Occurrence of inhibitory compounds in spent growth media that interfere with acid-tolerance mechanisms of enteric pathogens

This study investigated the survival and acid tolerance of Listeria monocytogenes during the 2-day processing stage and 90-day ripening of Savak tulum cheese, a traditional cheese in Turkey. Experimental Savak tulum cheese was produced from raw sheep's milk that was inoculated with a L. monocytogenes mixture consisting of five strains (average 7.0 log CFU/ml) and was ripened at 6°C for 90 days. Microbiological and chemical analyses and acid exposure experiments in synthetic gastric fluid (SGF) (pH 1.5 to 2.5) were carried out on days 1 and 2 during processing and on days 0, 15, 30, 45, 60, and 90 during ripening. The numbers of L. monocytogenes did not decrease during processing, but a total of 4.1 log CFU/g reduction was observed during ripening. Throughout the ripening period, L. monocytogenes cells survived direct 90-min exposures of the cheese samples to SGF. These results suggest that, although the pathogen numbers decreased in Savak tulum cheese ripened at 6°C for 90 days, a sublethal environment may have occurred in the cheese during the production stage, activating the acid-tolerance mechanisms of the pathogen and allowing L. monocytogenes to maintain its viability in the SGF for 90 min.

Download Full-text

Microbial response to acid stress: mechanisms and applications

Applied Microbiology and Biotechnology ◽

10.1007/s00253-019-10226-1 ◽

2019 ◽

Vol 104 (1) ◽

pp. 51-65 ◽

Cited By ~ 18

Author(s):

Ningzi Guan ◽

Long Liu

Keyword(s):

Synthetic Biology ◽

Metabolic Regulation ◽

Membrane Integrity ◽

Acid Stress ◽

Acid Tolerance ◽

Industrial Applications ◽

Cell Factory ◽

Ph Homeostasis ◽

Tolerance Mechanisms ◽

Microbial Cell Factory

AbstractMicroorganisms encounter acid stress during multiple bioprocesses. Microbial species have therefore developed a variety of resistance mechanisms. The damage caused by acidic environments is mitigated through the maintenance of pH homeostasis, cell membrane integrity and fluidity, metabolic regulation, and macromolecule repair. The acid tolerance mechanisms can be used to protect probiotics against gastric acids during the process of food intake, and can enhance the biosynthesis of organic acids. The combination of systems and synthetic biology technologies offers new and wide prospects for the industrial applications of microbial acid tolerance mechanisms. In this review, we summarize acid stress response mechanisms of microbial cells, illustrate the application of microbial acid tolerance in industry, and prospect the introduction of systems and synthetic biology to further explore the acid tolerance mechanisms and construct a microbial cell factory for valuable chemicals.

Download Full-text

Rapid procedure for acid adaptation of oral lactic-acid bacteria and further characterization of the response

Canadian Journal of Microbiology ◽

10.1139/m97-019 ◽

1997 ◽

Vol 43 (2) ◽

pp. 143-148 ◽

Cited By ~ 17

Author(s):

Yousheng Ma ◽

Timothy M. Curran ◽

Robert E. Marquis

Keyword(s):

Lactic Acid ◽

Lactic Acid Bacteria ◽

Streptococcus Mutans ◽

Acid Tolerance ◽

Growth Media ◽

Oral Microbiota ◽

Adaptive Responses ◽

Acid Adaptation ◽

General Importance ◽

Time Required

Acid-adaptive responses could be induced readily in oral lactic-acid bacteria by growing them in batch cultures with excess sugar or more conveniently and rapidly by transferring cells to acidified growth media for the time required for biomass doubling. The response of Streptococcus mutans GS-5 was induced in a progressive rather than all-or-nothing way, and the extent of acid tolerance was inversely related to the pH of the inducing medium over a range from 8.5 to 5. The weak acids fluoride, acetate, or lactate did not measurably enhance acid adaptation, and so the response did not appear to depend primarily on changes in ΔpH or the proton motive force across the cell membrane. Transcription and translation to form new proteins did appear to be necessary, as indicated by inhibition of adaptation by rifampin or chloramphenicol and by lack of adaptation by cells suspended in phosphate buffer at pH 5. Streptococcus salivarius and Lactobacillus casei were acid adapted by the rapid method, and the method appeared to be generally useful for oral lactic-acid bacteria. The rapid induction of the response in multiple oral lactic-acid bacteria suggests that it is of general importance for maintaining a diversity of organisms in the oral microbiota, which is regularly subjected to acid stresses.Key words: acid adaptation, oral lactic-acid bacteria, Streptococcus mutans.

Download Full-text

Enteric pathogens induce tissue tolerance and prevent neuronal loss from subsequent infections

10.1101/2021.04.09.439221 ◽

2021 ◽

Author(s):

Tomasz Ahrends ◽

Begüm Aydin ◽

Fanny Matheis ◽

Cajsa Classon ◽

Gláucia C. Furtado ◽

...

Keyword(s):

Adrenergic Receptors ◽

Sympathetic Neurons ◽

Neuronal Cell Death ◽

Neuronal Cell ◽

Neuronal Loss ◽

Enteric Pathogens ◽

Tolerance Mechanisms ◽

Enteric Infections ◽

Intestinal Functions ◽

Pathogen Exposure

AbstractThe enteric nervous system (ENS) controls several intestinal functions including motility and nutrient handling, which can be disrupted by infection-induced neuropathies or neuronal cell death. We investigated possible tolerance mechanisms preventing neuronal loss and disruption in gut motility after pathogen exposure. We found that following enteric infections, muscularis macrophages (MMs) acquire a tissue-protective phenotype that prevents neuronal loss and dysmotility during subsequent challenge with unrelated pathogens. Bacteria-induced neuroprotection relied on activation of gut-projecting sympathetic neurons and signaling via β2-adrenergic receptors (β2AR) on MMs. In contrast, helminth-mediated neuroprotection was dependent on T cells and systemic production of interleukin (IL)-4 and -13 by eosinophils, which induced arginase-expressing MMs that prevented neuronal loss from an unrelated infection located in a different intestinal region. Collectively, these data suggest that distinct enteric pathogens trigger a state of disease- or tissue tolerance that preserves ENS number and functionality.

Download Full-text

Phagosome Acidification Has Opposite Effects on Intracellular Survival of Bordetella pertussis andB. bronchiseptica

Infection and Immunity ◽

10.1128/iai.68.12.7039-7048.2000 ◽

2000 ◽

Vol 68 (12) ◽

pp. 7039-7048 ◽

Cited By ~ 33

Author(s):

Boris Schneider ◽

Roy Gross ◽

Albert Haas

Keyword(s):

Bordetella Pertussis ◽

Acid Tolerance ◽

Proton Pumping ◽

Close Relative ◽

Growth Media ◽

Macrophage Cell Line ◽

Macrophage Cell ◽

Differential Survival ◽

Acid Tolerant ◽

Mouse Macrophage Cell Line

ABSTRACT Bordetella pertussis is readily killed after uptake by professional phagocytes, whereas its close relative Bordetella bronchiseptica is not and can persist intracellularly for days. Phagocytosis of members of either species by a mouse macrophage cell line results in transport of the bacteria to a phagosomal compartment positive for the lysosome-associated membrane protein 1, the protease cathepsin D, and the late endosomal vacuolar proton-pumping ATPase but negative for the early endosome antigen 1 and the early endosomal transferrin receptor. In addition, we demonstrate thatBordetella-containing phagosomes rapidly acidify to pH 4.5 to 5.0. Taken together, these data demonstrate thatBordetella-containing phagosomes rapidly mature to an acidic late endosomal/lysosomal compartment. Following up on this observation, we determined that B. pertussis does not survive in bacterial growth media adjusted to a pH of 4.5, whereas this pH has only minor effects on the growth of B. bronchiseptica. Raising the intracellular pH in infected macrophages by the addition of bafilomycin A1, ammonium chloride, or monensin increases the survival of acid-sensitive B. pertussis but, surprisingly, decreases that of acid-tolerantB. bronchiseptica. In summary, we hypothesize that the differential survival of B. pertussis and B. bronchiseptica in macrophages is, at least in part, due to the differences in their acid tolerance.

Download Full-text