydrophobic antibiotic novobiocin is ineffective against enterobacteria, due to its failure to penetrate the OM barrier. This only applies to cultures in pH 7.0 media, however, cells growing at pH 5.0 being exquisitely sensitive to novobiocin, due to a conformational change to the antibiotic at acidic pH, which allows ready penetration through the OM. Second, acidic pHs affect the synthesis and effects of another antibiotic, namely colicin V. Thus pH 5.0 prevents both synthesis of this agent and its effects on sensitive cells. Exposure to external acidity leads to numerous other effects, including those that influence growth, cell division, plasmid transfer and chemotaxis; these have also been reviewed here.
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PMID:Enterobacterial responses to external protons, including responses that involve early warning against stress and the functioning of extracellular pheromones, alarmones and varisensors. 1588 59