Toll-like receptor 2 activation induces C-C motif chemokine ligand 5 production in canine keratinocytes
Contact us if these videos are not relevant.
Contact us if these videos are not relevant.
View abstract on PubMed
Summary
This summary is machine-generated.Toll-like receptor 2 (TLR2) activation boosts C-C motif chemokine ligand 5 (CCL5) production in canine keratinocytes, potentially worsening atopic dermatitis (AD) in dogs. Interferon-gamma (IFN-γ) enhances this effect, suggesting a role for bacteria in canine AD pathogenesis.
Area Of Science
- Veterinary Dermatology
- Immunology
- Molecular Biology
Background
- Canine atopic dermatitis (cAD) pathogenesis involves C-C motif chemokine ligand 5 (CCL5) and Toll-like receptor 2 (TLR2) activation by Staphylococcus species.
- The role of TLR2 activation in inducing CCL5 production in canine keratinocytes is not fully understood.
Purpose Of The Study
- To investigate the effect of TLR2 agonists on CCL5 production in canine keratinocytes.
- To examine potential synergistic effects of interferon (IFN)-γ, interleukin (IL)-13, or IL-4 on TLR2-induced CCL5 production.
- To elucidate the underlying molecular mechanisms.
Main Methods
- Canine progenitor epidermal keratinocyte (CPEK) cells were stimulated with TLR2 agonists, with or without pathway inhibitors or cytokines (IFN-γ, IL-13, IL-4).
- CCL5 protein levels were quantified using enzyme-linked immunosorbent assay (ELISA).
- TLR2 mRNA expression was assessed via real-time PCR following IFN-γ stimulation.
Main Results
- TLR2 agonists significantly increased CCL5 production in CPEK cells.
- Inhibitors of the TLR2 signaling pathway reduced CCL5 production.
- IFN-γ synergistically enhanced TLR2 agonist-induced CCL5 production, while IL-13 and IL-4 did not.
- IFN-γ partially upregulated TLR2 mRNA expression in CPEK cells.
Conclusions
- TLR2 activation by Staphylococcus species may induce CCL5 production in canine keratinocytes, contributing to immune cell recruitment in canine atopic dermatitis (cAD).
- During the Th1-polarized chronic phase of cAD, Staphylococcus-induced TLR2 activation could exacerbate skin inflammation.
- Further research is needed to clarify the clinical significance and mechanisms of skin bacteria-mediated CCL5 production in keratinocytes.
Contact us if these videos are not relevant.
Contact us if these videos are not relevant.
Related Concept Videos
T cells are integral to our adaptive immune system, recognizing and effectively responding to foreign antigens. T cell activation and clonal selection are pivotal in orchestrating this immune response. This article elucidates these mechanisms, detailing the roles of cluster of differentiation (CD) markers, major histocompatibility complex (MHC) molecules, costimulatory signals, and the process of clonal selection.
Naive T cells that have not yet encountered an antigen express two primary CD...
Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as SH2...
Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
The adaptive immune response, a sophisticated defense mechanism, relies on the activation and differentiation of B lymphocytes, or B cells. These processes enable our bodies to mount a tailored response against specific pathogens such as bacteria, free virus particles, toxins, and parasites.
When naive B cells encounter a specific antigen that can bind to the B cell receptor (BCR) on their surface, they undergo sensitization to respond to the antigen's presence. Sensitization begins with...
Receptor tyrosine kinases or RTKs are membrane-bound receptors that phosphorylate specific tyrosine on protein substrates. RTKs regulate cellular growth, differentiation, survival, and migration. They contain an extracellular ligand binding domain, a transmembrane domain, and a cytosolic tail with intrinsic kinase activity. Several extracellular signaling molecules activate RTKs in one or more ways and relay the signal downstream. Ligands such as platelet-derived growth factor (PDGF) or...