scholarly journals Role for Neutrophils in Host Immune Responses and Genetic Factors That Modulate Resistance to Salmonella enterica Serovar Typhimurium in the Inbred Mouse Strain SPRET/Ei

2010 ◽  
Vol 78 (9) ◽  
pp. 3848-3860 ◽  
Author(s):  
Lien Dejager ◽  
Iris Pinheiro ◽  
Pieter Bogaert ◽  
Liesbeth Huys ◽  
Claude Libert
Keyword(s):  
Mouse Strain ◽  
Salmonella Enterica ◽  
Genetic Factors ◽  
Inbred Mouse ◽  
Critical Role ◽  
Inbred Mouse Strain ◽  
Natural Resistance ◽  
Host Bacterium ◽  
A Genome ◽  
Serovar Typhimurium

ABSTRACT Infection with Salmonella enterica serovar Typhimurium is a complex disease in which the host-bacterium interactions are strongly influenced by genetic factors of the host. We demonstrate that SPRET/Ei, an inbred mouse strain derived from Mus spretus, is resistant to S. Typhimurium infections. The kinetics of bacterial proliferation, as well as histological examinations of tissue sections, suggest that SPRET/Ei mice can control bacterial multiplication and spreading despite significant attenuation of the cytokine response. The resistance of SPRET/Ei mice to S. Typhimurium infection is associated with increased leukocyte counts in the circulation and enhanced neutrophil influx into the peritoneum during the course of infection. A critical role of neutrophils was confirmed by neutrophil depletion: neutropenic SPRET/Ei mice were sensitive to infection with S. Typhimurium and showed much higher bacterial loads. To identify genes that modulate the natural resistance of SPRET/Ei mice to S. Typhimurium infection, we performed a genome-wide study using an interspecific backcross between C3H/HeN and SPRET/Ei mice. The results of this analysis demonstrate that at least two loci, located on chromosomes 6 and 11, affect survival following lethal infection with S. Typhimurium. These two loci contain several interesting candidate genes which may have important implications for the search for genetic factors controlling Salmonella infections in humans and for our understanding of complex host-pathogen interactions in general.

scholarly journals Contribution of Target Gene Mutations and Efflux to Decreased Susceptibility of Salmonella enterica Serovar Typhimurium to Fluoroquinolones and Other Antimicrobials

2006 ◽  
Vol 51 (2) ◽  
pp. 535-542 ◽  
Author(s):  
Sheng Chen ◽  
Shenghui Cui ◽  
Patrick F. McDermott ◽  
Shaohua Zhao ◽  
David G. White ◽  
...  
Keyword(s):  
Salmonella Enterica ◽  
Efflux Pump ◽  
Critical Role ◽  
Gene Mutations ◽  
Efflux Pumps ◽  
Fluoroquinolone Resistance ◽  
Naturally Occurring ◽  
Serovar Typhimurium ◽  
Resistant Mutants ◽  
Increased Susceptibility

ABSTRACT The mechanisms involved in fluoroquinolone resistance in Salmonella enterica include target alterations and overexpression of efflux pumps. The present study evaluated the role of known and putative multidrug resistance efflux pumps and mutations in topoisomerase genes among laboratory-selected and naturally occurring fluoroquinolone-resistant Salmonella enterica serovar Typhimurium strains. Strains with ciprofloxacin MICs of 0.25, 4, 32, and 256 μg/ml were derived in vitro using serovar Typhimurium S21. These mutants also showed decreased susceptibility or resistance to many nonfluoroquinolone antimicrobials, including tetracycline, chloramphenicol, and several β-lactams. The expression of efflux pump genes acrA, acrB, acrE, acrF, emrB, emrD, and mdlB were substantially increased (≥2-fold) among the fluoroquinolone-resistant mutants. Increased expression was also observed, but to a lesser extent, with three other putative efflux pumps: mdtB (yegN), mdtC (yegO), and emrA among mutants with ciprofloxacin MICs of ≥32 μg/ml. Deletion of acrAB or tolC in S21 and its fluoroquinolone-resistant mutants resulted in increased susceptibility to fluoroquinolones and other tested antimicrobials. In naturally occurring fluoroquinolone-resistant serovar Typhimurium strains, deletion of acrAB or tolC increased fluoroquinolone susceptibility 4-fold, whereas replacement of gyrA double mutations (S83F D87N) with wild-type gyrA increased susceptibility >500-fold. These results indicate that a combination of topoisomerase gene mutations, as well as enhanced antimicrobial efflux, plays a critical role in the development of fluoroquinolone resistance in both laboratory-derived and naturally occurring quinolone-resistant serovar Typhimurium strains.

Using the inbred mouse strain SPRET/EiJ to provide novel insights in inflammation and infection research

2018 ◽  
Vol 29 (7-8) ◽  
pp. 585-592
Author(s):  
Steven Timmermans ◽  
Jolien Souffriau ◽  
Jolien Vandewalle ◽  
Lise Van Wyngene ◽  
Kelly Van Looveren ◽  
...  
Keyword(s):  
Mouse Strain ◽  
Inbred Mouse ◽  
Inbred Mouse Strain

scholarly journals Transcriptional Regulation of sitABCD of Salmonella enterica Serovar Typhimurium by MntR and Fur

2005 ◽  
Vol 187 (3) ◽  
pp. 912-922 ◽  
Author(s):  
Jack S. Ikeda ◽  
Anuradha Janakiraman ◽  
David G. Kehres ◽  
Michael E. Maguire ◽  
James M. Slauch
Keyword(s):  
Transcriptional Regulation ◽  
Binding Sites ◽  
Transcriptional Repression ◽  
Salmonella Enterica ◽  
Transcriptional Control ◽  
Natural Resistance ◽  
Transport Systems ◽  
Transcriptional Level ◽  
Promoter Regions ◽  
Serovar Typhimurium

ABSTRACT Salmonella enterica serovar Typhimurium has two manganese transport systems, MntH and SitABCD. MntH is a bacterial homolog of the eukaryotic natural resistance-associated macrophage protein 1 (Nramp1), and SitABCD is an ABC-type transporter. Previously we showed that mntH is negatively controlled at the transcriptional level by the trans-acting regulatory factors, MntR and Fur. In this study, we examined the transcriptional regulation of sitABCD and compared it to the transcriptional regulation of mntH by constructing lacZ fusions to the promoter regions with and without mutations in putative MntR and/or Fur binding sites. The presence of Mn caused transcriptional repression of the sitABCD and mntH promoters primarily via MntR, but Fur was also capable of some repression in response to Mn. Likewise, Fe in the medium repressed transcription of both sit and mntH primarily via Fur, although MntR was also involved in this response. Transcriptional control by MntR and Fur was disrupted by site-specific mutations in the putative MntR and Fur binding sites, respectively. Transcription of the sit operon was also affected by the oxygen level and growth phase, but the increased expression observed under high oxygen conditions and higher cell densities is consistent with decreased availability of metals required for repression by the metalloregulatory proteins.

scholarly journals Impaired Pavlovian fear extinction is a common phenotype across genetic lineages of the 129 inbred mouse strain

2009 ◽  
Vol 8 (8) ◽  
pp. 744-752 ◽  
Author(s):  
M. Camp ◽  
M. Norcross ◽  
N. Whittle ◽  
M. Feyder ◽  
W. D’Hanis ◽  
...  
Keyword(s):  
Mouse Strain ◽  
Inbred Mouse ◽  
Inbred Mouse Strain ◽  
Fear Extinction ◽  
Genetic Lineages ◽  
Common Phenotype

scholarly journals Genetic differences between substrains of the inbred mouse strain 101 and designation of a new strain 102

1985 ◽  
Vol 46 (3) ◽  
pp. 349-352 ◽  
Author(s):  
John D. West ◽  
Mary F. Lyon ◽  
Josephine Peters ◽  
Paul B. Selby
Keyword(s):  
Inbred Strain ◽  
Genetic Polymorphisms ◽  
Mouse Strain ◽  
Inbred Mouse ◽  
Inbred Mouse Strain ◽  
Genetic Differences ◽  
The Other ◽  
Genetic Loci ◽  
Genetic Contamination

SUMMARYGenetic polymorphisms revealed two distinct substrains of the inbred strain 101. One group included substrains 101*/Rl, 101/H and 101/HOxe; the other group comprised 101/El and 101/Sl. The two groups differed at 5 of the 8 genetic loci tested. The accompanying paper (Evans, Burtenshaw & Adler, 1985) shows that the two groups also differ for several chromosome polymorphisms. We suggest that genetic contamination occurred during the derivation of 101/El from 101/Rl and was already present in 101/El when 101/Sl was produced from this substrain. We further propose that these substrains be renamed 102/El and 102/Sl respectively.

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