A Low-pH-Inducible, Stationary-Phase Acid Tolerance Response in Lactobacillus acidophilus CRL 639

2001 ◽  
Vol 42 (1) ◽  
pp. 21-25 ◽  
Author(s):  
G.L. Lorca ◽  
G. Font de Valdez
Keyword(s):  
Stationary Phase ◽  
Lactobacillus Acidophilus ◽  
Acid Tolerance ◽  
Low Ph ◽  
Acid Tolerance Response ◽  
Tolerance Response

scholarly journals Effects of Acid Stress on Vibrio parahaemolyticus Survival and Cytotoxicity

2004 ◽  
Vol 67 (7) ◽  
pp. 1328-1334 ◽  
Author(s):  
P. S. MARIE YEUNG ◽  
KATHRYN J. BOOR
Keyword(s):  
Stationary Phase ◽  
Vibrio Parahaemolyticus ◽  
Acid Stress ◽  
Acid Tolerance ◽  
Acid Exposure ◽  
Bacterial Survival ◽  
Acid Tolerance Response ◽  
Tolerance Response ◽  
Acidic Conditions ◽  
Acid Challenge

For several foodborne bacterial pathogens, an acid tolerance response appears to be an important strategy for counteracting acid stress imposed either during food processing or by the human host. The acid tolerance response enhances bacterial survival of lethal acid challenge following prior exposure to sublethal acidic conditions. Previous studies have revealed relationships between a foodborne pathogen's ability to survive acid challenge and its infectious dose. Vibrio parahaemolyticus is capable of causing gastroenteritis when sufficient cells of pathogenic strains are consumed. This study was designed to characterize acid sensitivities and to compare the effects of sublethal acid exposure (adaptation) on survival capabilities and cytotoxicities of different V. parahaemolyticus strains. Survival of acid challenge by stationary-phase cells differed by up to 3 log CFU/ml among the 25 isolates tested. No differences in acid resistance were found between strains when they were grouped by source (clinical isolates versus those obtained from food). Survival at pH 3.6 for log-phase cells that had been previously exposed to sublethal acidic conditions (pH 5.5) was enhanced compared with that for cells not previously exposed to pH 5.5. However, for stationary-phase cells, exposure to pH 5.5 impaired both subsequent survival at pH 3.6 and cytotoxicity to human epithelial cells. Relative cytotoxicities of nonadapted stationary-phase cells were 1.2- to 4.8-fold higher than those of adapted cells. Sublethal acid exposure appears to impose measurable growth phase–dependent effects on subsequent lethal acid challenge survival and cytotoxicity of V. parahaemolyticus.

scholarly journals Transcriptional analysis of the acid tolerance response in Streptococcus pneumoniae

Microbiology ◽  
2005 ◽  
Vol 151 (12) ◽  
pp. 3935-3946 ◽  
Author(s):  
Antonio J. Martín-Galiano ◽  
Karin Overweg ◽  
Maria J. Ferrándiz ◽  
Mark Reuter ◽  
Jerry M. Wells ◽  
...  
Keyword(s):  
Streptococcus Pneumoniae ◽  
Survival Rate ◽  
Stationary Phase ◽  
Acid Tolerance ◽  
Maintenance Phase ◽  
Transcriptional Analysis ◽  
Acid Tolerance Response ◽  
Tolerance Response ◽  
Adaptation Phase

Streptococcus pneumoniae, one of the major causes of morbidity and mortality in humans, faces a range of potentially acidic conditions in the middle and late stages of growth in vitro, in diverse human fluids during the infection process, and in biofilms present in the nasopharynx of carriers. S. pneumoniae was shown to develop a weak acid tolerance response (ATR), where cells previously exposed to sublethal pHs (5·8–6·6) showed an increased survival rate of up to one order of magnitude after challenge at the lethal pH (4·4, survival rate of 10−4). Moreover, the survival after challenge of stationary phase cells at pH 4·4 was three orders of magnitude higher than that of cells taken from the exponential phase, due to the production of lactic acid during growth and increasing acidification of the growth medium until stationary phase. Global expression analysis after short-term (5, 15 and 30 min, the adaptation phase) and long-term (the maintenance phase) acidic shock (pH 6·0) was performed by microarray experiments, and the results were validated by real-time RT-PCR. Out of a total of 126 genes responding to acidification, 59 and 37 were specific to the adaptation phase and maintenance phase, respectively, and 30 were common to both periods. In the adaptation phase, both up- and down-regulation of gene transcripts was observed (38 and 21 genes, respectively), whereas in the maintenance phase most of the affected genes were down-regulated (34 out of 37). Genes involved in protein fate (including those involved in the protection of the protein native structure) and transport (including transporters of manganese and iron) were overrepresented among the genes affected by acidification, 8·7 and 24·6 % of the acid-responsive genes compared to 2·8 % and 9·6 % of the genome complement, respectively. Cross-regulation with the response to oxidative and osmotic stress was observed. Potential regulatory motifs involved in the ATR were identified in the promoter regions of some of the regulated genes.

scholarly journals A Low pH-Inducible, PhoPQ-Dependent Acid Tolerance Response Protects Salmonella typhimurium against Inorganic Acid Stress

1998 ◽  
Vol 180 (9) ◽  
pp. 2409-2417 ◽  
Author(s):  
Bradley L. Bearson ◽  
Lee Wilson ◽  
John W. Foster
Keyword(s):  
Organic Acids ◽  
Salmonella Typhimurium ◽  
Organic Acid ◽  
Acid Stress ◽  
Acid Tolerance ◽  
Low Ph ◽  
Inorganic Acid ◽  
Acid Tolerance Response ◽  
Acid Shock ◽  
Tolerance Response

ABSTRACT The acid tolerance response enables Salmonella typhimurium to survive exposures to potentially lethal acidic environments. The acid stress imposed in a typical assay for acid tolerance (log-phase cells in minimal glucose medium) was shown to comprise both inorganic (i.e., low pH) and organic acid components. A gene previously determined to affect acid tolerance, atbR, was identified as pgi, the gene encoding phosphoglucoisomerase. Mutations in pgi were shown to increase acid tolerance by preventing the synthesis of organic acids. Protocols designed to separate the stresses of inorganic from organic acids revealed that the regulators ς38 (RpoS), Fur, and Ada have major effects on tolerance to organic acid stress but only minor effects on inorganic acid stress. In contrast, the two-component regulatory system PhoP (identified as acid shock protein ASP29) and PhoQ proved to be important for tolerance to organic acid stress but had little effect against organic acid stress. PhoP mutants also failed to induce four ASPs, confirming a role for this regulator in acid tolerance. Acid shock induction of PhoP appears to occur at the transcriptional level and requires the PhoPQ system. Furthermore, induction by acid occurs even in the presence of high concentrations of magnesium, the ion known to be sensed by PhoQ. These results suggest that PhoQ can sense both Mg2+ and pH. SincephoP mutants are avirulent, the low pH activation of this system has important implications concerning the pathogenesis ofS. typhimurium. The involvement of four regulators, two of which are implicated in virulence, underscores the complexity of the acid tolerance stress response and further suggests that features of acid tolerance and virulence are interwoven.

scholarly journals Global Analysis of Escherichia coli Gene Expression during the Acetate-Induced Acid Tolerance Response

2001 ◽  
Vol 183 (7) ◽  
pp. 2178-2186 ◽  
Author(s):  
Carrie N. Arnold ◽  
Justin McElhanon ◽  
Aaron Lee ◽  
Ryan Leonhart ◽  
Deborah A. Siegele
Keyword(s):  
Escherichia Coli ◽  
Global Analysis ◽  
Acid Tolerance ◽  
Short Chain Fatty Acids ◽  
Low Ph ◽  
Insertion Mutation ◽  
Acid Tolerance Response ◽  
E Coli ◽  
Serovar Typhimurium ◽  
Tolerance Response

ABSTRACT The ability of Escherichia coli to survive at low pH is strongly affected by environmental factors, such as composition of the growth medium and growth phase. Exposure to short-chain fatty acids, such as acetate, proprionate, and butyrate, at neutral or nearly neutral pH has also been shown to increase acid survival of E. coli and Salmonella enterica serovar Typhimurium. To investigate the basis for acetate-induced acid tolerance in E. coli O157:H7, genes whose expression was altered by exposure to acetate were identified using gene arrays. The expression of 60 genes was reduced by at least twofold; of these, 48 encode components of the transcription-translation machinery. Expression of 26 genes increased twofold or greater following treatment with acetate. This included six genes whose products are known to be important for survival at low pH. Five of these genes, as well as six other acetate-induced genes, are members of the E. coli RpoS regulon. RpoS, the stress sigma factor, is known to be required for acid tolerance induced by growth at nonlethal low pH or by entry into stationary phase. Disruption of therpoS gene by a transposon insertion mutation also prevented acetate-induced acid tolerance. However, induction of RpoS expression did not appear to be sufficient to activate the acid tolerance response. Treatment with either NaCl or sodium acetate (pH 7.0) increased expression of anrpoS::lacZ fusion protein, but only treatment with acetate increased acid survival.

scholarly journals Role of Listeria monocytogenes σB in Survival of Lethal Acidic Conditions and in the Acquired Acid Tolerance Response

2003 ◽  
Vol 69 (5) ◽  
pp. 2692-2698 ◽  
Author(s):  
Adriana Ferreira ◽  
David Sue ◽  
Conor P. O'Byrne ◽  
Kathryn J. Boor
Keyword(s):  
Listeria Monocytogenes ◽  
Stationary Phase ◽  
Growth Phase ◽  
Brain Heart Infusion ◽  
Relative Survival ◽  
Acid Tolerance ◽  
Inorganic Acid ◽  
Wild Type ◽  
Acid Tolerance Response ◽  
Tolerance Response

ABSTRACT The food-borne pathogen Listeria monocytogenes can acquire enhanced resistance to lethal acid conditions through multiple mechanisms. We investigated contributions of the stress-responsive alternative sigma factor, σB, which is encoded by sigB, to growth phase-dependent acid resistance (AR) and to the adaptive acid tolerance response in L. monocytogenes. At various points throughout growth, we compared the relative survival of L. monocytogenes wild-type and ΔsigB strains that had been exposed to either brain heart infusion (pH 2.5) or synthetic gastric fluid (pH 2.5) with and without prior acid adaptation. Under these conditions, survival of the ΔsigB strain was consistently lower than that of the wild-type strain throughout all phases of growth, ranging from 4 orders of magnitude less in mid-log phase to 2 orders of magnitude less in stationary phase. Survival of both ΔsigB and wild-type L. monocytogenes strains increased by 6 orders of magnitude upon entry into stationary phase, demonstrating that the L. monocytogenes growth phase-dependent AR mechanism is σB independent. σB-mediated contributions to acquired acid tolerance appear to be greatest in early logarithmic growth. Loss of a functional σB reduced the survival of L. monocytogenes at pH 2.5 to a greater extent in the presence of organic acid (100 mM acetic acid) than in the presence of inorganic acid alone (HCl), suggesting that L. monocytogenes protection against organic and inorganic acid may be mediated through different mechanisms. σB does not appear to contribute to pHi homeostasis through regulation of net proton movement across the cell membrane or by regulation of pHi buffering by the GAD system under the conditions examined in this study. In summary, a functional σB protein is necessary for full resistance of L. monocytogenes to lethal acid treatments.

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