Acid tolerance in Listeria monocytogenes influences invasiveness of enterocyte-like cells and macrophage-like cells

Conte, Miriam; Petrone, G; Biase, AM Di; Ammendolia, Maria Grazia; Superti, Fabiana; Seganti, L

doi:10.1006/mpat.2000.0379

Cited by 92 publications

(85 citation statements)

References 28 publications

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“…The acidtolerant L. monocytogenes strains are more invasive in vitro (Conte et al, 2000) and more virulent in vivo (O'Driscoll et al, 1996) than their acid-sensitive counterparts, and the reverse has also been established. Consistently, a mutant unable to induce acid tolerance response displays subdued virulence compared with its parent strain in mice (Marron et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

Lmo0036, an ornithine and putrescine carbamoyltransferase in Listeria monocytogenes, participates in arginine deiminase and agmatine deiminase pathways and mediates acid tolerance

et al. 2011

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Listeria monocytogenes is a foodborne pathogen causing listeriosis. Acid is one of the stresses that foodborne pathogens encounter most frequently. The ability to survive and proliferate in acidic environments is a prerequisite for infection. However, there is limited knowledge about the molecular basis of adaptation of L. monocytogenes to acid. Arginine deiminase (ADI) and agmatine deiminase (AgDI) systems are implicated in bacterial tolerance to acidic environments. Homologues of ADI and AgDI systems have been found in L. monocytogenes lineages I and II strains. Sequence analysis indicated that lmo0036 encodes a putative carbamoyltransferase containing conserved motifs and residues important for substrate binding. Lmo0036 acted as an ornithine carbamoyltransferase and putrescine carbamoyltransferase, representing the first example, to our knowledge, that catalyses reversible ornithine and putrescine carbamoyltransfer reactions. Catabolic ornithine and putrescine carbamoyltransfer reactions constitute the second step of ADI and AgDI pathways. However, the equilibrium of in vitro carbamoyltransfer reactions was overwhelmingly towards the anabolic direction, suggesting that catabolic carbamoyltransferase was probably the limiting step of the pathways. lmo0036 was induced at the transcriptional level when L. monocytogenes was subjected to low-pH stress. Its expression product in Escherichia coli exhibited higher catabolic carbamoyltransfer activities under acidic conditions. Consistently, absence of this enzyme impaired the growth of Listeria under mild acidic conditions (pH 4.8) and reduced its survival in synthetic human gastric fluid (pH 2.5), and corresponded to a loss in ammonia production, indicating that Lmo0036 was responsible for acid tolerance at both sublethal and lethal pH levels. Furthermore, Lmo0036 played a possible role in Listeria virulence.

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Section: Discussionmentioning

confidence: 99%

Lmo0036, an ornithine and putrescine carbamoyltransferase in Listeria monocytogenes, participates in arginine deiminase and agmatine deiminase pathways and mediates acid tolerance

et al. 2011

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“…Although the molecular strategies utilized by this pathogen to survive acid stress are well understood , there is little information on the influence of acid stress on EHEC O157 : H7 virulence. Several other gastrointestinal pathogens (Helicobacter pylori, Legionella pneumophila, Clostridium difficile, Salmonella typhimurium and Legionella monocytogenes) show enhanced virulence after exposure to acid stress, including increased host-cell adhesion and invasion, macrophage apoptosis, and lethality in mouse models (Conte et al, 2000;de Jesus et al, 2005;Fernandez et al, 1996;Hennequin et al, 2001;Hoffman & Garduno, 1999;Huesca et al, 1996;O'Driscoll et al, 1996;Waligora et al, 1999). The present study now demonstrates that there are also significant changes in EHEC O157 : H7 virulence properties after acid stress.…”

Section: Discussionmentioning

confidence: 99%

Acid-stress-induced changes in enterohaemorrhagic Escherichia coli O157 : H7 virulence

et al. 2009

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Enterohaemorrhagic Escherichia coli (EHEC) O157 : H7 is naturally exposed to a wide variety of stresses including gastric acid shock, and yet little is known about how this stress influences virulence. This study investigated the impact of acid stress on several critical virulence properties including survival, host adhesion, Shiga toxin production, motility and induction of host-cell apoptosis. Several acid-stress protocols with relevance for gastric passage as well as external environmental exposure were included. Acute acid stress at pH 3 preceded by acid adaptation at pH 5 significantly enhanced the adhesion of surviving organisms to epithelial cells and bacterial induction of host-cell apoptosis. Motility was also significantly increased after acute acid stress. Interestingly, neither secreted nor periplasmic levels of Shiga toxin were affected by acid shock. Pretreatment of bacteria with erythromycin eliminated the acid-induced adhesion enhancement, suggesting that de novo protein synthesis was required for the enhanced adhesion of acidshocked organisms. DNA microarray was used to analyse the transcriptome of an EHEC O157 : H7 strain exposed to three different acid-stress treatments. Expression profiles of acidstressed EHEC revealed significant changes in virulence factors associated with adhesion, motility and type III secretion. These results document profound changes in the virulence properties of EHEC O157 : H7 after acid stress, provide a comprehensive genetic analysis to substantiate these changes and suggest strategies that this pathogen may use during gastric passage and colonization in the human gastrointestinal tract.

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“…In these cells, four-to fivefoldgreater numbers of acid-adapted Listeria were present 4 h postinfection, relative to the number in untreated cells. At 8 h postinfection, the majority of acid-adapted cells were free in the cytoplasm whereas a large number of the nonadapted cells remained in intact phagosomes (46). Both adapted and nonadapted bacteria were phagocytosed and multiplied efficiently in nonactivated THP-1 macrophages.…”

Section: Listeria Monocytogenesmentioning

confidence: 99%

“…To further appreciate the consequences of the emergence of acid-resistant strains, spontaneous acid-tolerant mutants were isolated which were almost as resistant, without acid induction, as adapted wild-type cells and which could be further induced to display even greater levels of survival (46,170). Compared with wild-type cells, these mutants displayed enhanced acid tolerance during all stages of growth, enjoyed improved sur- (46), and caused higher rates of mortality in mice (170).…”

Section: Listeria Monocytogenesmentioning

confidence: 99%

Surviving the Acid Test: Responses of Gram-Positive Bacteria to Low pH

Cotter

Hill

2003

Microbiol Mol Biol Rev

1,030

828

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Gram-positive bacteria possess a myriad of acid resistance systems that can help them to overcome the challenge posed by different acidic environments. In this review the most common mechanisms are described: i.e., the use of proton pumps, the protection or repair of macromolecules, cell membrane changes, production of alkali, induction of pathways by transcriptional regulators, alteration of metabolism, and the role of cell density and cell signaling. We also discuss the reponses of Listeria monocytogenes, Rhodococcus, Mycobacterium, Clostridium perfringens, Staphylococcus aureus, Bacillus cereus, oral streptococci, and lactic acid bacteria to acidic environments and outline ways in which this knowledge has been or may be used to either aid or prevent bacterial survival in low-pH environments

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Acid tolerance in Listeria monocytogenes influences invasiveness of enterocyte-like cells and macrophage-like cells

Cited by 92 publications

References 28 publications

Lmo0036, an ornithine and putrescine carbamoyltransferase in Listeria monocytogenes, participates in arginine deiminase and agmatine deiminase pathways and mediates acid tolerance

Lmo0036, an ornithine and putrescine carbamoyltransferase in Listeria monocytogenes, participates in arginine deiminase and agmatine deiminase pathways and mediates acid tolerance

Acid-stress-induced changes in enterohaemorrhagic Escherichia coli O157 : H7 virulence

Surviving the Acid Test: Responses of Gram-Positive Bacteria to Low pH

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