Downregulation of Salmonella Virulence Gene Expression During Invasion of Epithelial Cells Treated with Lactococcus lactis subsp. cremoris JFR1 Requires OppA

2019 ◽  
Vol 12 (2) ◽  
pp. 577-588 ◽  
Author(s):  
J. S. Zhang ◽  
M. Corredig ◽  
R. Morales-Rayas ◽  
A. Hassan ◽  
M. W. Griffiths ◽  
...  
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Lactococcus Lactis ◽  
Virulence Gene ◽  
Virulence Gene Expression ◽  
Lactococcus Lactis Subsp ◽  
Salmonella Virulence

scholarly journals Formate PromotesShigellaIntercellular Spread and Virulence Gene Expression

mBio ◽  
2018 ◽  
Vol 9 (5) ◽  
Author(s):  
Benjamin J. Koestler ◽  
Carolyn R. Fisher ◽  
Shelley M. Payne
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Host Cell ◽  
Shigella Flexneri ◽  
Virulence Gene ◽  
Plaque Size ◽  
Acid Fermentation ◽  
Content Type ◽  
Virulence Gene Expression ◽  
Cell Spread

ABSTRACTThe intracellular human pathogenShigella flexneriinvades the colon epithelium, replicates to high cell density within the host cell, and then spreads to adjacent epithelial cells. WhenS. flexnerigains access to the host cytosol, the bacteria metabolize host cytosolic carbon using glycolysis and mixed acid fermentation, producing formate as a by-product. We show thatS. flexneriinfection results in the accumulation of formate within the host cell. Loss of pyruvate formate lyase (PFL; ΔpflB), which converts pyruvate to acetyl coenzyme A (CoA) and formate, eliminatesS. flexneriformate production and reduces the ability ofS. flexnerito form plaques in epithelial cell monolayers. This defect in PFL does not decrease the intracellular growth rate ofS. flexneri; rather, it affects cell-to-cell spread. TheS. flexneriΔpflBmutant plaque defect is complemented by supplying exogenous formate; conversely, deletion of theS. flexneriformate dehydrogenase genefdnGincreases host cell formate accumulation andS. flexneriplaque size. Furthermore, exogenous formate increases plaque size of the wild-type (WT)S. flexneristrain and promotesS. flexnericell-to-cell spread. We also demonstrate that formate increases the expression ofS. flexnerivirulence genesicsAandipaJ. IntracellularS. flexneriicsAandipaJexpression is dependent on the presence of formate, andipaJexpression correlates withS. flexneriintracellular density during infection. Finally, consistent with elevatedipaJ, we show that formate altersS. flexneri-infected host interferon- and tumor necrosis factor (TNF)-stimulated gene expression. We propose thatShigella-derived formate is an intracellular signal that modulates virulence in response to bacterial metabolism.IMPORTANCEShigellais an intracellular pathogen that invades the human host cell cytosol and exploits intracellular nutrients for growth, enabling the bacterium to create its own metabolic niche. ForShigellato effectively invade and replicate within the host cytoplasm, it must sense and adapt to changing environmental conditions; however, the mechanisms and signals sensed byS. flexneriare largely unknown. We have found that the secretedShigellametabolism by-product formate regulatesShigellaintracellular virulence gene expression and its ability to spread among epithelial cells. We propose thatShigellasenses formate accumulation in the host cytosol as a way to determine intracellularShigelladensity and regulate secreted virulence factors accordingly, enabling spatiotemporal regulation of effectors important for dampening the host immune response.

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

2012 ◽  
Vol 80 (12) ◽  
pp. 4344-4353 ◽  
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.

scholarly journals Association and Virulence Gene Expression Vary among Serotype III Group B Streptococcus Isolates following Exposure to Decidual and Lung Epithelial Cells

2014 ◽  
Vol 82 (11) ◽  
pp. 4587-4595 ◽  
Author(s):  
Michelle L. Korir ◽  
David Knupp ◽  
Kathryn LeMerise ◽  
Erica Boldenow ◽  
Rita Loch-Caruso ◽  
...  
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Virulence Genes ◽  
Virulence Gene ◽  
Lung Epithelial Cells ◽  
Host Cells ◽  
Virulence Gene Expression ◽  
Decidual Cells ◽  
Lung Epithelial ◽  
Group B

ABSTRACTGroup BStreptococcus(GBS) causes severe disease in neonates, the elderly, and immunocompromised individuals. GBS species are highly diverse and can be classified by serotype and multilocus sequence typing. Sequence type 17 (ST-17) strains cause invasive neonatal disease more frequently than strains of other STs. Attachment and invasion of host cells are key steps in GBS pathogenesis. We investigated whether four serotype III strains representing ST-17 (two strains), ST-19, and ST-23 differ in their abilities to attach to and invade both decidual cells and lung epithelial cells. Virulence gene expression following host cell association and exposure to amnion cells was also tested. The ST-17 strains differed in their abilities to attach to and invade decidual cells, whereas there were no differences with lung epithelial cells. The ST-19 and ST-23 strains, however, attached to and invaded decidual cells less than both ST-17 strains. Although the ST-23 strain attached to lung epithelial cells better than ST-17 and -19 strains, none of the strains effectively invaded the lung epithelial cells. Notably, the association with host cells resulted in the differential expression of several virulence genes relative to basal expression levels. Similar expression patterns of some genes were observed regardless of cell type used. Collectively, these results show that GBS strains differ in their abilities to attach to distinct host cell types and express key virulence genes that are relevant to the disease process. Enhancing our understanding of pathogenic mechanisms could aid in the identification of novel therapeutic targets or vaccine candidates that could potentially decrease morbidity and mortality associated with neonatal infections.

Vibrio harveyi virulence gene expression in vitro and in vivo during infection in black tiger shrimp Penaeus monodon

2020 ◽  
Vol 139 ◽  
pp. 153-160
Author(s):  
S Peeralil ◽  
TC Joseph ◽  
V Murugadas ◽  
PG Akhilnath ◽  
VN Sreejith ◽  
...  
Keyword(s):  
Gene Expression ◽  
Virulence Genes ◽  
Vibrio Harveyi ◽  
Penaeus Monodon ◽  
Challenge Test ◽  
Virulence Gene ◽  
Economic Losses ◽  
Virulence Gene Expression

Luminescent Vibrio harveyi is common in sea and estuarine waters. It produces several virulence factors and negatively affects larval penaeid shrimp in hatcheries, resulting in severe economic losses to shrimp aquaculture. Although V. harveyi is an important pathogen of shrimp, its pathogenicity mechanisms have yet to be completely elucidated. In the present study, isolates of V. harveyi were isolated and characterized from diseased Penaeus monodon postlarvae from hatcheries in Kerala, India, from September to December 2016. All 23 tested isolates were positive for lipase, phospholipase, caseinase, gelatinase and chitinase activity, and 3 of the isolates (MFB32, MFB71 and MFB68) showed potential for significant biofilm formation. Based on the presence of virulence genes, the isolates of V. harveyi were grouped into 6 genotypes, predominated by vhpA+ flaB+ ser+ vhh1- luxR+ vopD- vcrD+ vscN-. One isolate from each genotype was randomly selected for in vivo virulence experiments, and the LD50 ranged from 1.7 ± 0.5 × 103 to 4.1 ± 0.1 × 105 CFU ml-1. The expression of genes during the infection in postlarvae was high in 2 of the isolates (MFB12 and MFB32), consistent with the result of the challenge test. However, in MFB19, even though all genes tested were present, their expression level was very low and likely contributed to its lack of virulence. Because of the significant variation in gene expression, the presence of virulence genes alone cannot be used as a marker for pathogenicity of V. harveyi.

Sign in / Sign up

Export Citation Format

Share Document