Catabolic mediators from TLR2-mediated proteoglycan aggrecan peptide-stimulated chondrocytes are reduced by Lactobacillus-conditioned media.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
05 Aug 2024
Historique:
received: 20 09 2023
accepted: 23 07 2024
medline: 6 8 2024
pubmed: 6 8 2024
entrez: 5 8 2024
Statut: epublish

Résumé

In osteoarthritis (OA), extracellular matrix (ECM) digestion by cartilage-degrading enzymes drives cartilage destruction and generates ECM fragments, such as proteoglycan aggrecan (PG) peptides. PG peptides have been shown to induce immunological functions of chondrocytes. However, the role of PG peptides in stimulating catabolic mediators from chondrocytes has not been investigated. Therefore, we aim to determine the effects and its mechanism by which PG peptides induce chondrocytes to produce catabolic mediators in OA. Human chondrocytes were stimulated with IFNγ and various PG peptides either (i) with or (ii) without TLR2 blockade or (iii) with Lactobacillus species-conditioned medium (LCM), a genus of bacteria with anti-inflammatory properties. Transcriptomic analysis, cartilage-degrading enzyme production and TLR2-intracellular signaling activation were investigated. Chondrocytes treated with PG peptides p16-31 and p263-280 increased expression levels of genes associated with chondrocyte hypertrophy, cartilage degradation and proteolytic enzyme production. TLR2 downstream signaling proteins (STAT3, IkBα and MAPK9) were significantly phosphorylated in p263-280 peptide-stimulated chondrocytes. MMP-1 and ADAMTS-4 were significantly reduced in p263-280 peptides-treated condition with TLR2 blockade or LCM treatment. Phosphorylation levels of IkBa, ERK1/2 and MAPK9 were significantly decreased with TLR2 blockade, but only phosphorylation levels of MAPK9 was significantly decreased with LCM treatment. Our study showed that PG peptide stimulation via TLR2 induced cartilage-degrading enzyme production via activation of MAPK, NFκB and STAT3 pathways.

Identifiants

pubmed: 39103466
doi: 10.1038/s41598-024-68404-9
pii: 10.1038/s41598-024-68404-9
doi:

Substances chimiques

Toll-Like Receptor 2 0
Aggrecans 0
Culture Media, Conditioned 0
TLR2 protein, human 0
ADAMTS4 Protein EC 3.4.24.82
STAT3 Transcription Factor 0
Peptides 0
Proteoglycans 0
Matrix Metalloproteinase 1 EC 3.4.24.7
ADAMTS4 protein, human EC 3.4.24.82
NF-KappaB Inhibitor alpha 139874-52-5
NFKBIA protein, human 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

18043

Subventions

Organisme : Ratchadaphiseksompotch Fund, Faculty of Medicine, Chulalongkorn University
ID : RA62/112

Informations de copyright

© 2024. The Author(s).

Références

Terkawi, M. A. et al. Low-grade inflammation in the pathogenesis of osteoarthritis: Cellular and molecular mechanisms and strategies for future therapeutic intervention. Biomedicines 10 (2022).
Lambert, C. et al. The damage-associated molecular patterns (DAMPs) as potential targets to treat osteoarthritis: Perspectives from a review of the literature. Front. Med. (Lausanne) 7, 607186 (2020).
pubmed: 33537330 doi: 10.3389/fmed.2020.607186
Barreto, G., Manninen, M. & K, K.E. Osteoarthritis and toll-like receptors: When innate immunity meets chondrocyte apoptosis. Biology (Basel) 9 (2020).
Akkiraju, H. & Nohe, A. Role of chondrocytes in cartilage formation, progression of osteoarthritis and cartilage regeneration. J. Dev. Biol. 3, 177–192 (2015).
pubmed: 27347486 doi: 10.3390/jdb3040177
Zeng, G. Q., Chen, A. B., Li, W., Song, J. H. & Gao, C. Y. High MMP-1, MMP-2, and MMP-9 protein levels in osteoarthritis. Genet. Mol. Res. 14, 14811–14822 (2015).
pubmed: 26600542 doi: 10.4238/2015.November.18.46
Xin, X. et al. Potential Value of Matrix Metalloproteinase-13 as a Biomarker for Osteoarthritis. Front. Surg. 8, 750047 (2021).
pubmed: 34778362 pmcid: 8589078 doi: 10.3389/fsurg.2021.750047
Verma, P. & Dalal, K. ADAMTS-4 and ADAMTS-5: Key enzymes in osteoarthritis. J. Cell. Biochem. 112, 3507–3514 (2011).
pubmed: 21815191 doi: 10.1002/jcb.23298
Ashruf, O. S. & Ansari, M. Y. Natural compounds: Potential therapeutics for the inhibition of cartilage matrix degradation in osteoarthritis. Life (Basel) 13 (2022).
Slovacek, H. et al. Interrelationship of MMP-9, Proteoglycan-4, and inflammation in osteoarthritis patients undergoing total hip arthroplasty. Clin. Appl. Thromb. Hemost. 27, 1076029621995569 (2021).
pubmed: 33754883 pmcid: 7995300 doi: 10.1177/1076029621995569
Lees, S. et al. Bioactivity in an aggrecan 32-mer fragment is mediated via Toll-like receptor 2. Arthritis Rheumatol. 67, 1240–1249 (2015).
pubmed: 25707860 doi: 10.1002/art.39063
Jung, Y. K. et al. Degrading products of chondroitin sulfate can induce hypertrophy-like changes and MMP-13/ADAMTS5 production in chondrocytes. Sci. Rep. 9, 15846 (2019).
pubmed: 31676809 pmcid: 6825126 doi: 10.1038/s41598-019-52358-4
Maldonado, M. & Nam, J. The role of changes in extracellular matrix of cartilage in the presence of inflammation on the pathology of osteoarthritis. Biomed. Res. Int. 2013, 284873 (2013).
pubmed: 24069595 pmcid: 3771246 doi: 10.1155/2013/284873
Sengprasert, P. et al. Upregulation of antigen presentation function and inflammation in chondrocytes by induction of proteoglycan aggrecan peptides (P16–31 and P263–280). Clin. Exp. Rheumatol. 40, 596–607 (2022).
pubmed: 34128792 doi: 10.55563/clinexprheumatol/hjzqfs
Roughley, P. J. & Mort, J. S. The role of aggrecan in normal and osteoarthritic cartilage. J. Exp. Orthop. 1, 8 (2014).
pubmed: 26914753 pmcid: 4648834 doi: 10.1186/s40634-014-0008-7
de Jong, H. et al. Cartilage proteoglycan aggrecan epitopes induce proinflammatory autoreactive T-cell responses in rheumatoid arthritis and osteoarthritis. Ann. Rheum. Dis. 69, 255–262 (2010).
pubmed: 19213744 doi: 10.1136/ard.2008.103978
Dunn, C. M. & Jeffries, M. A. The microbiome in osteoarthritis: A narrative review of recent human and animal model literature. Curr. Rheumatol. Rep. 24, 139–148 (2022).
pubmed: 35389162 doi: 10.1007/s11926-022-01066-6
Jhun, J. et al. Oral Administration of Lactobacillus rhamnosus ameliorates the progression of osteoarthritis by inhibiting joint pain and inflammation. Cells 10 (2021).
Lei, M., Guo, C., Wang, D., Zhang, C. & Hua, L. The effect of probiotic Lactobacillus casei Shirota on knee osteoarthritis: A randomised double-blind, placebo-controlled clinical trial. Benef. Microbes 8, 697–703 (2017).
pubmed: 28726510 doi: 10.3920/BM2016.0207
So, J. S. et al. Lactobacillus casei enhances type II collagen/glucosamine-mediated suppression of inflammatory responses in experimental osteoarthritis. Life Sci. 88, 358–366 (2011).
pubmed: 21167838 doi: 10.1016/j.lfs.2010.12.013
Sengprasert, P., Kamenkit, O., Tanavalee, A. & Reantragoon, R. The immunological facets of chondrocytes in osteoarthritis: A narrative review. J. Rheumatol. (2023).
Chawla, S. et al. Chondrocyte hypertrophy in osteoarthritis: Mechanistic studies and models for the identification of new therapeutic strategies. Cells 11 (2022).
Pauli, C. et al. Comparison of cartilage histopathology assessment systems on human knee joints at all stages of osteoarthritis development. Osteoarthr Cartil 20, 476–485 (2012).
doi: 10.1016/j.joca.2011.12.018
Kim, H. A. et al. The catabolic pathway mediated by Toll-like receptors in human osteoarthritic chondrocytes. Arthritis Rheum. 54, 2152–2163 (2006).
pubmed: 16802353 doi: 10.1002/art.21951
Indira, M., Venkateswarulu, T. C., Abraham Peele, K., Nazneen Bobby, M. & Krupanidhi, S. Bioactive molecules of probiotic bacteria and their mechanism of action: A review. 3 Biotech 9, 306 (2019).
pubmed: 31355115 pmcid: 6656846 doi: 10.1007/s13205-019-1841-2
Robinson, W. H. et al. Low-grade inflammation as a key mediator of the pathogenesis of osteoarthritis. Nat. Rev. Rheumatol. 12, 580–592 (2016).
pubmed: 27539668 pmcid: 5500215 doi: 10.1038/nrrheum.2016.136
Boonma, P., Spinler, J. K., Venable, S. F., Versalovic, J. & Tumwasorn, S. Lactobacillus rhamnosus L34 and Lactobacillus casei L39 suppress Clostridium difficile-induced IL-8 production by colonic epithelial cells. BMC Microbiol. 14, 177 (2014).
pubmed: 24989059 pmcid: 4094603 doi: 10.1186/1471-2180-14-177
Panpetch, W., Spinler, J. K., Versalovic, J. & Tumwasorn, S. Characterization of Lactobacillus salivarius strains B37 and B60 capable of inhibiting IL-8 production in Helicobacter pylori-stimulated gastric epithelial cells. BMC Microbiol 16, 242 (2016).
pubmed: 27756217 pmcid: 5070129 doi: 10.1186/s12866-016-0861-x
Thiraworawong, T. et al. Anti-inflammatory properties of gastric-derived Lactobacillus plantarum XB7 in the context of Helicobacter pylori infection. Helicobacter 19, 144–155 (2014).
pubmed: 24387083 doi: 10.1111/hel.12105
Kalogera, S. et al. Relevance of biomarkers in serum vs. synovial fluid in patients with knee osteoarthritis. Int. J. Mol. Sci. 24 (2023).
Germaschewski, F. M. et al. Quantitation OF ARGS aggrecan fragments in synovial fluid, serum and urine from osteoarthritis patients. Osteoarthr. Cartil. 22, 690–697 (2014).
doi: 10.1016/j.joca.2014.02.930
Zou, J., Appel, H., Rudwaleit, M., Thiel, A. & Sieper, J. Analysis of the CD8+ T cell response to the G1 domain of aggrecan in ankylosing spondylitis. Ann. Rheum. Dis. 64, 722–729 (2005).
pubmed: 15539415 doi: 10.1136/ard.2004.024455
Li, T. et al. The mechanism and role of ADAMTS protein family in osteoarthritis. Biomolecules 12 (2022).
Szanto, S. et al. Induction of arthritis in HLA-DR4-humanized and HLA-DQ8-humanized mice by human cartilage proteoglycan aggrecan but only in the presence of an appropriate (non-MHC) genetic background. Arthritis Rheum. 50, 1984–1995 (2004).
pubmed: 15188376 doi: 10.1002/art.20285
Pollanen, R. et al. Microbial antigens mediate HLA-B27 diseases via TLRs. J. Autoimmun. 32, 172–177 (2009).
pubmed: 19299108 doi: 10.1016/j.jaut.2009.02.010
Taniguchi, N. et al. Stage-specific secretion of HMGB1 in cartilage regulates endochondral ossification. Mol. Cell. Biol. 27, 5650–5663 (2007).
pubmed: 17548469 pmcid: 1952123 doi: 10.1128/MCB.00130-07
Kuhne, M. et al. HLA-B27-restricted antigen presentation by human chondrocytes to CD8+ T cells: Potential contribution to local immunopathologic processes in ankylosing spondylitis. Arthritis Rheum. 60, 1635–1646 (2009).
pubmed: 19479861 doi: 10.1002/art.24549
Candia, L., Marquez, J., Hernandez, C., Zea, A. H. & Espinoza, L. R. Toll-like receptor-2 expression is upregulated in antigen-presenting cells from patients with psoriatic arthritis: A pathogenic role for innate immunity?. J. Rheumatol. 34, 374–379 (2007).
pubmed: 17183618
Oliveira-Nascimento, L., Massari, P. & Wetzler, L. M. The role of TLR2 in infection and immunity. Front. Immunol. 3, 79 (2012).
pubmed: 22566960 pmcid: 3342043 doi: 10.3389/fimmu.2012.00079
Holub, M. N. et al. Peptidoglycan in osteoarthritis synovial tissue is associated with joint inflammation. Res Sq (2023).
Avenoso, A. et al. The proteoglycan biglycan mediates inflammatory response by activating TLR-4 in human chondrocytes: Inhibition by specific siRNA and high polymerized Hyaluronan. Arch. Biochem. Biophys. 640, 75–82 (2018).
pubmed: 29339093 doi: 10.1016/j.abb.2018.01.007
Campo, G. M. et al. Small hyaluronan oligosaccharides induce inflammation by engaging both toll-like-4 and CD44 receptors in human chondrocytes. Biochem. Pharmacol. 80, 480–490 (2010).
pubmed: 20435021 doi: 10.1016/j.bcp.2010.04.024
Liu-Bryan, R. & Terkeltaub, R. Chondrocyte innate immune myeloid differentiation factor 88-dependent signaling drives procatabolic effects of the endogenous Toll-like receptor 2/Toll-like receptor 4 ligands low molecular weight hyaluronan and high mobility group box chromosomal protein 1 in mice. Arthritis Rheum. 62, 2004–2012 (2010).
pubmed: 20506365 pmcid: 2902571 doi: 10.1002/art.27475
Barreto, G. et al. Lumican is upregulated in osteoarthritis and contributes to TLR4-induced pro-inflammatory activation of cartilage degradation and macrophage polarization. Osteoarthr. Cartil. 28, 92–101 (2020).
doi: 10.1016/j.joca.2019.10.011
Hwang, H. S., Park, S. J., Cheon, E. J., Lee, M. H. & Kim, H. A. Fibronectin fragment-induced expression of matrix metalloproteinases is mediated by MyD88-dependent TLR-2 signaling pathway in human chondrocytes. Arthritis Res. Ther. 17, 320 (2015).
pubmed: 26563875 pmcid: 4643537 doi: 10.1186/s13075-015-0833-9
Lei, L. et al. Effect of cell receptors in the pathogenesis of osteoarthritis: Current insights. Open Life Sci. 17, 695–709 (2022).
pubmed: 35859614 pmcid: 9267313 doi: 10.1515/biol-2022-0075
Hu, X. et al. IFN-gamma suppresses IL-10 production and synergizes with TLR2 by regulating GSK3 and CREB/AP-1 proteins. Immunity 24, 563–574 (2006).
pubmed: 16713974 doi: 10.1016/j.immuni.2006.02.014
Li, Z., Huang, Z. & Bai, L. Cell interplay in osteoarthritis. Front. Cell Dev. Biol. 9, 720477 (2021).
pubmed: 34414194 pmcid: 8369508 doi: 10.3389/fcell.2021.720477
Tan, T. C., Chong, T. K. Y., Low, A. H. L. & Leung, Y. Y. Microbiome and osteoarthritis: New insights from animal and human studies. Int. J. Rheum. Dis. 24, 984–1003 (2021).
pubmed: 33961348 doi: 10.1111/1756-185X.14123
Jenab, A., Roghanian, R. & Emtiazi, G. Bacterial natural compounds with anti-inflammatory and immunomodulatory properties (mini review). Drug Des. Dev. Ther. 14, 3787–3801 (2020).
doi: 10.2147/DDDT.S261283
Kuleshov, M. V. et al. Enrichr: A comprehensive gene set enrichment analysis web server 2016 update. Nucleic Acids Res. 44, W90-97 (2016).
pubmed: 27141961 pmcid: 4987924 doi: 10.1093/nar/gkw377

Auteurs

Panjana Sengprasert (P)

Immunology Division, Department of Microbiology, Faculty of Medicine, Chulalongkorn University, 1873 Rama 4 Road, Bangkok, 10330, Thailand.

Palapun Waitayangkoon (P)

Immunology Division, Department of Microbiology, Faculty of Medicine, Chulalongkorn University, 1873 Rama 4 Road, Bangkok, 10330, Thailand.

Ousakorn Kamenkit (O)

Medical Microbiology Interdisciplinary Program, Graduate School, Chulalongkorn University, Bangkok, Thailand.

Ajcharaporn Sawatpanich (A)

Bacteriology Division, Department of Microbiology, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.

Thiamjit Chaichana (T)

Department of Pathology, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.

Jutamas Wongphoom (J)

Department of Pathology, King Chulalongkorn Memorial Hospital, Thai Red Cross Society, Bangkok, Thailand.

Srihatach Ngarmukos (S)

Department of Orthopedics, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
Biologics for Knee Osteoarthritis Research Unit, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.

Mana Taweevisit (M)

Department of Pathology, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.

Sutada Lotinun (S)

Department of Physiology, Faculty of Dentistry, Chulalongkorn University, Bangkok, Thailand.
Center of Excellence in Skeletal Disorders and Enzyme Reaction Mechanism, Faculty of Dentistry, Chulalongkorn University, Bangkok, Thailand.

Somying Tumwasorn (S)

Bacteriology Division, Department of Microbiology, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.

Aree Tanavalee (A)

Department of Orthopedics, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
Biologics for Knee Osteoarthritis Research Unit, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.

Rangsima Reantragoon (R)

Immunology Division, Department of Microbiology, Faculty of Medicine, Chulalongkorn University, 1873 Rama 4 Road, Bangkok, 10330, Thailand. rangsima.reantragoon@gmail.com.
Center of Excellence in Immunology and Immune-Mediated Diseases, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand. rangsima.reantragoon@gmail.com.
Center of Excellence in Skeletal Disorders and Enzyme Reaction Mechanism, Faculty of Dentistry, Chulalongkorn University, Bangkok, Thailand. rangsima.reantragoon@gmail.com.

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