Optimization of protective antibodies response against bacterial adhesins

NIH RePORTER · NIH · R21 · $173,664 · view on reporter.nih.gov ↗

Abstract

ABSTRACT The primary goal of this proposal is to understand how conformational properties of the major pathogenesis factor of E. coli - most common, type 1 fimbrial adhesin of E. coli - defines its ability to elicit a protective antibody response as a vaccine candidate against urinary tract infections caused by E. coli. FimH is an adhesive subunit of the type 1 fimbriae and is one of the major factors in the ability of E. coli to bing human urothelium and cause urinary tract infection. We determined that the mannose-binding lectin domain of FimH can assume two conformational states - with a high- and low-affinity towards terminally-exposed mannosyl residues. The conformational shift in FimH is highly dynamic in nature and is the basis of the ability of FimH to mediate shear-enhanced bacterial adhesion, bind fast and strongly human cell receptors and shed bound antibodies. We intend to perform a comprehensive functional analysis of antibodies against both conformational states of FimH to analyze the conformational switch in FimH in the context of the immune response against the adhesive protein.

Key facts

NIH application ID
10890155
Project number
5R21AI178593-02
Recipient
UNIVERSITY OF WASHINGTON
Principal Investigator
Mark Cartwright
Activity code
R21
Funding institute
NIH
Fiscal year
2024
Award amount
$173,664
Award type
5
Project period
2023-07-18 → 2025-12-31