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.

Induced Acid-Tolerance Response Confers Limited Nisin Resistance on Listeria monocytogenes Scott A

1996 ◽  
Vol 59 (9) ◽  
pp. 1003-1006 ◽  
Author(s):  
AMECHI OKEREKE ◽  
STERLING S. THOMPSON
Keyword(s):  
Listeria Monocytogenes ◽  
Acid Stress ◽  
Brain Heart Infusion ◽  
Acid Tolerance ◽  
Acid Resistance ◽  
Cross Protection ◽  
C Cells ◽  
Acid Tolerance Response ◽  
Tolerance Response ◽  
Resistance Trait

The presence of an inducible acid-tolerance response (ATR) in Listeria monocytogenes Scott A was established. Protection of cells with induced ATR against nisin-mediated inhibition and stress was also evaluated. ATR was induced in L. monocytogenes Scott A by culturing in brain heart infusion (BHI) broth buffered to pH 5.4. The unadapted cells were grown at pH 7.2. Both acid-adapted and unadapted cells were challenged at pH 3.3 and 4.3 at 35°C. The acid-adapted cells were 150- to 7,500-fold more resistant to acid stress at pH 3.3 than unadapted cells. Both cells were equally resistant to acid stress at pH 4.3. The acid-adapted and unadapted cells were exposed to 0, 0.3, 0.6, 1.2 and 1.5 μg of nisin per ml of buffered BHI broth at pH 6.0 for 90 min at 35°C. Cells with the induced acid-resistance trait were slightly more resistant to nisin than the unadapted cells. In the presence of 1.5 μg of nisin per ml, 47% of the acid-adapted cells survived compared to 41% of the unadapted cells. In the range of nisin concentration included in this study, there was no significant (P < 0.05) difference in the nisin resistance of adapted and unadapted cells. The data suggest that ATR induction confers very limited cross protection against nisin stress and kill.

Effect offurmutation on acid-tolerance response and in vivo virulence of avian septicemicEscherichia coli

2002 ◽  
Vol 48 (5) ◽  
pp. 458-462 ◽  
Author(s):  
Chengru Zhu ◽  
Musangu Ngeleka ◽  
Andrew A Potter ◽  
Brenda J Allan
Keyword(s):  
Parent Strain ◽  
Acid Tolerance ◽  
Wild Type ◽  
Acid Tolerance Response ◽  
E Coli ◽  
Regulator Protein ◽  
In The Wild ◽  
Tolerance Response ◽  
Wild Type Parent

The Fur (ferric uptake regulator) protein is a master regulator of iron metabolism in gram-negative bacteria. In the present study, the effect of a partial deletion of the fur gene on the acid-tolerance response and in vivo virulence of avian Escherichia coli was examined. The fur mutant was unable to trigger the acid-tolerance response as observed in the wild-type parent strain. However, the mutant was as virulent as the wild-type parent strain when tested in 1-day-old chickens by subcutaneous inoculation. These data indicate that the fur gene is involved in the acid-tolerance response but not involved in the virulence of E. coli, as detected by the ability to cause septicemia in our experimental infection.Key words: E. coli, fur, acid-tolerance response.

High-Salt Preadaptation of Vibrio parahaemolyticus Enhances Survival in Response to Lethal Environmental Stresses

2014 ◽  
Vol 77 (2) ◽  
pp. 246-253 ◽  
Author(s):  
SAI SIDDARTH KALBURGE ◽  
W. BRIAN WHITAKER ◽  
E. FIDELMA BOYD
Keyword(s):  
Stress Response ◽  
Marine Environment ◽  
Vibrio Parahaemolyticus ◽  
High Salinity ◽  
Acid Stress ◽  
Acid Tolerance ◽  
High Salt ◽  
Wild Type ◽  
Acid Tolerance Response ◽  
Tolerance Response

Adaptation to changing environmental conditions is an important strategy for survival of foodborne bacterial pathogens. Vibrio parahaemolyticus is a gram-negative seafoodborne enteric pathogen found in the marine environment both free living and associated with oysters. This pathogen is a moderate halophile, with optimal growth at 3% NaCl. Among the several stresses imposed upon enteric bacteria, acid stress is perhaps one of the most important. V. parahaemolyticus has a lysine decarboxylase system responsible for decarboxylation of lysine to the basic product cadaverine, an important acid stress response system in bacteria. Preadaptation to mild acid conditions, i.e., the acid tolerance response, enhances survival under lethal acid conditions. Because of the variety of conditions encountered by V. parahaemolyticus in the marine environment and in oyster postharvest facilities, we examined the nature of the V. parahaemolyticus acid tolerance response under high-salinity conditions. Short preadaptation to a 6% salt concentration increased survival of the wild-type strain but not that of a cadA mutant under lethal acid conditions. However, prolonged exposure to high salinity (16 h) increased survival of both the wild-type and the cadA mutant strains. This phenotype was not dependent on the stress response sigma factor RpoS. Although this preadaptation response is much more pronounced in V. parahaemolyticus, this characteristic is not limited to this species. Both Vibrio cholerae and Vibrio vulnificus also survive better under lethal acid stress conditions when preadapted to high-salinity conditions. High salt both protected the organism against acid stress and increased survival under −20°C cold stress conditions. High-salt adaptation of V. parahaemolyticus strains significantly increases survival under environmental stresses that would otherwise be lethal to these bacteria.

scholarly journals Defects in d-Alanyl-Lipoteichoic Acid Synthesis in Streptococcus mutans Results in Acid Sensitivity

2000 ◽  
Vol 182 (21) ◽  
pp. 6055-6065 ◽  
Author(s):  
David A. Boyd ◽  
Dennis G. Cvitkovitch ◽  
Arnold S. Bleiweis ◽  
Michael Y. Kiriukhin ◽  
Dmitri V. Debabov ◽  
...  
Keyword(s):  
Streptococcus Mutans ◽  
Growth Yield ◽  
Acid Tolerance ◽  
Lipoteichoic Acid ◽  
Wild Type ◽  
Lower Growth ◽  
Acid Tolerance Response ◽  
Acid Sensitivity ◽  
Permeabilized Cells ◽  
Tolerance Response

ABSTRACT In the cariogenic organism, Streptococcus mutans, low pH induces an acid tolerance response (ATR). To identify acid-regulated proteins comprising the ATR, transposon mutagenesis with the thermosensitive plasmid pGh9:ISS1 was used to produce clones that were able to grow at neutral pH, but not in medium at pH 5.0. Sequence analysis of one mutant (IS1A) indicated that transposition had created a 6.3-kb deletion, one end of which was indltB of the dlt operon encoding four proteins (DltA-DltD) involved in the synthesis ofd-alanyl-lipoteichoic acid. Inactivation of thedltC gene, encoding the d-alanyl carrier protein (Dcp), resulted in the generation of the acid-sensitive mutant, BH97LC. Compared to the wild-type strain, LT11, the mutant exhibited a threefold-longer doubling time and a 33% lower growth yield. In addition, it was unable to initiate growth below pH 6.5 and unadapted cells were unable to survive a 3-h exposure in medium buffered at pH 3.5, while a pH of 3.0 was required to kill the wild type in the same time period. Also, induction of the ATR in BH97LC, as measured by the number of survivors at a pH killing unadapted cells, was 3 to 4 orders of magnitude lower than that exhibited by the wild type. While the LTA of both strains contained a similar average number of glycerolphosphate residues, permeabilized cells of BH97LC did not incorporated-[14C]alanine into this amphiphile. This defect was correlated with the deficiency of Dcp. Chemical analysis of the LTA purified from the mutant confirmed the absence ofd-alanine-esters. Electron micrographs showed that BH97LC is characterized by unequal polar caps and is devoid of a fibrous extracellular matrix present on the surface of the wild-type cells. Proton permeability assays revealed that the mutant was more permeable to protons than the wild type. This observation suggests a mechanism for the loss of the characteristic acid tolerance response in S. mutans.

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