Lactic acid is a potential virulence factor for group B Streptococcus

Kling, David E.; Cavicchio, Amanda J.; Sollinger, Christina; Madoff, Lawrence C.; Schnitzer, Jay J.; Kinane, T. Bernard

doi:10.1016/j.micpath.2008.10.009

Cited by 16 publications

(22 citation statements)

References 46 publications

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“…We found that lactic acid production was enhanced when E. faecalis V583 is treated with SP. Lactic acid produced by the lactate dehydrogenase (LDH) enzyme, is implicated in multiple stress resistance and virulence in E. faecalis [23] and was also demonstrated to be a potential virulence factor in Streptococcus [31]. In our study, the increase of lactic acid production during exposure of the bacteria to SP didn’t result to a fall in pH.…”

Section: Discussionmentioning

confidence: 56%

Substance P enhances lactic acid and tyramine production in Enterococcus faecalis V583 and promotes its cytotoxic effect on intestinal Caco-2/TC7 cells

et al. 2017

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Background Enterococcus faecalis, generally considered as a saprophytic bowel commensal, has recently emerged as an important nosocomial pathogen causing severe urinary tract infections, surgical wound infections, bacteremia, and bacterial endocarditis. This bacterium is capable of forming biofilms on various surfaces and its high level of antibiotic resistance contributes to its pathogenicity. The aim of this study was to evaluate the effect on E. faecalis, of Substance P (SP), an antimicrobial peptide that is produced in the gut and skin.ResultsWe found that SP did not have antibacterial activity against E. faecalis V583 (MIC >1000 µg/ml). Conversely, SP stimulated aggregation, hydrophobicity, lactic acid and tyramine production in this bacterium. The cytotoxicity and bacterial translocation were also accelerated when E. faecalis V583 were pretreated with SP before infection of intestinal Caco-2/TC7 cells.ConclusionSP can modulate the physiology of E. faecalis. Extensive studies are now needed to screen within the human microbiota which bacteria are responsive to host molecules, and to identify their sensors.

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Section: Discussionmentioning

confidence: 56%

Substance P enhances lactic acid and tyramine production in Enterococcus faecalis V583 and promotes its cytotoxic effect on intestinal Caco-2/TC7 cells

et al. 2017

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“…To determine if the above observations were unique to GBS infections, explants were also infected with either heat-killed (EC-HK) or live E. coli strain EC1 (EC-L), a nonlethal derivative of strain DH5α [24]. Figure 1 shows that explants infected with EC1-L failed to show tissue atrophy observed in the live GBS infections.…”

Section: Resultsmentioning

confidence: 99%

“…The GBS strains A909 (serotype Ia) and COH1 (serotype III) were obtained from the Channing Laboratory [25]. The E. coli strain EC1 is a derivative of the laboratory strain DH5α [24]. Antibodies used in these studies are shown in Table I.…”

Section: Methodsmentioning

confidence: 99%

“…Analysis of L-Lactate in the spent media samples was carried out essentially as previously described [24]. Assays were scaled to a 96-well microplate format using black/clear Imaging Plates (BD Falcon) and samples were read at 340 nm using a Synergy H4 Hybrid (Biotek, Winooski, VT) microplate reader.…”

Section: Methodsmentioning

confidence: 99%

“…Therefore, GBS pathogenic mechanisms were studied via an ex vivo model, which enables the observation of dynamic host-pathogen interactions with an intact tissue bed over the course of an infection [24]. The data herein suggest that GBS infections are associated not only with profound lung morphological changes, but GBS targets the lung interstitial cells inducing caspase-dependent apoptosis.…”

Section: Introductionmentioning

confidence: 99%

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Group B Streptococcus induces a caspase-dependent apoptosis in fetal rat lung interstitium

Kling

Tsvang

Murphy

et al. 2013

Microbial Pathogenesis

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Group B Streptococcus (GBS) is an important pathogen and is associated with sepsis and meningitis in neonates and infants. An ex vivo model that facilitates observations of GBS interactions with multiple host cell types over time was used to study its pathogenicity. GBS infections were associated with profound reductions in fetal lung; explant size, and airway branching. Elevated levels of apoptosis subsequent to GBS infections were observed by whole-mount confocal immunofluorescence using activated-caspase-3-antibodies and terminal deoxynucleotidyl transferase dUTP nick end-labeling (TUNEL) assays. The caspase inhibitor Z-VAD-FMK abolished the increase in TUNEL-positive cells associated with GBS infections, indicating that the GBS-induced apoptosis was caspase-dependent. Digital image analyses revealed that both GBS and the active form of caspase-3 were distributed primarily within the lung interstitium, suggesting that these tissues are important targets for GBS. Antibodies to the active form of caspase-3 colocalized with both macrophage- and erythroblast-markers, suggesting that these hematopoietic cells are vulnerable to GBS-mediated pathogenesis. These studies suggest that GBS infections profoundly alter lung morphology and caspase-dependent hematopoietic cell apoptosis within the lung interstitium play roles in GBS pathophysiology in this model.

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Nitrofen induces apoptosis independently of retinaldehyde dehydrogenase (RALDH) inhibition

Kling

Cavicchio

Sollinger

et al. 2010

Birth Defects Research Pt B

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Lactic acid is a potential virulence factor for group B Streptococcus

Cited by 16 publications

References 46 publications

Substance P enhances lactic acid and tyramine production in Enterococcus faecalis V583 and promotes its cytotoxic effect on intestinal Caco-2/TC7 cells

Substance P enhances lactic acid and tyramine production in Enterococcus faecalis V583 and promotes its cytotoxic effect on intestinal Caco-2/TC7 cells

Group B Streptococcus induces a caspase-dependent apoptosis in fetal rat lung interstitium

Nitrofen induces apoptosis independently of retinaldehyde dehydrogenase (RALDH) inhibition

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