Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

Toll-like receptor 5 (TLR5) mediates innate immune responses to bacterial pathogens by binding to flagellin. A polymorphism in the TLR5 gene introduces a premature stop codon (TLR5(392STOP)) that is associated with susceptibility to legionnaires disease. Here we investigated whether TLR5(392STOP) was associated with typhoid fever. The frequency of TLR5(392STOP) was not significantly different in 565 patients with typhoid fever and 281 ethnically matched control subjects. Furthermore, TLR5 deficiency had no measurable effect on a number of clinical parameters associated with typhoid fever, including fever clearance time, pathogen burden, disease severity, or age at acquisition of disease. TLR5 may not play an important role in TLR-stimulated innate immune responses to human infection with Salmonella enterica serovar Typhi. Initiation of these responses may rely on other TLRs that recognize different bacterial ligands.

Original publication

DOI

10.1086/428593

Type

Journal article

Journal

J Infect Dis

Publication Date

01/04/2005

Volume

191

Pages

1068 - 1071

Keywords

Adolescent, Adult, Aged, Child, Child, Preschool, Flagellin, Genetic Predisposition to Disease, Genetic Testing, Humans, Immunity, Innate, Infant, Membrane Glycoproteins, Middle Aged, Polymorphism, Genetic, Receptors, Cell Surface, Salmonella enterica, Toll-Like Receptor 5, Toll-Like Receptors, Typhoid Fever, Vietnam