Heat stable toxin of E. coli (STa) stimulates duodenal mucosal bicarbonate secretion in cystic fibrosis knockout mice

DNA probes that identify genes coding for heat-labile type I (LT-I) and heat-stable type 1 (ST-I) enterotoxins, enteropathogenic Escherichia coli adherence factor (EAF), and Shigella-like, invasiveness (INV) are used to evaluate the sensitivity and specificity of stool blots in comparison with the sensitivity and specificity of colony blots in detecting enteropathoghens. The sensitivities of the probes in stool blots are 91.7% for the LT-I probe, 76.9% for the ST-I probes, 78.9% for the EAF probe, and 45.5% for the INV probe. The specificity of all probes is higher than 95%. In general, the stool blot method identifies as many if not more LT-I-, ST-I-, and EAF-producing E. coli infections than the colony blots. Key words: DNA probes, stool blots, enteropathogens, diagnosis.

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Nutritional Effects on Host Response to Lung Infections with Mucoid Pseudomonas aeruginosa in Mice

Infection and Immunity ◽

10.1128/iai.72.3.1479-1486.2004 ◽

2004 ◽

Vol 72 (3) ◽

pp. 1479-1486 ◽

Cited By ~ 15

Author(s):

Anna M. van Heeckeren ◽

Mark Schluchter ◽

Lintong Xue ◽

Juan Alvarez ◽

Steven Freedman ◽

...

Keyword(s):

Cystic Fibrosis ◽

Pseudomonas Aeruginosa ◽

Docosahexaenoic Acid ◽

Knockout Mice ◽

Host Response ◽

Inflammatory Responses ◽

Liquid Diet ◽

Wild Type ◽

Agarose Beads ◽

Lung Infections

ABSTRACT In cystic fibrosis, a recessive genetic disease caused by defects in the cystic fibrosis conductance regulator (CFTR), the main cause of death is lung infection and inflammation. Nutritional deficits have been proposed to contribute to the excessive host inflammatory response in both humans and Cftr-knockout mice. Cftr-knockout mice and gut-corrected Cftr-knockout mice expressing human CFTR primarily in the gut were challenged with Pseudomonas aeruginosa-laden agarose beads; they responded similarly with respect to bronchoalveolar lavage cell counts and levels of the acute-phase cytokines tumor necrosis factor alpha, interleukin-1β (IL-1β), and IL-6. Wild-type mice fed the liquid diet used to prevent intestinal obstruction in Cftr-knockout mice had inflammatory responses to P. aeruginosa-laden agarose beads similar to those of wild-type mice fed an enriched solid diet, so dietary effects are unlikely to account for differences between wild-type mice and mice with cystic fibrosis. Finally, since cystic fibrosis patients and Cftr-knockout mice have an imbalance in fatty acids (significantly lower-than-normal levels of docosahexaenoic acid), the effects of specific supplementation with docosahexaenoic acid of wild-type and Cftr-knockout mice on their inflammatory responses to P. aeruginosa-laden agarose beads were tested. There were no significant differences (P = 0.35) in cumulative survival rates between Cftr-knockout mice and wild-type mice provided with either the liquid diet Peptamen or Peptamen containing docosahexaenoic acid. In conclusion, diet and docosahexaenoic acid imbalances alone are unlikely to explain the differences in the host response to lung infections with mucoid P. aeruginosa between mice with cystic fibrosis and their wild-type counterparts.

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Loci of intestinal distress in cystic fibrosis knockout mice

Physiological Genomics ◽

10.1152/physiolgenomics.00114.2002 ◽

2003 ◽

Vol 12 (2) ◽

pp. 79-84 ◽

Cited By ~ 15

Author(s):

Christina K. Haston ◽

Lap-Chee Tsui

Keyword(s):

Cystic Fibrosis ◽

X Chromosome ◽

Knockout Mice ◽

Mendelian Inheritance ◽

Genetic Dissection ◽

Male Mice ◽

Female Mice ◽

Genome Wide ◽

A Genome ◽

Strain Dependent

The strain-dependent survival of cystic fibrosis (CF) knockout mice has been used to map a modifier of CF, Cfm1, in mice and, subsequently, in humans. To identify additional modifiers of the CF phenotype, in this study, the survival of F2 CF mice derived from a cross between congenic C57BL/6J CF and BALB/cJ CF heterozygotes was followed up to 12 wk of age. A genome-wide linkage scan completed in F2 CF mice revealed a chromosome 10 locus ( P = 1.2 × 10−4) to predict for intestinal distress in CF male mice. An X chromosome locus for which non-Mendelian inheritance favoring B6 alleles in the surviving CF mice and BALB alleles in mice of a control population, was identified. The survival of female mice, both F2 CF and F2 control, was linked to loci on chromosomes 3 and 5. The identification of additional putative CF modifier loci may permit further genetic dissection of the complex CF phenotype.

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CFTR Deficiency Affects Glucose Homeostasis via Regulating GLUT4 Plasma Membrane Transportation

Frontiers in Cell and Developmental Biology ◽

10.3389/fcell.2021.630654 ◽

2021 ◽

Vol 9 ◽

Author(s):

Junzhong Gu ◽

Weiwei Zhang ◽

Lida Wu ◽

Yuchun Gu

Keyword(s):

Cystic Fibrosis ◽

Glucose Homeostasis ◽

Knockout Mice ◽

Glucose Transporter ◽

Autosomal Recessive Disorder ◽

Cellular Level ◽

Transmembrane Conductance Regulator ◽

Glut4 Translocation ◽

Altered Glucose ◽

Insulin Responses

Cystic Fibrosis (CF) is an autosomal recessive disorder caused by mutations in the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) gene. CF-related diabetes (CFRD) is one of the most prevalent comorbidities of CF. Altered glucose homeostasis has been reported in CF patients. The mechanism has not been fully elucidated. Besides the consequence of pancreatic endocrine dysfunction, we focus on insulin-responsive tissues and glucose transportation to explain glucose homeostasis alteration in CFRD. Herein, we found that CFTR knockout mice exhibited insulin resistance and glucose tolerance. Furthermore, we demonstrated insulin-induced glucose transporter 4 (GLUT4) translocation to the cell membrane was abnormal in the CFTR knockout mice muscle fibers, suggesting that defective intracellular GLUT4 transportation may be the cause of impaired insulin responses and glucose homeostasis. We further demonstrated that PI(4,5)P2 could rescue CFTR related defective intracellular GLUT4 transportation, and CFTR could regulate PI(4,5)P2 cellular level through PIP5KA, suggesting PI(4,5)P2 is a down-stream signal of CFTR. Our results revealed a new signal mechanism of CFTR in GLUT4 translocation regulation, which helps explain glucose homeostasis alteration in CF patients.

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Erratum

Epidemiology and Infection ◽

10.1017/s0950268803009592 ◽

2003 ◽

Vol 130 (3) ◽

pp. 573-573

Author(s):

Z. ZHOU ◽

J. OGASAWARA ◽

Y. NISHIKAWA

Keyword(s):

Escherichia Coli ◽

E Coli ◽

Heat Stable ◽

Epidemiol Infect

Epidemiol. Infect. 128 (2002), 363–371An outbreak of gastroenteritis in Osaka, Japan due toEscherichia coliserogroup O166[ratio ]H15 that had a coding gene for enteroaggregativeE. coliheat-stable enterotoxin 1 (EAST1)Tables 1 and 2 were omitted

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Evolution of diarrheagenic Escherichia coli pathotypes in India

Journal of Laboratory Physicians ◽

10.4103/jlp.jlp_58_19 ◽

2019 ◽

Vol 11 (04) ◽

pp. 346-351

Author(s):

Pankaj Singh ◽

Sharda C. Metgud ◽

Subarna Roy ◽

Shashank Purwar

Keyword(s):

Escherichia Coli ◽

Cross Sectional Study ◽

Clinical Settings ◽

Accurate Identification ◽

Cross Sectional ◽

E Coli ◽

Medical College ◽

Diarrheagenic Escherichia Coli ◽

Proper Management ◽

Heat Stable

Abstract CONTEXT: Diarrheagenic Escherichia coli (DEC) is the leading cause of infectious diarrhea in developing countries. On the basis of virulence and phenotypic characteristics, the DEC is categorized into multiple pathotypes. Each pathotype has different pathogenesis and geographical distribution. Thus, the proper management of disease relies on rapid and accurate identification of DEC pathotypes. AIMS: The aim of the study was to determine the prevalence of DEC pathotypes in India. MATERIALS AND METHODS: A cross-sectional study was carried out between January 2008 and December 2012 at Jawaharlal Nehru Medical College and KLES Dr. Prabhakar Kore Hospital and Medical Research Center, Belgaum (Karnataka), India. A total of 300 stool samples were collected from diarrhea patients with age >3 months. The DEC was identified by both conventional and molecular methods. RESULTS: Of 300 samples, E. coli were detected in 198 (66%) and 170 (56.6%) samples by culture and polymerase chain reaction, respectively. Among DEC (n = 198) isolates, eae gene (59.5%) was the most prevalent followed by stx (27.7%), east (27.2%), elt (12.6%), est (10.6%), ipaH (5.5%), and eagg (1.5%) genes. On the basis of virulence genes, enteropathogenic E. coli (33.8%) was the most common pathotype followed by Shiga toxin-producing E. coli (STEC, 23.2%), enterotoxigenic E. coli (ETEC, 13.6%), enteroinvasive E. coli (5.5%), enteroaggregative heat-stable enterotoxin 1-harboring E. coli (EAST1EC, 4.5%), STEC/ETEC (3.5%), STEC/enteroaggregative E. coli (STEC/EAEC, 1.0%), and EAEC (0.05%). CONCLUSIONS: The hybrid DEC is potentially more virulent than basic pathotypes. The pathotyping should be included in clinical settings for the proper management of DEC-associated diarrhea.

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