Effect of Two Probiotic Strains of Lactobacillus on In Vitro Adherence of Listeria monocytogenes, Streptococcus agalactiae, and Staphylococcus aureus to Vaginal Epithelial Cells

Ortíz, Luisa; Ruíz, Francisco; Pascual, Liliana; Barberis, Lucila

doi:10.1007/s00284-014-0524-9

Cited by 36 publications

(25 citation statements)

References 18 publications

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“…Interestingly, an inverse relationship between Lactobacillus and GBS has also been observed in cows with subclinical mastitis ( 79 ). Certain Lactobacillus strains have the capacity to inhibit GBS adherence to vaginal epithelial cells ( 80 , 81 ), and antimicrobial activity of Lactobacillus against GBS has been documented in vitro ( 82 ) and reduction of colonization seen in vivo ( 83 , 84 ). Although the full complexity of the vaginal microbiome is only now being characterized, preliminary in vitro studies have begun to probe GBS communication and cooperation with other microbes in this host microenvironment.…”

Section: Influence Of Vaginal Microbiota On Gbs Colonizationmentioning

confidence: 99%

Group B Streptococcal Maternal Colonization and Neonatal Disease: Molecular Mechanisms and Preventative Approaches

2018

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Group B Streptococcus (GBS) colonizes the gastrointestinal and vaginal epithelium of a significant percentage of healthy women, with potential for ascending intrauterine infection or transmission during parturition, creating a risk of serious disease in the vulnerable newborn. This review highlights new insights on the bacterial virulence determinants, host immune responses, and microbiome interactions that underpin GBS vaginal colonization, the proximal step in newborn infectious disease pathogenesis. From the pathogen perspective, the function GBS adhesins and biofilms, β-hemolysin/cytolysin toxin, immune resistance factors, sialic acid mimicry, and two-component transcriptional regulatory systems are reviewed. From the host standpoint, pathogen recognition, cytokine responses, and the vaginal mucosal and placental immunity to the pathogen are detailed. Finally, the rationale, efficacy, and potential unintended consequences of current universal recommended intrapartum antibiotic prophylaxis are considered, with updates on new developments toward a GBS vaccine or alternative approaches to reducing vaginal colonization.

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Section: Influence Of Vaginal Microbiota On Gbs Colonizationmentioning

confidence: 99%

Group B Streptococcal Maternal Colonization and Neonatal Disease: Molecular Mechanisms and Preventative Approaches

2018

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“…Our study revealed that colonization of A. baumannii in the presence of either GBS and/or C. albicans did not increase the possibility of PPROM. We postulate that vaginal microbiota, especially Lactobacilli, may outcompete the adherence of GBS and other pathogens to the vaginal epithelial cells as previously demonstrated by Ortiz et al (2014) and Parolin et al (2015). Apart from that, epithelial cells of the vagina were also reported to produce antimicrobial compounds (Yarbrough et al, 2015).…”

Section: Discussionmentioning

confidence: 53%

Colonization of Acinetobacter baumannii, Streptococcus agalactiae (GBS) and Candida albicans in preterm premature rupture of membrane (PPROM) compared to normal labor at term

Mohd-Zain¹,

Yahcob²,

Sood³

et al. 2019

MJM

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Aims: Preterm premature rupture of membrane (PPROM) is usually associated with maternal vaginal colonization of Group B Streptococci (GBS). However, there are reports on isolation of Acinetobacter baumannii in PPROM cases. In order to ascertain A. baumannii's role in PPROM, we determine the colonization of A. baumannii and other common vaginal tract flora, i.e. GBS and Candida albicans, in women with PPROM, and compared them to those with normal labor at term (NLT). The transmissibility of the organisms to their babies was also investigated. Methodology and results: A total of 218 high vaginal swabs from 108 and 100 women with PPROM and NLT respectively were collected. The transmission of these organisms to their 215 babies was determined by swabbing the ears and axillae. These were cultured for isolation of A. baumannii, GBS and C. albicans. Results showed that mothers with PPROM were predominantly colonized with GBS (32.4%), followed by C. albicans (19.4%) and A. baumannii (7.4%), compared to 10.9%, 17.3% and 7.2% respectively, in women with NLT. Between 34 to 50% of the babies of mothers with PPROM acquired the organisms, with GBS being the most significantly (p=0.000) transferred compared to other organisms. Coexistence of A. baumannii with either GBS or C. albicans, or both, did not enhance the occurrence of PPROM. Conclusion, significance and impact of study: Colonization of A. baumannii in vaginal tract of pregnant women does not increase the possibility of PPROM, as compared to GBS.

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“…These interactions vary between the microorganisms: cooperation with E. faecalis and Candida albicans (Engelmann et al, 2011; Nair et al, 2014; Zago et al, 2015), competition with Lactobacillus sp. (Ortiz et al, 2014), and Streptococcus pneumoniae (Margolis et al, 2010). S. aureus can also have both interactions (competition and cooperation) with the same pathogen depending of the disease and the conditions such as Pseudomonas aeruginosa (Hoffman et al, 2006; Baldan et al, 2014; Serra et al, 2015; Frydenlund Michelsen et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

Decrease of Staphylococcus aureus Virulence by Helcococcus kunzii in a Caenorhabditis elegans Model

Essebe

Visvikis

Fines-Guyon

et al. 2017

Front. Cell. Infect. Microbiol.

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Social bacterial interactions are considered essential in numerous infectious diseases, particularly in wounds. Foot ulcers are a common complication in diabetic patients and these ulcers become frequently infected. This infection is usually polymicrobial promoting cell-to-cell communications. Staphylococcus aureus is the most prevalent pathogen isolated. Its association with Helcococcus kunzii, commensal Gram-positive cocci, is frequently described. The aim of this study was to assess the impact of co-infection on virulence of both H. kunzii and S. aureus strains in a Caenorhabditis elegans model. To study the host response, qRT-PCRs targeting host defense genes were performed. We observed that H. kunzii strains harbored a very low (LT50: 5.7 days ± 0.4) or an absence of virulence (LT50: 6.9 days ± 0.5). In contrast, S. aureus strains (LT50: 2.9 days ± 0.4) were significantly more virulent than all H. kunzii (P < 0.001). When H. kunzii and S. aureus strains were associated, H. kunzii significantly reduced the virulence of the S. aureus strain in nematodes (LT50 between 4.4 and 5.2 days; P < 0.001). To evaluate the impact of these strains on host response, transcriptomic analysis showed that the ingestion of S. aureus led to a strong induction of defense genes (lys-5, sodh-1, and cyp-37B1) while H. kunzii did not. No statistical difference of host response genes expression was observed when C. elegans were infected with either S. aureus alone or with S. aureus + H. kunzii. Moreover, two well-characterized virulence factors (hla and agr) present in S. aureus were down-regulated when S. aureus were co-infected with H. kunzii. This study showed that H. kunzii decreased the virulence of S. aureus without modifying directly the host defense response. Factor(s) produced by this bacterium modulating the staphylococci virulence must be investigated.

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Effect of Two Probiotic Strains of Lactobacillus on In Vitro Adherence of Listeria monocytogenes, Streptococcus agalactiae, and Staphylococcus aureus to Vaginal Epithelial Cells

Cited by 36 publications

References 18 publications

Group B Streptococcal Maternal Colonization and Neonatal Disease: Molecular Mechanisms and Preventative Approaches

Group B Streptococcal Maternal Colonization and Neonatal Disease: Molecular Mechanisms and Preventative Approaches

Colonization of Acinetobacter baumannii, Streptococcus agalactiae (GBS) and Candida albicans in preterm premature rupture of membrane (PPROM) compared to normal labor at term

Decrease of Staphylococcus aureus Virulence by Helcococcus kunzii in a Caenorhabditis elegans Model

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