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Aballay A: Worms and flies as genetically tractable animal models to study host-pathogen interactions. Infection and Immunity
, 2005
"... This article cites 86 articles, 35 of which can be accessed free ..."
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This article cites 86 articles, 35 of which can be accessed free
Sequence variants in Toll-like receptor gene cluster (TLR6-TLR1-TLR10) and prostate cancer risk
- J Natl Cancer Inst
, 2005
"... Background: Chronic infl ammation plays an important role in several human cancers and may be involved in the etiology of prostate cancer. Toll-like receptors (TLRs) are important in the innate immune response to pathogens and in cross-talk between innate immunity and adaptive immunity. Our previ-ou ..."
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Background: Chronic infl ammation plays an important role in several human cancers and may be involved in the etiology of prostate cancer. Toll-like receptors (TLRs) are important in the innate immune response to pathogens and in cross-talk between innate immunity and adaptive immunity. Our previ-ous fi nding of an association of TLR4 gene sequence variants and prostate cancer risk provides evidence for a role of TLRs in prostate cancer. In this study, we investigated whether sequence variants in the TLR6-TLR1-TLR10 gene cluster, residing within a 54-kb region on 4p14, were associated with prostate cancer risk. Methods: We selected 32 single-nucleotide polymorphisms (SNPs) covering these three genes and genotyped these SNPs in 96 control subjects from the Cancer Prostate in Sweden (CAPS) population-based pros-tate cancer case – control study. Five distinct haplotype blocks
Lipopolysaccharide opposes the induction of CYP26A1 and CYP26B1 gene expression by retinoic acid in the rat liver in vivo. Am J Physiol Gastrointest Liver Physiol 292: G1029–36
, 2007
"... Retinoic acid (RA), a principal metabolite of vitamin A (retinol), is an essential endogenous regulator of gene transcription and an important therapeutic agent. The catabolism of RA must be well regulated to maintain physiological concentrations of RA. The cytochrome P450 (CYP) gene family CYP26, w ..."
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Retinoic acid (RA), a principal metabolite of vitamin A (retinol), is an essential endogenous regulator of gene transcription and an important therapeutic agent. The catabolism of RA must be well regulated to maintain physiological concentrations of RA. The cytochrome P450 (CYP) gene family CYP26, which encodes RA-4-hydroxylase activ-ity, is strongly implicated in the oxidation of RA. Inflammation alters the expression of numerous genes; however, whether inflammation affects CYP26 expression is not well understood. We investigated the regulation of CYP26A1 and CYP26B1 mRNA levels by RA and LPS in the rat liver, as the liver is centrally involved in retinoid metabolism and the acute-phase response to LPS. Both CYP26A1 and CYP26B1 mRNA were induced in 4 h by a single oral dose of all-trans-RA. RA-induced responses of both CYP26A1 and CYP26B1 were signif-icantly attenuated in rats with LPS-induced inflammation whether LPS was given concurrently with RA or after the RA-induced increase
LPS activation of Tolllike receptor 4 signals CD11b/CD18 expression in neutrophils
- Am J Physiol Lung Cell Mol Physiol 288: L655–62
, 2005
"... identify herein a novel signaling function of the Toll-like receptor-4 (TLR4), the lipopolysaccharide (LPS) receptor mediating the innate immune response, in inducing the expression of CD11b/CD18 inte-grin in polymorphonuclear leukocytes (PMNs). Studies were made in PMNs isolated from TLR4-deficient ..."
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identify herein a novel signaling function of the Toll-like receptor-4 (TLR4), the lipopolysaccharide (LPS) receptor mediating the innate immune response, in inducing the expression of CD11b/CD18 inte-grin in polymorphonuclear leukocytes (PMNs). Studies were made in PMNs isolated from TLR4-deficient (TLR4/) and C57BL/6 [wild-type (WT)] mice. We observed increased CD11b expression in WT PMNs within 3 h after LPS challenge, whereas CD11b was not expressed in TLR4/ PMNs above basal levels. TLR4-activated CD11b expression was cycloheximide sensitive and involved the activation of transcription factors, NF-B and c-Jun/PU.1. TLR4/ PMNs challenged with LPS were functionally defective as the result of the impaired CD11b expression in that they failed to adhere and did not migrate across endothelial cells in response to N-formylmethio-nyl-leucyl-phenylalanine. TLR4 also promoted increased binding of LPS to PMNs on the basis of expression of CD11b. Thus TLR4
Cellular immune reactions in the lung
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Pathopharmacology of excessive hemorrhage in mifepristone abortions
- Ann Pharmacother 2007;41:2002-7. DOI 10.1345/aph.1K351
"... Hemorrhage and infection are theleading causes of mifepristone-relat- ..."
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Hemorrhage and infection are theleading causes of mifepristone-relat-
The R753Q Polymorphism Abrogates Toll-Like Receptor 2 Signaling in Response to Human
, 2009
"... Toll-like receptor 2 (TLR2) serves as a pattern recognition receptor that signals the presence of cytomegalovirus. Herein, we report that R753Q polymorphism paralyzes TLR2-me-diated immune signaling in cells exposed to cytomegalovirus glycoprotein B. This immunologic impairment could serve as a biol ..."
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Toll-like receptor 2 (TLR2) serves as a pattern recognition receptor that signals the presence of cytomegalovirus. Herein, we report that R753Q polymorphism paralyzes TLR2-me-diated immune signaling in cells exposed to cytomegalovirus glycoprotein B. This immunologic impairment could serve as a biologic mechanism underlying the association between the TLR2 R753Q polymorphism and cytomegalovirus disease in humans. Toll-like receptors (TLRs) are germline-encoded innate im-mune sensors of microbial pathogens [1]. Activation of TLR signaling results in induction of proinflammatory cytokines and antimicrobial peptides [1]. Experimental observations suggest that TLR2 is involved in the innate immune response to cy-tomegalovirus (CMV) [2, 3]. Stimulation of TLR2 by CMV in vitro, specifically by its envelope glycoproteins B (gB) and H
Polymorphism and Cytomegalovirus Disease after Liver Transplantation
"... Background. Experimental data suggest that cytomegalovirus (CMV) initiates innate immunity through the activation of Toll-like receptor 2 (TLR2). To assess the clinical relevance of this experimental observation, we assessed the association between the specific single-nucleotide polymorphism that re ..."
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Background. Experimental data suggest that cytomegalovirus (CMV) initiates innate immunity through the activation of Toll-like receptor 2 (TLR2). To assess the clinical relevance of this experimental observation, we assessed the association between the specific single-nucleotide polymorphism that results in the substitution of arginine for glutamine in position 753 of TLR2 (the TLR2 Arg753Gln polymorphism) and CMV replication and disease after liver transplantation. Methods. Ninety-two liver transplant recipients with chronic hepatitis C were screened for the presence of the TLR2 Arg753Gln polymorphism. CMV load was determined in serially collected blood samples using CMV DNA polymerase chain reaction. Kaplan-Meier estimation and univariable and multivariable stepwise Cox proportional hazard models were used to assess associations. Results. The degree of CMV replication, as measured by CMV load, was significantly higher in patients who were homozygous (mean maximum viral load, 37,059 copies/mL) and heterozygous (mean maximum viral load, 29,718 copies/mL) for this polymorphism, compared with patients without the TLR2 Arg753Gln polymorphism (mean maximum viral load, 3252 copies/mL;). Kaplan-Meier survival analysis demonstrated an associationPp.003 between being homozygous for the TLR2 Arg753Gln polymorphism and CMV disease (). A multivariatePp.04 Cox proportional hazard model demonstrated a trend towards a higher risk of CMV disease among patients who
Running Title: Inflammation opposes retinoid induced CYP26 expression Address for reprint requests and other correspondence:
"... Retinoic acid (RA), a principal metabolite of vitamin A (retinol), is an essential endogenous regulator of gene transcription, and an important therapeutic agent. The catabolism of RA must be well regulated to maintain physiological concentrations of RA. The cytochrome P450 gene family, CYP26, which ..."
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Retinoic acid (RA), a principal metabolite of vitamin A (retinol), is an essential endogenous regulator of gene transcription, and an important therapeutic agent. The catabolism of RA must be well regulated to maintain physiological concentrations of RA. The cytochrome P450 gene family, CYP26, which encodes retinoic acid-4-hydroxylase activity, is strongly implicated in the oxidation of RA. Inflammation alters the expression of numerous genes; however, whether inflammation affects CYP26 expression is not well understood. We have investigated the regulation of CYP26A1 and CYP26B1 mRNA levels by RA and lipopolysaccharide (LPS) in rat liver, as the liver is centrally involved in retinoid metabolism and the acute phase response to LPS. Both CYP26A1 and CYP26B1 mRNA were induced in <4-h by a single oral dose of all-trans-RA. The RA-induced response of both CYP26A1 and CYP26B1 was significantly attenuated in rats with LPS-induced inflammation, whether LPS was given concurrently with RA, or after the RA-induced increase in CYP26A1 and CYP26B1 mRNA levels. When RA and LPS were administered simultaneously (6 h study), LPS alone had little effect on either CYP26A1 or CP26B1 mRNA, but LPS reduced by 80 % the RA-induced increase in CYP26A1 mRNA (P <0.02), with a similar trend for CYP26B1 mRNA. When LPS
unknown title
"... Abstract Introduction. TLR´s play a role in host defense in HIV infection recognizing the viral DNA or RNA. Their activation induces a signaling pathway that includes the proteins MyD88, IRAK4, TRAF6 and the transcription factor NF-kBp65. Objective. To determine the expression of TLR7, TLR8 and TLR ..."
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Abstract Introduction. TLR´s play a role in host defense in HIV infection recognizing the viral DNA or RNA. Their activation induces a signaling pathway that includes the proteins MyD88, IRAK4, TRAF6 and the transcription factor NF-kBp65. Objective. To determine the expression of TLR7, TLR8 and TLR9, and activation of its signaling pathway in monocytes from patients infected with HIV. Methods. Expression of TLR7, TLR8 and TLR9 was determined in monocytes from HIV-infected patients (n = 13) and control subjects (n = 13), which were activated with specific ligands. The expression of MyD88 and NF-kBp65 were determined by flow cytometry; IRAK4 and TRAF6 were studied by immunoblotting. Results. No statistical difference was found in the expression of TLR7, 8 and 9 in monocytes from patients compared to controls, but we observed the non-significant increased expression of TLR9 in patients. The activation showed no significant difference in the expression of MyD88 and NF-kBp65 in patients when compared to controls, but were decreased in stimulated cells over non-stimulated cells. IRAK4 and TRAF6 were not detected. Conclusions. No statistical difference was observed in the expression of intracellular TLRs, MyD88 and NFkBp65 in monocytes from patients compared to controls. This was probably due to effective antiretroviral therapy being received at the time of study entry. Additional studies are needed (ARTV) under controlled conditions that include infected patients with and without ARVT, responders and non-responders, and work with different cell populations. Original Article Expression and activation of intracellular receptors TLR7, TLR8 and TLR9 in peripheral blood monocytes from HIV-infected patients Expresión y activación de receptores intracelulares TLR7, TLR8 y TLR9 en monocitos de sangre periférica de pacientes infectados con VIH.
