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Bacterial virulence in urinary tract infection.

https://arctichealth.org/en/permalink/ahliterature60098
Source
Infect Dis Clin North Am. 1987 Dec;1(4):731-50
Publication Type
Article
Date
Dec-1987
Author
C. Svanborg Edén
P. de Man
Author Affiliation
Department of Clinical Immunology, University of Götenborg, Sweden.
Source
Infect Dis Clin North Am. 1987 Dec;1(4):731-50
Date
Dec-1987
Language
English
Publication Type
Article
Keywords
Adult
Bacterial Adhesion
Bacterial Typing Techniques
Escherichia coli - classification - isolation & purification - pathogenicity
Escherichia coli Infections - microbiology
Female
Glycolipids - metabolism
Humans
Hydroxamic Acids - metabolism
Infant
Lipopolysaccharides - metabolism
Male
Polysaccharides, Bacterial - metabolism
Research Support, Non-U.S. Gov't
Sweden
Urinary Tract Infections - microbiology
Virulence
Abstract
The severity of an infection is a function of the resistance of the host and the virulence of the infecting strain. Infections of the urinary tract can be caused by a wide range of gram-negative and gram-positive bacteria, which also are constituents of the normal flora. Indeed, most uropathogens originate from the intestinal tract. Still, the virulence concept implies that bacteria associated with urinary tract infections differ from members of the indigenous flora not causing infections. This review attempts to summarize the mechanisms known to contribute to bacterial virulence in the urinary tract and their relevance in different patient groups.
PubMed ID
3333656 View in PubMed
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Expression of toll-like receptor 4 and endotoxin responsiveness in mice during perinatal period.

https://arctichealth.org/en/permalink/ahliterature63265
Source
Pediatr Res. 2005 May;57(5 Pt 1):644-8
Publication Type
Article
Date
May-2005
Author
Kirsi Harju
Marja Ojaniemi
Samuli Rounioja
Virpi Glumoff
Reija Paananen
Reetta Vuolteenaho
Mikko Hallman
Author Affiliation
Department of Pediatrics and Biocenter Oulu, University of Oulu, FIN-90014 Oulu, Finland.
Source
Pediatr Res. 2005 May;57(5 Pt 1):644-8
Date
May-2005
Language
English
Publication Type
Article
Keywords
Alleles
Animals
Animals, Newborn
Blotting, Western
Cytokines - metabolism
Disease Models, Animal
Endotoxins - metabolism
Inflammation
Interleukin-1 - biosynthesis
Interleukin-10 - biosynthesis
Interleukin-6 - biosynthesis
Lipopolysaccharides - metabolism
Lung Diseases - microbiology
Membrane Glycoproteins - biosynthesis
Mice
Mice, Inbred DBA
Monokines - biosynthesis
Placenta - metabolism
RNA - metabolism
RNA, Messenger - metabolism
Receptors, Cell Surface - biosynthesis
Receptors, Interleukin-1 - biosynthesis
Research Support, Non-U.S. Gov't
Ribonucleases - metabolism
Signal Transduction
Time Factors
Toll-Like Receptor 4
Toll-Like Receptors
Tumor Necrosis Factor-alpha - biosynthesis
Up-Regulation
Abstract
Endotoxin [lipopolysaccharide (LPS)] from Gram-negative bacteria is found in amniotic fluid in intrauterine infections that associate with the risk for spontaneous premature birth, bronchopulmonary dysplasia (BPD), and respiratory distress syndrome. Toll-like receptor 4 (TLR4) is the signaling receptor for LPS. The aim was to investigate the primary inflammatory response in mice shortly after administration of LPS to the dam (14 and 17 d of pregnancy), to the newborn, or into the amniotic fluid. The expression levels of TLR4, IL-1, tumor necrosis factor-alpha, IL-6, IL-10, macrophage inflammatory protein-2, and IL-1 receptor 1 were studied with ribonuclease protection assay. In addition, TLR4 protein was analyzed with Western blotting. The fetal membranes expressed TLR4 mRNA and protein and showed an acute cytokine response to LPS when LPS was administrated into the amniotic fluid. There was distinct ontogeny in the responsiveness of fetal lung to LPS: on fetal day 14 (term 20 d), both the expression of TLR4 and the acute cytokine response were undetectable 5 h after LPS; they became detectable by fetal day 17. TLR4 and the cytokine response further increased after birth. In maternal lung, the TLR4 expression was strongest and up-regulated in parallel with the induction of the cytokines. We propose that TLR4 controls the magnitude of the LPS-induced cytokine response during the perinatal period.
PubMed ID
15718365 View in PubMed
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[Immunological reactivity conditions of burned children]

https://arctichealth.org/en/permalink/ahliterature32113
Source
Fiziol Zh. 2000;46(6):68-74
Publication Type
Article
Date
2000
Author
H M Boiars'ka
O I Osadcha
H P Kozynets'
Author Affiliation
Institute of Haematology and Transfusiology, Kiev.
Source
Fiziol Zh. 2000;46(6):68-74
Date
2000
Language
Ukrainian
Publication Type
Article
Keywords
B-Lymphocytes - immunology
Burns - immunology - physiopathology
Child
English Abstract
Humans
Immunoglobulin A - immunology
Immunoglobulin G - immunology
Lipopolysaccharides - metabolism
T-Lymphocytes - immunology
Abstract
Analysis of the immunological reactivity conditions of burned children was conducted. The factors witch have influence on the functional activity of blood leucocytes were studied. The decrease of immunological reactivity proportionale to the grave of the trauma was discovered. The secondary immunodeficiency in T-indepent type developed. The protein fraction of the blood serum influenced on the T-lymphocytes to the highest degree. Simultaneously decrease of the toleranse to the autologus erytrocytes with the hyperproduction of antibodies was discovered.
PubMed ID
11424566 View in PubMed
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