Protection against Escherichia coli-induced urinary tract infections with hybridoma antibodies directed against type 1 fimbriae or complementary d-mannose receptors

S. N. Abraham, Jegdish Babu, C. S. Giampapa, D. L. Hasty, W. A. Simpson, E. H. Beachey

Research output: Contribution to journalArticle

50 Citations (Scopus)

Abstract

Hybridoma antibodies directed against quaternary structural epitopes of the type 1 fimbrial adhesin of Escherichia coli or against d-mannose, the sugar determinant in the complementary host cell receptor, prevented the attachment of mannose-sensitive E. coli to various eucaryotic cells. Passive intraperitoneal administration of the fimbria-specific or d-mannose-specific antibodies protected mice against retrograde colonization with mannose-sensitive E. coli instilled into their urinary bladders. Monoclonal antibodies directed against fimbrial subunits rather than quaternary structural epitopes or against N-acetylgalactosamine rather than d-mannose residues lacked protective activity. These studies provide evidence that bacterial colonization can be blocked or interrupted by antibodies directed against either the adhesin or the complementary host cell receptor of pathogenic microorganisms.

Original languageEnglish (US)
Pages (from-to)625-628
Number of pages4
JournalInfection and Immunity
Volume48
Issue number3
StatePublished - Nov 20 1985
Externally publishedYes

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Hybridomas
Mannose
Urinary Tract Infections
Escherichia coli
Antibodies
Epitopes
Bacterial Adhesins
Acetylgalactosamine
Urinary Bladder
Monoclonal Antibodies
mannose receptor

All Science Journal Classification (ASJC) codes

  • Parasitology
  • Microbiology
  • Immunology
  • Infectious Diseases

Cite this

Protection against Escherichia coli-induced urinary tract infections with hybridoma antibodies directed against type 1 fimbriae or complementary d-mannose receptors. / Abraham, S. N.; Babu, Jegdish; Giampapa, C. S.; Hasty, D. L.; Simpson, W. A.; Beachey, E. H.

In: Infection and Immunity, Vol. 48, No. 3, 20.11.1985, p. 625-628.

Research output: Contribution to journalArticle

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