Colonization factors of diarrheagenicE. coli and their intestinal receptors

1995 ◽  
Vol 15 (3) ◽  
pp. 214-226 ◽  
Author(s):  
FJ Cassels ◽  
MK Wolf

2003 ◽  
Vol 185 (12) ◽  
pp. 3547-3557 ◽  
Author(s):  
Deborah S. Millikan ◽  
Edward G. Ruby

ABSTRACT Flagellum-mediated motility of Vibrio fischeri is an essential factor in the bacterium's ability to colonize its host, the Hawaiian squid Euprymna scolopes. To begin characterizing the nature of the flagellar regulon, we have cloned a gene, designated flrA, from V. fischeri that encodes a putative σ54-dependent transcriptional activator. Genetic arrangement of the flrA locus in V. fischeri is similar to motility master-regulator operons of Vibrio cholerae and Vibrio parahaemolyticus. In addition, examination of regulatory regions of a number of flagellar operons in V. fischeri revealed apparent σ54 recognition motifs, suggesting that the flagellar regulatory hierarchy is controlled by a similar mechanism to that described in V. cholerae. However, in contrast to its closest known relatives, flrA mutant strains of V. fischeri ES114 were completely abolished in swimming capability. Although flrA provided in trans restored motility to the flrA mutant, the complemented strain was unable to reach wild-type levels of symbiotic colonization in juvenile squid, suggesting a possible role for the proper expression of FlrA in regulating symbiotic colonization factors in addition to those required for motility. Comparative RNA arbitrarily primed PCR analysis of the flrA mutant and its wild-type parent revealed several differentially expressed transcripts. These results define a regulon that includes both flagellar structural genes and other genes apparently not involved in flagellum elaboration or function. Thus, the transcriptional activator FlrA plays an essential role in regulating motility, and apparently in modulating other symbiotic functions, in V. fischeri.



2008 ◽  
Vol 76 (11) ◽  
pp. 5247-5256 ◽  
Author(s):  
Emily Hart ◽  
Ji Yang ◽  
Marija Tauschek ◽  
Michelle Kelly ◽  
Matthew J. Wakefield ◽  
...  

ABSTRACT Citrobacter rodentium is an attaching and effacing pathogen which causes transmissible colonic hyperplasia in mice. Infection with C. rodentium serves as a model for infection of humans with enteropathogenic and enterohemorrhagic Escherichia coli. To identify novel colonization factors of C. rodentium, we screened a signature-tagged mutant library of C. rodentium in mice. One noncolonizing mutant had a single transposon insertion in an open reading frame (ORF) which we designated regA because of its homology to genes encoding members of the AraC family of transcriptional regulators. Deletion of regA in C. rodentium resulted in markedly reduced colonization of the mouse intestine. Examination of lacZ transcriptional fusions using promoter regions of known and putative virulence-associated genes of C. rodentium revealed that RegA strongly stimulated transcription of two newly identified genes located close to regA, which we designated adcA and kfcC. The cloned adcA gene conferred autoaggregation and adherence to mammalian cells to E. coli strain DH5α, and a kfc mutation led to a reduction in the duration of intestinal colonization, but the kfc mutant was far less attenuated than the regA mutant. These results indicated that other genes of C. rodentium whose expression required activation by RegA were required for colonization. Microarray analysis revealed a number of RegA-regulated ORFs encoding proteins homologous to known colonization factors. Transcription of these putative virulence determinants was activated by RegA only in the presence of sodium bicarbonate. Taken together, these results show that RegA is a global regulator of virulence in C. rodentium which activates factors that are required for intestinal colonization.



2006 ◽  
Vol 75 (2) ◽  
pp. 745-752 ◽  
Author(s):  
Clara Belzer ◽  
Bart A. M. van Schendel ◽  
Ernst J. Kuipers ◽  
Johannes G. Kusters ◽  
Arnoud H. M. van Vliet

ABSTRACT Persistent colonization of mucosal surfaces by bacteria in the mammalian host requires concerted expression of colonization factors, depending on the environmental conditions. Helicobacter hepaticus is a urease-positive pathogen that colonizes the intestinal and hepatobiliary tracts of rodents. Here it is reported that urease expression of H. hepaticus is iron repressed by the transcriptional regulator Fur. Iron restriction of growth medium resulted in a doubling of urease activity in wild-type H. hepaticus strain ATCC 51449 and was accompanied by increased levels of urease subunit proteins and ureA mRNA. Insertional inactivation of the fur gene abolished iron-responsive repression of urease activity, whereas inactivation of the perR gene did not affect iron-responsive regulation of urease activity. The iron-responsive promoter element was identified directly upstream of the H. hepaticus ureA gene. Recombinant H. hepaticus Fur protein bound to this ureA promoter region in a metal-dependent matter, and binding resulted in the protection of a 41-bp, Fur box-containing operator sequence located at positions −35 to −75 upstream of the transcription start site. In conclusion, H. hepaticus Fur controls urease expression at the transcriptional level in response to iron availability. This represents a novel type of urease regulation in ureolytic bacteria and extends the already diverse regulatory repertoire of the Fur protein.



1987 ◽  
Vol 253 (5) ◽  
pp. H1167-H1176 ◽  
Author(s):  
L. C. Weaver ◽  
S. Genovesi ◽  
A. Stella ◽  
A. Zanchetti

Stimulation of visceral receptors with bradykinin has been shown to cause reflex increases in sympathetic nerve activity and systemic arterial pressure. In this investigation, serosal receptors of the intestine were stimulated by bradykinin in anesthetized cats to 1) compare mesenteric and renal sympathetic responses, 2) compare hemodynamic responses in mesenteric and renal beds, and 3) determine changes in renal function. This stimulation in intact animals caused pressor responses, significantly greater excitation of mesenteric than renal nerves, significantly greater mesenteric than renal vasoconstriction, diuresis, natriuresis, and, in denervated kidneys, increases in fractional sodium excretion. In vagotomized, sinoaortic-denervated cats, stimulation of intestinal receptors caused excitation of mesenteric nerve activity greater than renal for only 30 s. This sympathetic reflex response led to pressor responses, equal mesenteric and renal vasoconstriction, diuresis, natriuresis, and increased fractional excretion of sodium only in denervated kidneys. When abdominal perfusion pressure was held constant with an aortic snare in these same animals, the sympathetic reflexes initially caused greater mesenteric than renal vasoconstriction and antidiuresis and antinatriuresis only in innervated kidneys. These findings demonstrate that the intensity of hemodynamic and renal responses to stimulation of visceral receptors correlates well with the magnitude of sympathetic nerve responses.



Endocrinology ◽  
1985 ◽  
Vol 117 (6) ◽  
pp. 2267-2273 ◽  
Author(s):  
A. B. KORKOR ◽  
J. KUCHIBOTLA ◽  
M. ARRIEH ◽  
R. W. GRAY ◽  
W. A. GLEASON
Keyword(s):  


2006 ◽  
Vol 47 (2) ◽  
pp. 199-206 ◽  
Author(s):  
Simone Corrêa ◽  
Patricia Palmeira ◽  
Magda Maria Sales Carneiro-Sampaio ◽  
Lucília Sanae Nishimura ◽  
Beatriz Ernestina Cabilio Guth


2020 ◽  
Vol 8 (11) ◽  
pp. 1662
Author(s):  
Zachary R. Stromberg ◽  
Rick E. Masonbrink ◽  
Melha Mellata

Foodborne pathogens are a public health threat globally. Shiga toxin-producing Escherichia coli (STEC), particularly O26, O111, and O157 STEC, are often associated with foodborne illness in humans. To create effective preharvest interventions, it is critical to understand which factors STEC strains use to colonize the gastrointestinal tract of cattle, which serves as the reservoir for these pathogens. Several colonization factors are known, but little is understood about initial STEC colonization factors. Our objective was to identify these factors via contrasting gene expression between nonpathogenic E. coli and STEC. Colonic explants were inoculated with nonpathogenic E. coli strain MG1655 or STEC strains (O26, O111, or O157), bacterial colonization levels were determined, and RNA was isolated and sequenced. STEC strains adhered to colonic explants at numerically but not significantly higher levels compared to MG1655. After incubation with colonic explants, flagellin (fliC) was upregulated (log2 fold-change = 4.0, p < 0.0001) in O157 STEC, and collectively, Lon protease (lon) was upregulated (log2 fold-change = 3.6, p = 0.0009) in STEC strains compared to MG1655. These results demonstrate that H7 flagellum and Lon protease may play roles in early colonization and could be potential targets to reduce colonization in cattle.



2019 ◽  
Vol 6 (Supplement_2) ◽  
pp. S907-S907
Author(s):  
Teresa C Fox ◽  
Paul Thuras ◽  
Connie Clabots ◽  
Stephen Porter ◽  
James R Johnson

Abstract Background Extraintestinal Escherichia coli infections are an ever-growing threat, to which specific clonal lineages and virulence factors contribute disproportionately. Despite the gut being the main reservoir for such E. coli strains, relationships between clonal lineages, virulence factors, and fecal colonization patterns are poorly understood. Accordingly, we defined E. coli fecal colonization patterns within households (HHs) and assessed specific lineages and virulence genes (VGs) as predictors of colonization behaviors. Methods Veterans with an E. coli clinical isolate (n = 22: 11 fluoroquinoline [FQ]-resistant, 11 FQ-susceptible) and their HH members provided stool samples on 2–6 occasions each. Stools were screened for total and FQ-resistant E. coli. Distinct E. coli strains were resolved by genomic profiling of 10 colonies/sample. Strains underwent molecular lineage identification, VG detection, and comparison with the veteran’s clinical isolate. Clonal lineages and VGs were assessed (Wilcoxon rank-sum test) as predictors of strains’ (i) predominance within the fecal sample, (ii) persistence across serial fecal samples, (iii) within-HH strain sharing, and (iv) overall within-HH colonization prevalence. Results From the 22 veterans and 46 HH members (27 humans, 19 pets) we recovered 139 unique-by-household fecal E. coli strains. Sixty-four traits were evaluated (16 clonal lineages, 48 VGs). Of these, 44 exhibited n ≥ 5, so could be analyzed statistically. Among these 44 traits, the proportion significantly associated with ≥ 1 outcome variable was 5/6 (83%) for clonal lineages and 18/38 (47%) for VGs. Additionally, fecal strains that matched the veteran’s clinical isolate exhibited significantly greater sharing, persistence, and overall colonization. Conclusion The studied E. coli traits – known for their associations with clinical infections –here were significantly associated with within-HH colonization behavior. These findings support that “virulence factors” may be regarded also (or perhaps best) as “colonization factors,” and “virulent lineages” as “colonizing lineages.” This suggests the possibility that future interventions that disrupt colonization behavior also could prevent E. coli infections. Disclosures All authors: No reported disclosures.



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