Chemokine and Cytokine Profiles in Patients with Hand Osteoarthritis
Jazyk angličtina Země Švýcarsko Médium electronic
Typ dokumentu časopisecké články, práce podpořená grantem
Grantová podpora
023728
ministry of health of czech republic - International
023728
ministry of health of czech republic for conceptual research development - International
260 523
Specific Academic Research Projects Competition - International
PubMed
33375165
PubMed Central
PMC7822191
DOI
10.3390/biom11010004
PII: biom11010004
Knihovny.cz E-zdroje
- Klíčová slova
- chemokines, cytokines, erosive disease, hand osteoarthritis,
- MeSH
- chemokin CCL11 krev MeSH
- chemokin CCL2 krev MeSH
- chemokiny krev MeSH
- cytokiny krev MeSH
- interleukin-8 krev MeSH
- lidé středního věku MeSH
- lidé MeSH
- osteoartróza krev patologie MeSH
- progrese nemoci MeSH
- ruka patofyziologie MeSH
- senioři MeSH
- TNF-alfa krev MeSH
- zánět krev patofyziologie MeSH
- Check Tag
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- chemokin CCL11 MeSH
- chemokin CCL2 MeSH
- chemokiny MeSH
- cytokiny MeSH
- interleukin-8 MeSH
- TNF-alfa MeSH
BACKGROUND: The development of hand osteoarthritis (HOA) and its progression into the erosive subset are unclear, but inflammation is suspected to be the main source. To verify the involvement of inflammation in HOA pathogenesis, we evaluate serum inflammatory mediators and their association with HOA-related clinical features in patients. METHODS: 153 participants (50 non-erosive HOA patients, 54 erosive HOA patients, and 49 healthy control subjects) were included in this study. All patients underwent clinical examination, which included assessment of tender and swollen small hand joints, ultrasound (US) examination, and self-reported measures (e.g., AUSCAN or algofunctional indexes). Serum inflammatory mediators were quantified using human cytokine 27-plex immunoassay. We employed linear modelling, correlation analysis, and resampling statistics to evaluate the association of these mediators to HOA. RESULTS: We identified increased levels of nine inflammatory mediators (e.g., eotaxin, monocyte chemoattractant protein 1, interleukin-8, and tumour necrosis factor) in HOA patients compared to healthy controls. Increased mediators correlated with ultrasound findings as well as with clinically tender and swollen joint counts in patients with erosive HOA. However, none of the mediators distinguished between erosive and non-erosive HOA subtypes. CONCLUSION: Our findings support the hypothesis on the involvement of inflammation in HOA.
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