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Title: Toll-like receptor 2 and Toll-like receptor 4 polymorphisms in invasive pneumococcal disease
Authors: Moens, Leen
Verhaegen, Jan
Pierik, Marie
Vermeire, Severine
De Boeck, Kris
Peetermans, Willy
Bossuyt, Xavier # ×
Issue Date: Jan-2007
Publisher: Elsevier
Series Title: Microbes and infection vol:9 issue:1 pages:15-20
Abstract: BACKGROUND: Toll-like receptors (TLRs) recognize distinct pathogen-associated molecular patterns and trigger anti-microbial host defense responses. Several in vitro and in vivo studies in mice indicate that TLR2 and TLR4 are involved in the defense against Streptococcus pneumoniae. Studies have revealed associations between polymorphisms in TLRs and human diseases. The effect of polymorphisms in TLR2 and TLR4 in the human defense to S. pneumoniae has not been studied. METHODS: We genotyped 99 Caucasian patients with invasive pneumococcal disease and 178 Caucasian controls for the known R579H, P631H and R753Q polymorphisms in TLR2 and the D299G polymorphism in TLR4 with PCR-RFLP methods. RESULTS: The distribution of the TLR2 R579H, P631H and R753Q and TLR4 D299G variants was not significantly different between the patients and the controls. After stratification of the patient population by age, sex, diagnosis, and mortality no significant differences for the TLR2 R753Q genotype and TLR4 D299G genotype were found between various patient subgroups and between patient subgroups and the control population. It should be mentioned that for the TLR2 polymorphisms neither the control group nor the patient group contains homozygous mutant individuals. CONCLUSION: We found no association between TLR2 and TLR4 polymorphisms and invasive pneumococcal infection.
ISSN: 1286-4579
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Laboratory of Clinical Bacteriology and Mycology
Clinical Residents Medicine
Laboratory for Clinical Infectious and Inflammatory Disorders
Translational Research in GastroIntestinal Disorders
Experimental Laboratory Immunology
× corresponding author
# (joint) last author

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