The Toll-like receptor 2 R753Q polymorphism defines a subgroup of patients with atopic dermatitis having severe phenotype 
Available from: Johanna U Ericson Sollid
- "Epidemiological studies show no or little association between TLR2 R753Q and/or the GT repeat and severe S. aureus infection (Lorenz et al., 2000; Moore et al., 2004); however, an association between a TLR2 R753Q polymorphism and nasopharyngeal S. aureus carriage among healthy infants was recently found (Vuononvirta et al., 2011). Also, among AD patients, which are often colonized with the bacteria, 9 out of 78 patients (11.5%) carried the TLR2 R753Q variant (Ahmad-Nejad et al., 2004). Only a few studies in mice have addressed the involvement of TLR2, IL-1R, or MyD88 in nasal carriage of S. aureus. "
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ABSTRACT: Staphylococcus aureus may cause serious skin and soft tissue infections, deep abscesses, endocarditis, osteomyelitis, pneumonia, and sepsis. S. aureus persistently colonizes 25-30% of the adult human population, and S. aureus carriers have an increased risk for infections caused by the bacterium. The major site of colonization is the nose, i.e., the vestibulum nasi, which is covered with ordinary skin and hair follicles. Several host and microbe determinants are assumed to be associated with colonization. These include the presence and expression level of bacterial adhesins, which can adhere to various proteins in the extracellular matrix or on the cellular surface of human skin. The host expresses several antimicrobial peptides and lipids. The level of β-defensin 3, free sphingosine, and cis-6-hexadecenoic acid are found to be associated with nasal carriage of S. aureus. Other host factors are certain polymorphisms in Toll-like receptor 2, mannose-binding lectin, C-reactive protein, glucocorticoid-, and vitamin D receptor. Additional putative determinants for carriage include genetic variation and expression of microbial surface components recognizing adhesive matrix molecules and their interaction partners, as well as variation among humans in the ability of recognizing and responding appropriately to the bacteria. Moreover, the available microflora may influence the success of S. aureus colonization. In conclusion, colonization is a complex interplay between the bacteria and its host. Several bacterial and host factors are involved, and an increased molecular understanding of these are needed.
Frontiers in Cellular and Infection Microbiology 05/2012; 2(56):56. DOI:10.3389/fcimb.2012.00056 · 3.72 Impact Factor
Available from: PubMed Central
- "Toll-like receptors (TLRs) are a family of evolutionarily conserved receptors that recognize pathogen-associated molecular patterns (PAMPs), leading to an inflammatory response by induction of interleukins and other pro-inflammatory proteins . Polymorphisms in TLR genes have been implicated in various diseases  including AD . Yet, the effect of genetic variation in TLR downstream signalling pathways has not been sufficiently studied yet. "
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ABSTRACT: Atopic dermatitis (AD) is a common inflammatory skin disorder, affecting up to 15% of children in industrialized countries. Toll-interacting protein (TOLLIP) is an inhibitory adaptor protein within the toll-like receptor (TLR) pathway, a part of the innate immune system that recognizes structurally conserved molecular patterns of microbial pathogens, leading to an inflammatory immune response.
In order to detect a possible role of TOLLIP variation in the pathogenesis of AD, we screened the entire coding sequence of the TOLLIP gene by SSCP in 50 AD patients. We identified an amino acid exchange in exon 6 (Ala222Ser) and a synonymous variation in exon 4 (Pro139Pro). Subsequently, these two variations and four additional non-coding polymorphisms (-526 C/G, two polymorphisms in intron 1 and one in the 3'UTR) were genotyped in 317 AD patients and 224 healthy controls.
The -526G allele showed borderline association with AD in our cohort (p = 0.012; significance level after correction for multiple testing 0.0102). Haplotype analysis did not yield additional information. Evaluation of mRNA expression by quantitative real-time polymerase chain reaction in six probands with the CC and six with the GG genotype at the -526 C/G locus did not reveal significant differences between genotypes.
Variation in the TOLLIP gene may play a role in the pathogenesis of AD. Yet, replication studies in other cohorts and populations are warranted to confirm these association results.
BMC Dermatology 02/2007; 7(1):3. DOI:10.1186/1471-5945-7-3
Available from: Marshall V Williams
- "Assuming that the EBV-encoded dUTPase preparations contained 0.9 ng of DNA/ml, then the maximal amount of dsDNA that could be present in any assay is 0.5 ng which is at least 3-fold less that what has been reported previously to stimulate Toll receptors (TLR) (Ahmad-Nejad et al., 2004). We also demonstrated using the SLP-HS assay, which has a detection limit of 10 pg/ml of peptidoglycan, that the EBVencoded dUTPase preparations were free of contaminating peptidoglycan. "
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ABSTRACT: Epstein-Barr virus (EBV) encodes for several enzymes that are involved in viral DNA replication. There is evidence that some viral proteins, by themselves, can induce immune dysregulation that may contribute to the pathophysiology of the virus infection. In this study, we focused on the EBV-encoded deoxyuridine triphosphate nucleotidohydrolase (dUTPase) and present the first evidence that the dUTPase is able to induce immune dysregulation in vitro as demonstrated by the inhibition of the replication of stimulated peripheral blood mononuclear cells (PBMCs) and the upregulation of several proinflammatory cytokines including TNF-alpha, IL-1beta, IL-8, IL-6, and IL-10 produced by unstimulated PBMCs treated with purified EBV-encoded dUTPase. Depletion of CD14-positive cells (monocytes) eliminated the cytokine profile induced by EBV dUTPase treatment. The data support the hypothesis that at least one protein of the EBV early antigen complex can induce immune dysregulation and may be involved in the pathophysiology of EBV-associated disease.
Virology 04/2006; 346(1):205-18. DOI:10.1016/j.virol.2005.10.034 · 3.32 Impact Factor
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