Effects of Environmental Conditions (temperature, pH, and glucose) on Biofilm Formation of Salmonella enterica serotype Kentucky and Virulence Gene Expression

Abstract Background The aim of this study was to investigate the association among biofilm formation, virulence gene expression, and antibiotic resistance in P. mirabilis isolates collected from diarrhetic animals (n = 176) in northeast China between September 2014 and October 2016. Results Approximately 92.05% of the isolates were biofilm producers, whereas 7.95% of the isolates were non-producers. The prevalence of virulence genes in biofilm producers was significantly higher than that in non-producers. Biofilm production was significantly associated with the expression of ureC , zapA , rsmA , hmpA , mrpA , atfA , and pmfA ( P < 0.05). Drug susceptibility tests revealed that approximately 76.7% of the isolates were multidrug-resistant (MDR) and extensively drug-resistant (XDR). Biofilm production was significantly associated with resistance to doxycycline, tetracycline, sulfamethoxazole, kanamycin, and cephalothin ( P < 0.05). Although the pathogenicity of the biofilm producers was stronger than that of the non-producers, the biofilm-forming ability of the isolates was not significantly associated with morbidity and mortality in mice ( P > 0.05). Conclusion Our findings suggested that a high level of multidrug resistance in diarrhetic animals infected with P. mirabilis in northeast China.The results of this study indicated that the positive rates of the genes expressed by biofilm-producing P. mirabilis isolates were significantly higher than those expressed by non-producing isolates.

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Novel Inhibitors of Staphylococcus aureus Virulence Gene Expression and Biofilm Formation

PLoS ONE ◽

10.1371/journal.pone.0047255 ◽

2012 ◽

Vol 7 (10) ◽

pp. e47255 ◽

Cited By ~ 37

Author(s):

Yibao Ma ◽

Yuanxi Xu ◽

Bryan D. Yestrepsky ◽

Roderick J. Sorenson ◽

Meng Chen ◽

...

Keyword(s):

Gene Expression ◽

Staphylococcus Aureus ◽

Biofilm Formation ◽

Virulence Gene ◽

Virulence Gene Expression

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Diffusible Signal Factors Act through AraC-Type Transcriptional Regulators as Chemical Cues To Repress Virulence of Enteric Pathogens

Infection and Immunity ◽

10.1128/iai.00226-20 ◽

2020 ◽

Vol 88 (10) ◽

Author(s):

Erick Maosa Bosire ◽

Colleen R. Eade ◽

Carl J. Schiltz ◽

Amanda J. Reid ◽

Jerry Troutman ◽

...

Keyword(s):

Gene Expression ◽

Fatty Acids ◽

Salmonella Enterica ◽

Unsaturated Fatty Acids ◽

Virulence Gene ◽

Transcriptional Regulators ◽

Enteric Pathogens ◽

Hexadecenoic Acid ◽

Content Type ◽

Virulence Gene Expression

ABSTRACT Successful colonization by enteric pathogens is contingent upon effective interactions with the host and the resident microbiota. These pathogens thus respond to and integrate myriad signals to control virulence. Long-chain fatty acids repress the virulence of the important enteric pathogens Salmonella enterica and Vibrio cholerae by repressing AraC-type transcriptional regulators in pathogenicity islands. While several fatty acids are known to be repressive, we show here that cis-2-unsaturated fatty acids, a rare chemical class used as diffusible signal factors (DSFs), are highly potent inhibitors of virulence functions. We found that DSFs repressed virulence gene expression of enteric pathogens by interacting with transcriptional regulators of the AraC family. In Salmonella enterica serovar Typhimurium, DSFs repress the activity of HilD, an AraC-type activator essential to the induction of epithelial cell invasion, by both preventing its interaction with target DNA and inducing its rapid degradation by Lon protease. cis-2-Hexadecenoic acid (c2-HDA), a DSF produced by Xylella fastidiosa, was the most potent among those tested, repressing the HilD-dependent transcriptional regulator hilA and the type III secretion effector sopB >200- and 68-fold, respectively. Further, c2-HDA attenuated the transcription of the ToxT-dependent cholera toxin synthesis genes of V. cholerae. c2-HDA significantly repressed invasion gene expression by Salmonella in the murine colitis model, indicating that the HilD-dependent signaling pathway functions within the complex milieu of the animal intestine. These data argue that enteric pathogens respond to DSFs as interspecies signals to identify appropriate niches in the gut for virulence activation, which could be exploited to control the virulence of enteric pathogens.

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Interplay between the QseC and QseE Bacterial Adrenergic Sensor Kinases in Salmonella enterica Serovar Typhimurium Pathogenesis

Infection and Immunity ◽

10.1128/iai.00803-12 ◽

2012 ◽

Vol 80 (12) ◽

pp. 4344-4353 ◽

Cited By ~ 34

Author(s):

Cristiano G. Moreira ◽

Vanessa Sperandio

Keyword(s):

Gene Expression ◽

Epithelial Cells ◽

Salmonella Enterica ◽

Double Mutant ◽

Virulence Gene ◽

Virulence Gene Expression ◽

Regulatory Cascade ◽

Serovar Typhimurium ◽

Sensor Kinases

ABSTRACTThe bacterial adrenergic sensor kinases QseC and QseE respond to epinephrine and/or norepinephrine to initiate a complex phosphorelay regulatory cascade that modulates virulence gene expression in several pathogens. We have previously shown that QseC activates virulence gene expression inSalmonella entericaserovar Typhimurium. Here we report the role of QseE inS. Typhimurium pathogenesis as well as the interplay between these two histidine sensor kinases in gene regulation. AnS. TyphimuriumqseEmutant is hampered in the invasion of epithelial cells and intramacrophage replication. The ΔqseCstrain is highly attenuated for intramacrophage survival but has only a minor defect in invasion. However, the ΔqseECstrain has only a slight attenuation in invasion, mirroring the ΔqseCstrain, and has an intermediary intramacrophage replication defect in comparison to the ΔqseEand ΔqseCstrains. The expressions of thesipAandsopBgenes, involved in the invasion of epithelial cells, are activated by epinephrine via QseE. The expression levels of these genes are still decreased in the ΔqseECdouble mutant, albeit to a lesser extent, congruent with the invasion phenotype of this mutant. The expression level of thesifAgene, important for intramacrophage replication, is decreased in theqseEmutant and the ΔqseECdouble mutant grownin vitro. However, as previously reported by us, the epinephrine-dependent activation of this gene occurs via QseC. In the systemic model ofS. Typhimurium infection of BALB/c mice, theqseCandqseEmutants are highly attenuated, while the double mutant has an intermediary phenotype. Altogether, these data suggest that both adrenergic sensors play an important role in modulating several aspects ofS. Typhimurium pathogenesis.

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Host stress hormone norepinephrine stimulates pneumococcal growth, biofilm formation and virulence gene expression

BMC Microbiology ◽

10.1186/1471-2180-14-180 ◽

2014 ◽

Vol 14 (1) ◽

pp. 180 ◽

Cited By ~ 33

Author(s):

Sara Sandrini ◽

Fayez Alghofaili ◽

Primrose Freestone ◽

Hasan Yesilkaya

Keyword(s):

Gene Expression ◽

Biofilm Formation ◽

Virulence Gene ◽

Stress Hormone ◽

Virulence Gene Expression

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Yunnan Baiyao reduces hospital-acquired pressure ulcers via suppressing virulence gene expression and biofilm formation of Staphylococcus aureus

International Journal of Medical Sciences ◽

10.7150/ijms.33723 ◽

2019 ◽

Vol 16 (8) ◽

pp. 1078-1088

Author(s):

Jun Liu ◽

Mufa Cai ◽

Huimin Yan ◽

Jiawu Fu ◽

Guocai Wu ◽

...

Keyword(s):

Gene Expression ◽

Staphylococcus Aureus ◽

Biofilm Formation ◽

Pressure Ulcers ◽

Virulence Gene ◽

Virulence Gene Expression ◽

Yunnan Baiyao ◽

Hospital Acquired

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Norfloxacin Sub-Inhibitory Concentration Affects Streptococcus suis Biofilm Formation and Virulence Gene Expression

Indian Journal of Animal Research ◽

10.18805/ijar.b-1192 ◽

2020 ◽

Author(s):

Baobao Li ◽

Li Yi ◽

Jinpeng Li ◽

Shenglong Gong ◽

Xiao Dong ◽

...

Keyword(s):

Gene Expression ◽

Biofilm Formation ◽

Inhibitory Concentration ◽

Mrna Level ◽

Virulence Gene ◽

Streptococcus Suis ◽

Economic Losses ◽

Swine Industry ◽

Virulence Gene Expression ◽

Viable Bacteria

Streptococcus suis (S. suis) is a major pathogen causing economic losses to the swine industry. Norfloxacins are usually used at sub-MIC (Minimum Inhibitory Concentration) doses to prevent S. suis infection. This study demonstrates the effect of norfloxacin sub-MIC on biofilm formation and virulence gene expression in S. suis.It was found that 1/4 MIC of norfloxacin increased biofilm formation in S. suis, the biofilms formed contained a higher number of viable bacteria. Additionally, bacterial growth rates were inhibited at 1/2 MIC of norfloxacin. Furthermore, the mRNA level of S. suis virulence gene cps, ef, sly, fpbs, gdh and gapdh increased by real-time PCR, while the virulence gene mrp decreased at 1/4 MIC. In conclusion, Norfloxacin sub-MICs affects biofilm formation and virulence gene expression in S. suis. These findings suggest that investigating the effect of the administration of antibiotics sub-MICs on bacterial biofilms and infection may lead to the development of future antibiotic treatments modalities.

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