Background: In recent reports, human toll-like receptor (TLR) 8 mediates the antiviral response by recognizing single-stranded RNA. The inflammatory response against enteroviral (EV) RNA replication may play an important role in dilated cardiomyopathy (DCM). The purpose of this study was to determine whether TLR8 was expressed with EV replication in patients with enterovirus-associated DCM.
Methods: Reverse transcriptase-polymerase chain reaction analysis was performed to screen the detection of myocardial EV RNA in 198 consecutive patients with DCM. Seventy-two EV RNA-positive patients with DCM and 20 control samples constituted the study population of the present study. Levels of TLR8 and myeloid differentiation factor (MyD) 88 adaptor protein mRNA and EV RNA (plus- and minus-strand RNAs) were measured by real-time RT-PCR. Immunohistochemistry was performed to identify the cellular source of these molecules.
Results: Toll-like receptor 8 and MyD88 mRNA levels were higher in patients with DCM than in controls (P < .001). Immunostainings of TLR8, MyD88, and EV protein showed localization of these proteins in cardiac myocytes in patients with DCM. After a mean follow-up of 426 days, clinical outcomes (development of heart failure n = 11, cardiac death n = 3) were associated with increased levels of TLR8 and MyD88 (P < .05). Multivariate analysis showed that TLR8 (relative risk 3.2, 95% CI 1.6-6.2) was a strong predictor of heart failure and cardiac death after adjustment for baseline characteristics.
Conclusion: Toll-like receptor 8 and MyD88 expressions may be involved in the immune response to EV replication in enterovirus-associated DCM. In addition, TLR8 may provide important prognostic information in patients with enterovirus-associated DCM.
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http://dx.doi.org/10.1016/j.ahj.2007.05.010 | DOI Listing |
J Dermatol Sci
November 2024
Department of Dermatology, Plastic Surgery Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. Electronic address:
Background: Mutations in gamma-secretase complex (GSC) genes are associated with hidradenitis suppurativa (HS), and toll-like receptor (TLR) 2 is elevated in HS lesions. However, it remains unclear whether TLR2 is upregulated in the skin lesions of patients with HS with GSC gene variants, and the role of its upregulation in the pathogenesis of this disease are unknown.
Objective: To investigate the role of TLR2 upregulation in NCSTN and PSENEN knockdown keratinocytes.
Mol Med
December 2024
Disease Prevention and Health Management Center, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, 310006, Zhejiang, China.
Background: Nonalcoholic fatty liver disease (NAFLD) has developed as a leading public wellness challenge as a result of changes in dietary patterns. Unfortunately, there is still a lack of effective pharmacotherapy methods for NAFLD. Wang's empirical formula (WSF) has demonstrated considerable clinical efficacy in treating metabolic disorders for years.
View Article and Find Full Text PDFInt Dent J
December 2024
Center of Excellence for Dental Stem Cell Biology, Faculty of Dentistry, Chulalongkorn University, Bangkok, Thailand; Faculty of Dentistry, Department of Anatomy, Chulalongkorn University, Bangkok, Thailand.
Human periodontal ligament (hPDL) is continuously exposed to mechanical forces that can induce inflammatory responses in resident stem cells (hPDLSCs). Here, we review the impact of mechanical force on hPDLSCs, focusing on the activation of inflammatory cytokines and related signalling pathways, which subsequently influence periodontal tissue remodelling. The effects of various mechanical forces, including compressive, shear, and tensile forces, on hPDLSCs are discussed.
View Article and Find Full Text PDFTrends Biochem Sci
December 2024
Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, VIC 3052, Australia; Department of Medical Biology, University of Melbourne, Parkville, VIC 3052, Australia; Drug Discovery Biology, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, VIC 3052, Australia. Electronic address:
Necroptosis is a mode of programmed cell death executed by the mixed lineage kinase domain-like (MLKL) pseudokinase following its activation by the upstream receptor-interacting protein kinase-3 (RIPK3), subsequent to activation of death, Toll-like, and pathogen receptors. The pathway originates in innate immunity, although interest has surged in therapeutically targeting necroptosis owing to its dysregulation in inflammatory diseases. Here, we explore how protein conformation and higher order assembly of the pathway effectors - Z-DNA-binding protein-1 (ZBP1), RIPK1, RIPK3, and MLKL - can be modulated by post-translational modifications, such as phosphorylation, ubiquitylation, and lipidation, and intermolecular interactions to tune activities and modulate necroptotic signaling flux.
View Article and Find Full Text PDFPLoS One
December 2024
International Vaccine Institute, Seoul, Republic of Korea.
The involvement of Toll-like receptor 2 (TLR2) in leptospirosis is poorly understood. Our systematic review examined its role across in-vitro, in-vivo, ex-vivo, and human studies. Original articles published in English up to January 2024, exploring the role of TLR2 during leptospirosis, were selected from databases including PubMed, Web of Science, Scopus, Trip, and Google Scholar.
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