scholarly journals Type 1 Fimbriae of Salmonella enterica Serovar Typhimurium Bind to Enterocytes and Contribute to Colonization of Swine In Vivo

2003 ◽  
Vol 71 (11) ◽  
pp. 6446-6452 ◽  
Author(s):  
Carrie Althouse ◽  
Sheila Patterson ◽  
Paula Fedorka-Cray ◽  
Richard E. Isaacson
Keyword(s):  
Salmonella Enterica ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Phase Variation ◽  
Gene Encoding ◽  
Type 1 Fimbriae ◽  
Systemic Spread ◽  
Serovar Typhimurium ◽  
Asymptomatic Infections

ABSTRACT Salmonella enterica serovar Typhimurium strain 798 is a clinical isolate from a pig and is known to be able to cause persistent, asymptomatic infections. This strain also is known to exist in two phenotypes (adhesive and nonadhesive to enterocytes) and can switch between the two phenotypes at a rate consistent with phase variation. Cells in the adhesive phenotype are more readily phagocytosed by leukocytes than nonadhesive cells. Once in a leukocyte, adhesive-phase cells survive while nonadhesive-phase cells die. In the present study, nonadhesive mutants were obtained with the transposon TnphoA. A nonadhesive mutant was selected for study and was shown by electron microscopy not to produce fimbriae. The gene encoding the adhesin was cloned and sequenced. Based on its sequence, the adhesin was shown to be FimA, the major subunit of type 1 fimbriae. The nonadhesive mutant was attenuated in its ability to colonize both mouse and pig intestines, but remained capable of systemic spread in mice. The nonadhesive mutant was phagocytosed to the same extent as parental cells in the adhesive phase and then survived intracellularly. These results demonstrated that type 1 fimbriae were important for attachment to enterocytes and promoted intestinal colonization. However, they were not important in promoting phagocytosis or intracellular survival.

scholarly journals Two DNA Invertases Contribute to Flagellar Phase Variation in Salmonella enterica Serovar Typhimurium Strain LT2

2006 ◽  
Vol 188 (3) ◽  
pp. 950-957 ◽  
Author(s):  
Kazuhiro Kutsukake ◽  
Hisashi Nakashima ◽  
Akira Tominaga ◽  
Tatsuhiko Abo
Keyword(s):  
Salmonella Enterica ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Genomic Sequence ◽  
Phase Variation ◽  
Disruption Mutant ◽  
Typhimurium Strain ◽  
Alternative Expression ◽  
Serovar Typhimurium

ABSTRACT Salmonella enterica serovar Typhimurium strain LT2 possesses two nonallelic structural genes, fliC and fljB, for flagellin, the component protein of flagellar filaments. Flagellar phase variation occurs by alternative expression of these two genes. This is controlled by the inversion of a DNA segment, called the H segment, containing the fljB promoter. H inversion occurs by site-specific recombination between inverted repetitious sequences flanking the H segment. This recombination has been shown in vivo and in vitro to be mediated by a DNA invertase, Hin, whose gene is located within the H segment. However, a search of the complete genomic sequence revealed that LT2 possesses another DNA invertase gene that is located adjacent to another invertible DNA segment within a resident prophage, Fels-2. Here, we named this gene fin. We constructed hin and fin disruption mutants from LT2 and examined their phase variation abilities. The hin disruption mutant could still undergo flagellar phase variation, indicating that Hin is not the sole DNA invertase responsible for phase variation. Although the fin disruption mutant could undergo phase variation, fin hin double mutants could not. These results clearly indicate that both Hin and Fin contribute to flagellar phase variation in LT2. We further showed that a phase-stable serovar, serovar Abortusequi, which is known to possess a naturally occurring hin mutation, lacks Fels-2, which ensures the phase stability in this serovar.

scholarly journals FimA, FimF, and FimH Are Necessary for Assembly of Type 1 Fimbriae on Salmonella enterica Serovar Typhimurium

2012 ◽  
Vol 80 (9) ◽  
pp. 3289-3296 ◽  
Author(s):  
Sarah A. Zeiner ◽  
Brett E. Dwyer ◽  
Steven Clegg
Keyword(s):  
Salmonella Enterica ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Food Poisoning ◽  
Enteric Bacteria ◽  
Transcriptional Unit ◽  
Content Type ◽  
E Coli ◽  
Type 1 Fimbriae ◽  
Serovar Typhimurium

ABSTRACTSalmonella entericaserovar Typhimurium is a Gram-negative member of the familyEnterobacteriaceaeand is a common cause of bacterial food poisoning in humans. The fimbrial appendages are found on the surface of many enteric bacteria and enable the bacteria to bind to eukaryotic cells.S. Typhimurium type 1 fimbriae are characterized by mannose-sensitive hemagglutination and are assembled via the chaperone/usher pathway.S. Typhimurium type 1 fimbrial proteins are encoded by thefimgene cluster (fimAICDHFZYW), withfimAICDHFexpressed as a single transcriptional unit. The structural components of the fimbriae are FimA (major subunit), FimI, FimH (adhesin), and FimF (adaptor). In order to determine which components are required for fimbrial formation inS. Typhimurium, mutations infimA,fimI,fimH, andfimFwere constructed and examined for their ability to produce surface-assembled fimbriae.S. Typhimurium SL1344ΔfimA, -ΔfimH, and -ΔfimFmutants were unable to assemble fimbriae, indicating that these genes are necessary for fimbrial production inS. Typhimurium. However, SL1344ΔfimIwas able to assemble fimbriae. InEscherichia colitype 1 and Pap fimbriae, at least two adaptors are expressed in addition to the adhesins. However,E. colitype 1 and Pap fimbriae have been reported to be able to assemble fimbriae in the absence of these proteins. These results suggest differences between theS. Typhimurium type 1 fimbrial system and theE. colitype 1 and Pap fimbrial systems.

The expression of the rpoE operon is fine-tuned by the internal rseAp promoter in Salmonella enterica serovar Typhimurium

Biologia ◽  
2010 ◽  
Vol 65 (6) ◽  
Author(s):  
Dagmar Homerova ◽  
Bronislava Rezuchova ◽  
Henrieta Skovierova ◽  
Jan Kormanec
Keyword(s):  
Sigma Factor ◽  
Salmonella Enterica ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Consensus Sequence ◽  
Coding Region ◽  
Gene Encoding ◽  
In Vivo Experiments ◽  
Envelope Stress ◽  
Serovar Typhimurium

AbstractThree promoters, located upstream of the rpoE gene encoding an extracytoplasmic sigma factor σ E, direct expression of the rpoE operon (rpoE, rseA, rseB, rseC) in Salmonella enterica serovar Typhimurium (S. Typhimurium). One of them, rpoEp3, has been found to be directly recognized by RNA polymerase containing sigma factor σ E. Using the Northern blot analysis we detected a complex pattern of transcripts indicating an internal promoter in the coding region of the rpoE gene. The promoter, rseAp, has been located by S1 mapping analysis. Its proposed −10 and −35 elements with 15 intervening nucleotides exhibited high similarity with the consensus sequence of σ E promoters, suggesting the direct dependence of rseAp upon σ E. Activity of rseAp increased towards stationary phase, after heat shock, cold shock, and in the presence of artificially induced rpoE expression, the conditions previously shown to activate σ E-dependent promoters. In vivo experiments revealed increase of the rseAp activity during growth and confirmed its clear dependence upon σ E. The proposed role of the internal rseAp promoter is to facilitate a feedback control of σ E level after the envelope stress is removed.

scholarly journals Attenuation of Salmonella enterica Serovar Typhimurium by Altering Biological Functions of Murein Lipoprotein and Lipopolysaccharide

2005 ◽  
Vol 73 (12) ◽  
pp. 8433-8436 ◽  
Author(s):  
A. A. Fadl ◽  
J. Sha ◽  
G. R. Klimpel ◽  
J. P. Olano ◽  
C. L. Galindo ◽  
...  
Keyword(s):  
Salmonella Enterica ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Biological Functions ◽  
Double Knockout ◽  
In Vivo Models ◽  
Background Strain ◽  
Knockout Mutants ◽  
Serovar Typhimurium

ABSTRACT We constructed Salmonella enterica serovar Typhimurium double-knockout mutants in which either the lipoprotein A (lppA) or the lipoprotein B (lppB) gene was deleted from an msbB-negative background strain by marker exchange mutagenesis. These mutants were highly attenuated when tested with in vitro and in vivo models of Salmonella pathogenesis.

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