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.

The ex vivo cytokine response to lipopolysaccharide (LPS) of whole blood from patients with typhoid fever was investigated. Tumor necrosis factor (TNF)-alpha release by LPS-stimulated blood was found to be lower during acute typhoid fever than after a course of antimicrobial therapy (P<or=.001). Ex vivo interleukin (IL)-1beta, but not IL-1 receptor antagonist, release was also depressed during the acute stage of typhoid fever. Low ex vivo production of TNF-alpha was associated with delayed recovery. No association was found between the TNFA-308 promoter polymorphism and LPS-induced TNF-alpha release, either during an active infection or after treatment. In acute typhoid fever, the ability of peripheral blood leukocytes to release proinflammatory cytokines in response to an inflammatory stimulus is depressed, and this may contribute to delayed recovery following antibiotic treatment.

Original publication

DOI

10.1086/341298

Type

Journal article

Journal

J Infect Dis

Publication Date

15/07/2002

Volume

186

Pages

240 - 245

Keywords

Adult, Anti-Bacterial Agents, Azithromycin, Cytokines, DNA, Bacterial, Enzyme-Linked Immunosorbent Assay, Female, Fluoroquinolones, Humans, In Vitro Techniques, Interleukin-1, Lipopolysaccharides, Male, Polymerase Chain Reaction, Receptors, Interleukin-1, Salmonella typhi, Statistics, Nonparametric, Tumor Necrosis Factor-alpha, Typhoid Fever