| 1. |
- Adlerberth, Ingegerd, 1959, et al.
(författare)
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Intestinal colonization with Enterobacteriaceae in Pakistani and Swedish hospital-delivered infants.
- 1991
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Ingår i: Acta paediatrica Scandinavica. - 0001-656X. ; 80:6-7, s. 602-10
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Tidskriftsartikel (refereegranskat)abstract
- Rectal cultures from Swedish and Pakistani hospital-delivered newborn infants were analysed regarding the early acquisition of enterobacteria. Swedish infants were delivered vaginally, Pakistani infants were delivered either vaginally or by caesarean section. The Swedish infants were all breast-fed, whereas breastfeeding was incomplete and often started late among the Pakistani infants. Both groups of Pakistani infants were more rapidly colonized with enterobacteria than were the Swedish infants. Cultures from Swedish infants seldom yielded more than one kind of enterobacteria; E. coli and Klebsiella were most frequently isolated. E. coli dominated in both Pakistani groups, but especially caesarean section delivered infants were in addition often colonized with Proteus, Klebsiella, Enterobacter or Citrobacter species. Breastfeeding from the first day of life reduced colonization with Klebsiella/Enterobacter/Citrobacter. The results suggest that environmental exposure, delivery mode and early feeding habits all influence the early intestinal colonization with enterobacteria.
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| 2. |
- Adlerberth, Ingegerd, 1959, et al.
(författare)
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Adhesins of Escherichia coli associated with extra-intestinal pathogenicity confer binding to colonic epithelial cells.
- 1995
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Ingår i: Microbial pathogenesis. - 0882-4010. ; 18:6, s. 373-85
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Tidskriftsartikel (refereegranskat)abstract
- Escherichia coli adhesins are virulence factors in intestinal and extra-intestinal infections, but their role in normal intestinal colonization has not been defined. We investigated the intestinal adherence of E. coli with Dr hemagglutinin, S fimbriae, CFA/I or CFA/II, using freshly isolated ileal or colonic enterocytes and cells from the human colonic cell line HT-29. E. coli with S-fimbrial adhesins (Sfa I or Sfa II), P or type 1 fimbriae, adhered in a non-polarized manner, and in similar numbers to colonic and ileal enterocytes. S fimbriae of the variety Sfa II (originating from a meningitis isolate), mediated a stronger binding than Sfa I (of uropathogenic origin). Strains expressing Dr hemagglutinin adhered preferentially to the brush borders, slightly better to colonic than ileal enterocytes. Strains expressing CFA/I or II adhered to colonic and ileal enterocytes, although brush border adherence was predominantly observed with ileal cells. Binding to HT-29 cells paralleled binding to colonic enterocytes for all adhesin specificities except CFA/I. The results suggest that Dr hemagglutinin, P-, type 1- and S-fimbrial adhesins mediate binding to both colonic and ileal enterocytes. These specificities may contribute to the establishment of E. coli in the intestinal microflora, which precedes their spread to extra-intestinal sites.
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| 3. |
- Adlerberth, Ingegerd, 1959, et al.
(författare)
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Interaction of P-fimbriated Escherichia coli with human meconium.
- 1991
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Ingår i: FEMS microbiology letters. - 0378-1097. ; 68:1, s. 57-62
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Tidskriftsartikel (refereegranskat)abstract
- The ability of Escherichia coli with different receptor specificities to interact with meconium was studied. E. coli strains expressing P-fimbriae, specific for Gal alpha 1-4Gal beta-containing receptors, were agglutinated by meconium at high titres. This reaction was inhibited by globotetraosylceramide. The attachment of P-fimbriated E. coli to human colonic epithelial cells of the HT-29 cell line was inhibited by meconium. Some type 1 fimbriated strains were agglutinated by meconium, but the agglutination was rarely blocked by methyl alpha-D-mannoside. The attachment by type 1 fimbriated strains to HT-29 cells was reduced by meconium only in some cases. These results suggest that meconium interacts with the P-fimbriae of E. coli, in a way that may influence bacterial colonization of the neonatal intestine.
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| 4. |
- Friman, Vanda, 1952, et al.
(författare)
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Decreased expression of mannose-specific adhesins by Escherichia coli in the colonic microflora of immunoglobulin A-deficient individuals.
- 1996
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Ingår i: Infection and immunity. - 0019-9567. ; 64:7, s. 2794-8
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Tidskriftsartikel (refereegranskat)abstract
- Most Escherichia coli isolates can express type 1 fimbriae with mannose-specific adhesins. These adhesins bind to the oligosaccharide chains of secretory immunoglobulin A (IgA). Thus, in addition to specific antibody activity, secretory IgA possesses a broad reactivity with bacteria expressing type 1 fimbriae. The absence of secretory IgA in colonic secretions, as seen in IgA deficiency, might therefore alter the ability of type 1-fimbriated E. coli to colonize the large intestines of these individuals. In the present study, 10 E. coli isolates from each of 17 IgA-deficient and 17 age-matched control individuals were assessed for the carriage of the fim gene cluster by DNA-DNA hybridization and for the expression of type 1 fimbriae by hemagglutination of guinea pig erythrocytes. The contribution of type 1-fimbria-mediated adherence to HT-29 colonic cells was also analyzed. The proportion of fim+ E. coli isolates was lower in IgA-deficient than in control individuals (74 versus 94%, P < 0.05), as was the proportion of isolates expressing type 1 fimbriae in vitro (69% versus 85%, P < 0.05). The median mannose-sensitive adherence to HT-29 cells was lower for isolates from IgA-deficient individuals than from the controls (9 versus 26 bacteria per cell, P < 0.05). Isolates expressing type 1 fimbriae showed lower adherence to HT-29 cells when they were derived from IgA-deficient individuals than when they were derived from control individuals (15 versus 27 bacteria per cell, P < 0.05). The results suggest that the interaction of type 1 fimbriae with secretory IgA contributes to the large intestinal colonization by these bacteria.
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| 5. |
- Plos, Kaety, 1944, et al.
(författare)
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Intestinal carriage of P fimbriated Escherichia coli and the susceptibility to urinary tract infection in young children.
- 1995
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Ingår i: The Journal of infectious diseases. - : Oxford University Press (OUP). - 0022-1899 .- 1537-6613. ; 171:3, s. 625-31
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Tidskriftsartikel (refereegranskat)abstract
- This prospective study analyzed the intestinal carriage of P fimbriated Escherichia coli as a host susceptibility factor in urinary tract infection (UTI). P fimbriation was defined by the pap and G adhesin (papG1A2, prsGJ96) genotypes. Children with UTI carried pap+ E. coli in the fecal flora more often than healthy controls both at diagnosis (86% vs. 29%) and during infection-free intervals (approximately 40%; P < .01). P1 blood group-positive children carried pap+ E. coli in the fecal flora more often (88%) than those with P2 blood group (40%; P < .05). A pap+ E. coli strain caused UTI in 53 of 55 patients who carried both pap+ and pap- strains in their fecal flora. These results suggest that persons who develop UTI have an increased tendency to carry pap+ E. coli in the large intestine and that these pap+ E. coli cause UTI more often than pap E. coli strains in the fecal flora of the same host.
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| 6. |
- Wold, Agnes E, 1955, et al.
(författare)
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Resident colonic Escherichia coli strains frequently display uropathogenic characteristics.
- 1992
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Ingår i: The Journal of infectious diseases. - 0022-1899. ; 165:1, s. 46-52
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Tidskriftsartikel (refereegranskat)abstract
- Bacterial factors associated with long-term persistence in the colon have not been defined. Individual Escherichia coli strains in the colonic flora of 13 schoolgirls with asymptomatic bacteriuria were identified by electromorphic typing of chromosomally encoded enzymes and defined as resident or transient. The strains were characterized as to serotype, receptor specificity, and adherence to the human colonic epithelial cell line HT-29. Colonic resident strains expressed P fimbriae, adhered to colonic epithelial cells via a mannose-resistant mechanism, and expressed the uropathogenic serotypes O1, O2, O6, O7, O18, O25, or O75 more often than did the transient strains, which were often nontypeable. The serotype and hemagglutination pattern were generally retained during intestinal carriage, in contrast to the loss of such properties upon prolonged colonization of the urinary tract. P fimbriae with Gal alpha 1----4Gal beta-specific adherence may, in fact, have evolved to increase persistence in the colon.
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| 7. |
- Ambite, Ines, et al.
(författare)
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Susceptibility to urinary tract infection : Benefits and hazards of the antibacterial host response
- 2016
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Ingår i: Microbiology spectrum. - Washington, DC, USA : ASM Press. - 2165-0497. ; 4:3
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Forskningsöversikt (refereegranskat)abstract
- A paradigm shift is needed to improve and personalize the diagnosis of infectious disease and to select appropriate therapies. For many years, only the most severe and complicated bacterial infections received more detailed diagnostic and therapeutic attention as the efficiency of antibiotic therapy has guaranteed efficient treatment of patients suffering from the most common infections. Indeed, treatability almost became a rationale not to analyze bacterial and host parameters in these larger patient groups. Due to the rapid spread of antibiotic resistance, common infections like respiratory tract- or urinary-tract infections (UTIs) now pose new and significant therapeutic challenges. It is fortunate and timely that infectious disease research can offer such a wealth of new molecular information that is ready to use for the identification of susceptible patients and design of new suitable therapies. Paradoxically, the threat of antibiotic resistance may become a window of opportunity, by encouraging the implementation of new diagnostic and therapeutic approaches. The frequency of antibiotic resistance is rising rapidly in uropathogenic organisms and the molecular and genetic understanding of UTI susceptibility is quite advanced. More bold translation of the new molecular diagnostic and therapeutic tools would not just be possible but of great potential benefit in this patient group. This chapter reviews the molecular basis for susceptibility to UTI, including recent advances in genetics, and discusses the consequences for diagnosis and therapy. By dissecting the increasingly well-defined molecular interactions between bacteria and host and the molecular features of excessive bacterial virulence or host-response malfunction, it is becoming possible to isolate the defensive from the damaging aspects of the host response. Distinguishing "good" from "bad" inflammation has been a long-term quest of biomedical science and in UTI, patients need the "good" aspects of the inflammatory response to resist infection while avoiding the "bad" aspects, causing chronicity and tissue damage.
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| 8. |
- Baker, N, et al.
(författare)
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Glycosphingolipid receptors for Pseudomonas aeruginosa.
- 1990
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Ingår i: Infection and immunity. - 0019-9567. ; 58:7, s. 2361-6
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Tidskriftsartikel (refereegranskat)abstract
- The binding of Pseudomonas aeruginosa to glycosphingolipids and to buccal and bronchial epithelial cells was analyzed. Three independently expressed specificities were found by bacterial binding to glycosphingolipids separated by thin-layer chromatography. All strains bound gangliotria- and gangliotetrasylceramide. All but one of the strains bound sialic acid-containing glycosphingolipids and lactosylceramide. The latter two specificities could be separated in that the lactosylceramide binding was retained and the sialic acid binding was suppressed when bovine serum albumin was used as a blocking agent in the thin-layer chromatography assay. The attachment to buccal epithelial cells, like the binding to sialylated compounds and lactosylceramide, was abolished by Formalin treatment of the bacteria, suggesting the importance of these specificities for cell adherence. In contrast, the binding to gangliotria- and gangliotetraosylceramide was retained by nonattaching Formalin-treated bacteria.
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| 9. |
- Benson, Mikael, et al.
(författare)
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Interleukin (IL)-6 and IL-8 in children with febrile urinary tract infection and asymptomatic bacteriuria
- 1996
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Ingår i: Journal of Infectious Diseases. - : Oxford University Press (OUP). - 0022-1899 .- 1537-6613. ; 174:5, s. 1080-1084
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Tidskriftsartikel (refereegranskat)abstract
- Urine and serum interleukin (IL)-6 and IL-8 responses were higher in children with febrile urinary tract infection (n = 61) than in those with asymptomatic bacteriuria (n = 39). By univariate analysis, cytokine levels were related to age, sex, reflux, renal scarring, urine leukocytes, C- reactive protein (CRP), erythrocyte sedimentation rate (ESR), and bacterial properties (P fimbriae but not hemolysin). Multivariate modeling showed that urine IL-6 responds were higher in girls than boys, increased with age, and were positively associated with CRP, ESR, serum IL-6, and urine leukocyte counts. The urine IL-8 response was not influenced by age, but it was influenced by P fimbriae and was associated with ESR, CRP, urine leukocytes, and female sex. The results show that cytokine responses to urinary tract infection vary with the severity of infection and that cytokine activation is influenced by a variety of host and bacterial variables.
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| 10. |
- Bergsten, Göran, et al.
(författare)
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PapG-dependent adherence breaks mucosal inertia and triggers the innate host response
- 2004
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Ingår i: Journal of Infectious Diseases. - : Oxford University Press (OUP). - 1537-6613 .- 0022-1899. ; 189:9, s. 1734-1742
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Tidskriftsartikel (refereegranskat)abstract
- Mucosal pathogens differ from normal flora constituents in that they provoke a host response that upsets mucosal integrity. We investigated whether the elaboration of discrete adherence factors is sufficient to break the inertia of the mucosal barrier. PapG-mediated adherence was selected as an example, because P fimbrial expression characterizes uropathogenic Escherichia coli and because adherence starts the attack on the mucosal barrier. Patients were inoculated intravesically with transformed nonvirulent E. coli strains expressing functional P fimbriae (E. coli pap(+)) or mutant fimbriae lacking the adhesin (E. coli DeltapapG). E. coli pap(+) was shown to activate the innate host response, and adherent gfp(+) bacteria were observed on excreted uroepithelial cells. E. coli DeltapapG failed to trigger a response and was nonadhesive. We conclude that PapG-mediated adherence breaks mucosal inertia in the human urinary tract by triggering innate immunity and propose that this activation step differentiates asymptomatic carriage from infection.
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