scholarly journals Type I interferons differentially modulate maternal host immunity to infection by Listeria monocytogenes and Salmonella enterica serovar Typhimurium during pregnancy

2018 ◽  
Vol 81 (1) ◽  
pp. e13068 ◽  
Author(s):  
Gerard Agbayani ◽  
Kristina Wachholz ◽  
Shawn P. Murphy ◽  
Subash Sad ◽  
Lakshmi Krishnan
Keyword(s):  
Listeria Monocytogenes ◽  
Salmonella Enterica ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Host Immunity ◽  
Type I Interferons ◽  
Type I ◽  
Serovar Typhimurium

Influence of the Treatment of Listeria monocytogenes and Salmonella enterica Serovar Typhimurium with Citral on the Efficacy of Various Antibiotics

2014 ◽  
Vol 11 (4) ◽  
pp. 265-271 ◽  
Author(s):  
Surama F. Zanini ◽  
Angela B. Silva-Angulo ◽  
Amauri Rosenthal ◽  
Dolores Rodrigo Aliaga ◽  
Antonio Martínez
Keyword(s):  
Listeria Monocytogenes ◽  
Salmonella Enterica ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Serovar Typhimurium

scholarly journals Type I interferon induces necroptosis in macrophages during infection with Salmonella enterica serovar Typhimurium

2012 ◽  
Vol 13 (10) ◽  
pp. 954-962 ◽  
Author(s):  
Nirmal Robinson ◽  
Scott McComb ◽  
Rebecca Mulligan ◽  
Renu Dudani ◽  
Lakshmi Krishnan ◽  
...  
Keyword(s):  
Salmonella Enterica ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Type I Interferon ◽  
Type I ◽  
Serovar Typhimurium

scholarly journals Role of FimW, FimY, and FimZ in Regulating the Expression of Type I Fimbriae in Salmonella enterica Serovar Typhimurium

2009 ◽  
Vol 191 (9) ◽  
pp. 3003-3010 ◽  
Author(s):  
Supreet Saini ◽  
Jeffrey A. Pearl ◽  
Christopher V. Rao
Keyword(s):  
Gene Expression ◽  
Negative Feedback ◽  
Salmonella Enterica ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Phase Variation ◽  
Type I ◽  
Serovar Typhimurium ◽  
Type I Fimbriae ◽  
Positive And Negative Feedback

ABSTRACT Type I fimbriae in Salmonella enterica serovar Typhimurium are surface appendages that facilitate binding to eukaryotic cells. Expression of the fim gene cluster is known to be regulated by three proteins—FimW, FimY, and FimZ—and a tRNA encoded by fimU. In this work, we investigated how these proteins and tRNA coordinately regulate fim gene expression. Our results indicate that FimY and FimZ independently activate the P fimA promoter which controls the expression of the fim structural genes. FimY and FimZ were also found to strongly activate each other's expression and weakly activate their own expression. FimW was found to negatively regulate fim gene expression by repressing transcription from the P fimY promoter, independent of FimY or FimZ. Moreover, FimW and FimY interact within a negative feedback loop, as FimY was found to activate the P fimW promoter. In the case of fimU, the expression of this gene was not found to be regulated by FimW, FimY, or FimZ. We also explored the effect of fim gene expression on Salmonella pathogenicity island 1 (SPI1). Our results indicate that FimZ alone is able to enhance the expression of hilE, a known repressor of SPI1 gene expression. Based on our results, we were able to propose an integrated model for the fim gene circuit. As this model involves a combination of positive and negative feedback, we hypothesized that the response of this circuit may be bistable and thus a possible mechanism for phase variation. However, we found that the response was continuous and not bistable.

scholarly journals Coordinate Regulation of Salmonella Pathogenicity Island 1 (SPI1) and SPI4 in Salmonella enterica Serovar Typhimurium

2007 ◽  
Vol 76 (3) ◽  
pp. 1024-1035 ◽  
Author(s):  
Kara L. Main-Hester ◽  
Katherine M. Colpitts ◽  
Gracie A. Thomas ◽  
Ferric C. Fang ◽  
Stephen J. Libby
Keyword(s):  
Mutant Strain ◽  
Salmonella Enterica ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Pathogenicity Island ◽  
Open Reading Frames ◽  
Type I ◽  
Coordinate Regulation ◽  
Serovar Typhimurium ◽  
Epithelial Invasion ◽  
Secretory System

ABSTRACT Salmonella enterica serovar Typhimurium harbors five pathogenicity islands (SPI) required for infection in vertebrate hosts. Although the role of SPI1 in promoting epithelial invasion and proinflammatory cell death has been amply documented, SPI4 has only more recently been implicated in Salmonella virulence. SPI4 is a 24-kb pathogenicity island containing six open reading frames, siiA to siiF. Secretion of the 595-kDa SiiE protein requires a type I secretory system encoded by siiC, siiD, and siiF. An operon polarity suppressor (ops) sequence within the 5′ untranslated region upstream of siiA is required for optimal SPI4 expression and predicted to bind the antiterminator RfaH. SiiE concentrations are decreased in a SPI1 mutant strain, suggesting that SPI1 and SPI4 may have common regulatory inputs. SPI1 gene expression is positively regulated by the transcriptional activators HilA, HilC, and HilD, encoded within SPI1, and negatively regulated by the regulators HilE and PhoP. Here, we show that mutations in hilA, hilC, or hilD similarly reduce expression of siiE, and mutations in hilE or phoP enhance siiE expression. Individual overexpression of HilA, HilC, or HilD in the absence of SPI1 cannot activate siiE expression, suggesting that these transcriptional regulators act in concert or in combination with additional SPI1-encoded regulatory loci to activate SPI4. HilA is no longer required for siiE expression in an hns mutant strain, suggesting that HilA promotes SPI4 expression by antagonizing the global transcriptional silencer H-NS. Coordinate regulation suggests that SPI1 and SPI4 play complementary roles in the interaction of S. enterica serovar Typhimurium with the host intestinal mucosa.

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