دورية أكاديمية
Type 1 fimbrial expression enhances Escherichia coli virulence for the urinary tract.
| العنوان: | Type 1 fimbrial expression enhances Escherichia coli virulence for the urinary tract. |
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| المؤلفون: | Connell I; Department of Medical Microbiology, Lund University, Sweden., Agace W, Klemm P, Schembri M, Mărild S, Svanborg C |
| المصدر: | Proceedings of the National Academy of Sciences of the United States of America [Proc Natl Acad Sci U S A] 1996 Sep 03; Vol. 93 (18), pp. 9827-32. |
| نوع المنشور: | Journal Article; Research Support, Non-U.S. Gov't |
| اللغة: | English |
| بيانات الدورية: | Publisher: National Academy of Sciences Country of Publication: United States NLM ID: 7505876 Publication Model: Print Cited Medium: Print ISSN: 0027-8424 (Print) Linking ISSN: 00278424 NLM ISO Abbreviation: Proc Natl Acad Sci U S A Subsets: MEDLINE |
| أسماء مطبوعة: | Original Publication: Washington, DC : National Academy of Sciences |
| مواضيع طبية MeSH: | Escherichia coli/*pathogenicity , Escherichia coli Infections/*microbiology , Pili, Sex/*metabolism , Receptors, Immunologic/*metabolism , Urinary Tract Infections/*microbiology, Animals ; Blotting, Southern ; Child ; DNA, Bacterial/chemistry ; Escherichia coli/ultrastructure ; Genotype ; Humans ; Mice ; Microscopy, Immunoelectron ; Nucleic Acid Hybridization ; Phenotype ; Receptors, Immunologic/genetics ; Restriction Mapping |
| مستخلص: | Type 1 fimbriae are adhesion organelles expressed by many Gram-negative bacteria. They facilitate adherence to mucosal surfaces and inflammatory cells in vitro, but their contribution to virulence has not been defined. This study presents evidence that type 1 fimbriae increase the virulence of Escherichia coli for the urinary tract by promoting bacterial persistence and enhancing the inflammatory response to infection. In a clinical study, we observed that disease severity was greater in children infected with E. coli O1:K1:H7 isolates expressing type 1 fimbriae than in those infected with type 1 negative isolates of the same serotype. The E. coli O1:K1:H7 isolates had the same electrophoretic type, were hemolysin-negative, expressed P fimbriae, and carried the fim DNA sequences. When tested in a mouse urinary tract infection model, the type 1-positive E. coli O1:K1:H7 isolates survived in higher numbers, and induced a greater neutrophil influx into the urine, than O1:K1:H7 type 1-negative isolates. To confirm a role of type 1 fimbriae, a fimH null mutant (CN1016) was constructed from an O1:K1:H7 type 1-positive parent. E. coli CN1016 had reduced survival and inflammatogenicity in the mouse urinary tract infection model. E. coli CN1016 reconstituted with type 1 fimbriae (E. coli CN1018) had restored virulence similar to that of the wild-type parent strain. These results show that type 1 fimbriae in the genetic background of a uropathogenic strain contribute to the pathogenesis of E. coli in the urinary tract. |
| References: | J Bacteriol. 1990 Nov;172(11):6557-67. (PMID: 2172216) Infect Immun. 1990 Sep;58(9):3073-7. (PMID: 2201644) Biochem Biophys Res Commun. 1977 Sep 9;78(1):455-60. (PMID: 334169) J Clin Invest. 1979 Jul;64(1):333-6. (PMID: 376560) J Infect Dis. 1979 Mar;139(3):329-32. (PMID: 376757) J Mol Biol. 1980 Apr;138(2):179-207. (PMID: 6997493) Infect Immun. 1981 Feb;31(2):564-70. (PMID: 7012012) Infect Immun. 1982 Nov;38(2):739-44. (PMID: 6128310) Infect Immun. 1983 Apr;40(1):265-72. (PMID: 6131870) Infect Immun. 1983 Apr;40(1):273-83. (PMID: 6339403) Infect Immun. 1985 Jun;48(3):625-8. (PMID: 2860067) Infect Immun. 1985 Aug;49(2):407-13. (PMID: 2410366) Mol Gen Genet. 1985;199(3):410-4. (PMID: 2863734) Infect Immun. 1986 Sep;53(3):693-6. (PMID: 2875030) J Immunol. 1987 May 15;138(10):3475-80. (PMID: 3553327) Mol Gen Genet. 1987 Jul;208(3):439-45. (PMID: 2890081) Infect Immun. 1988 Apr;56(4):815-22. (PMID: 2894361) J Biol Chem. 1988 Apr 15;263(11):5362-7. (PMID: 2895767) J Bacteriol. 1988 Jun;170(6):2575-83. (PMID: 2836362) Nucleic Acids Res. 1988 Jul 11;16(13):6127-45. (PMID: 3041370) Microb Pathog. 1988 Mar;4(3):231-8. (PMID: 2904111) Clin Microbiol Rev. 1991 Jan;4(1):80-128. (PMID: 1672263) Infect Immun. 1991 Sep;59(9):2915-21. (PMID: 1879917) Infect Immun. 1992 Apr;60(4):1295-301. (PMID: 1347759) Infect Immun. 1992 Dec;60(12):5197-203. (PMID: 1360450) J Biol Chem. 1993 Feb 5;268(4):3009-15. (PMID: 8094080) J Clin Invest. 1993 Aug;92(2):780-5. (PMID: 8349817) J Bacteriol. 1994 Feb;176(3):748-55. (PMID: 7905476) J Bacteriol. 1994 Apr;176(8):2227-34. (PMID: 7908902) J Clin Invest. 1994 Apr;93(4):1645-53. (PMID: 7512987) Mol Microbiol. 1994 Apr;12(1):131-41. (PMID: 8057833) Proc Natl Acad Sci U S A. 1994 Dec 6;91(25):11889-93. (PMID: 7991552) Microbiology. 1995 Nov;141 ( Pt 11):2839-48. (PMID: 8535512) FEMS Microbiol Lett. 1996 Apr 1;137(2-3):257-63. (PMID: 8998995) J Pathol Bacteriol. 1955 Oct;70(2):335-48. (PMID: 13295908) Trends Microbiol. 1995 Jul;3(7):266-70. (PMID: 7551639) J Immunol. 1989 Feb 1;142(3):992-8. (PMID: 2563273) J Pediatr. 1989 Jul;115(1):40-5. (PMID: 2661790) Nucleic Acids Res. 1989 Nov 11;17(21):8893. (PMID: 2587246) Infect Immun. 1990 Jun;58(6):1995-8. (PMID: 1971261) Nature. 1977 Feb 17;265(5595):623-5. (PMID: 323718) |
| المشرفين على المادة: | 0 (DNA, Bacterial) 0 (Receptors, Immunologic) 0 (fimbriae receptor, type 1) |
| تواريخ الأحداث: | Date Created: 19960903 Date Completed: 19961024 Latest Revision: 20190501 |
| رمز التحديث: | 20240627 |
| مُعرف محوري في PubMed: | PMC38514 |
| DOI: | 10.1073/pnas.93.18.9827 |
| PMID: | 8790416 |
| قاعدة البيانات: | MEDLINE |
| تدمد: | 0027-8424 |
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| DOI: | 10.1073/pnas.93.18.9827 |