Lipocalin-2 Serum Levels in Rheumatoid Arthritis Patients Treated with Adalimumab and Its Correlation with Proinflammatory Factors.


Journal

Mediators of inflammation
ISSN: 1466-1861
Titre abrégé: Mediators Inflamm
Pays: United States
ID NLM: 9209001

Informations de publication

Date de publication:
2024
Historique:
received: 11 01 2024
revised: 15 08 2024
accepted: 04 09 2024
medline: 15 10 2024
pubmed: 15 10 2024
entrez: 15 10 2024
Statut: epublish

Résumé

Obesity is associated with an increased risk for different chronic diseases such as osteoarthritis (OA) or rheumatoid arthritis (RA). In fact, adipose tissue is now recognized as an endocrine organ able to secrete a wide variety of factors called adipokines, which have been demonstrated to participate in the pathophysiology of RA by regulating inflammation and immunity. LCN2 is one of these adipose tissue-derived factors. However, scarce information is available about the levels of this adipokine in different rheumatic diseases. Therefore, we aimed to analyze LCN2 serum levels in healthy, OA, and RA patients under different treatments. Serum levels of LCN2, among other proinflammatory and chemotactic factors, have been measured by ELISA or Multiplex in the following four groups of individuals: healthy, OA, and RA patients treated with conventional treatment or adalimumab. We found increased serum levels of LCN2 in OA and RA patients. Interestingly, LCN2 serum levels show a similar pattern to that observed for different proinflammatory and chemotactic factors, being increased in RA conventional treated patients in comparison to RA patients treated with adalimumab. Also, RA patients under conventional treatment revealed a positive and significant correlation between LCN2 and CCL2, CCL3, IL-8, IL-1 Our results clearly suggest that LCN2 is modulated and associated with inflammation in rheumatic diseases. Therefore, the serum levels of this adipokine might be used as an additional biomarker of the inflammatory/disease activity.

Sections du résumé

Background UNASSIGNED
Obesity is associated with an increased risk for different chronic diseases such as osteoarthritis (OA) or rheumatoid arthritis (RA). In fact, adipose tissue is now recognized as an endocrine organ able to secrete a wide variety of factors called adipokines, which have been demonstrated to participate in the pathophysiology of RA by regulating inflammation and immunity. LCN2 is one of these adipose tissue-derived factors. However, scarce information is available about the levels of this adipokine in different rheumatic diseases. Therefore, we aimed to analyze LCN2 serum levels in healthy, OA, and RA patients under different treatments.
Methods UNASSIGNED
Serum levels of LCN2, among other proinflammatory and chemotactic factors, have been measured by ELISA or Multiplex in the following four groups of individuals: healthy, OA, and RA patients treated with conventional treatment or adalimumab.
Results UNASSIGNED
We found increased serum levels of LCN2 in OA and RA patients. Interestingly, LCN2 serum levels show a similar pattern to that observed for different proinflammatory and chemotactic factors, being increased in RA conventional treated patients in comparison to RA patients treated with adalimumab. Also, RA patients under conventional treatment revealed a positive and significant correlation between LCN2 and CCL2, CCL3, IL-8, IL-1
Conclusions UNASSIGNED
Our results clearly suggest that LCN2 is modulated and associated with inflammation in rheumatic diseases. Therefore, the serum levels of this adipokine might be used as an additional biomarker of the inflammatory/disease activity.

Identifiants

pubmed: 39403549
doi: 10.1155/2024/7264704
pmc: PMC11473169
doi:

Substances chimiques

Adalimumab FYS6T7F842
Lipocalin-2 0
Chemokine CCL2 0
Interleukin-6 0
LCN2 protein, human 0
Interleukin-8 0
Interleukin-1beta 0
Chemokine CCL3 0
C-Reactive Protein 9007-41-4

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

7264704

Informations de copyright

Copyright © 2024 Javier Conde-Aranda et al.

Déclaration de conflit d'intérêts

The authors have no conflicts of interest to declare.

Auteurs

Javier Conde-Aranda (J)

Molecular and Cellular Gastroenterology, Health Research Institute of Santiago de Compostela (IDIS), Santiago de Compostela, Spain.

Morena Scotece (M)

SERGAS (Health Service from Galicia) and IDIS (Health Research Institute of Santiago de Compostela), The NEIRID Lab (Neuroendocrine Interactions in Rheumatology and Inflammatory Diseases), Research Laboratory 9, Santiago University Clinical Hospital, Santiago de Compostela, Spain.

María Varela-García (M)

SERGAS (Health Service from Galicia) and IDIS (Health Research Institute of Santiago de Compostela), The NEIRID Lab (Neuroendocrine Interactions in Rheumatology and Inflammatory Diseases), Research Laboratory 9, Santiago University Clinical Hospital, Santiago de Compostela, Spain.

Carlos Torrijos-Pulpón (C)

SERGAS (Health Service from Galicia) and IDIS (Health Research Institute of Santiago de Compostela), The NEIRID Lab (Neuroendocrine Interactions in Rheumatology and Inflammatory Diseases), Research Laboratory 9, Santiago University Clinical Hospital, Santiago de Compostela, Spain.

Laura Arosa (L)

Molecular and Cellular Gastroenterology, Health Research Institute of Santiago de Compostela (IDIS), Santiago de Compostela, Spain.

Miguel Camba-Gómez (M)

Molecular and Cellular Gastroenterology, Health Research Institute of Santiago de Compostela (IDIS), Santiago de Compostela, Spain.

Jesús Pino (J)

SERGAS (Health Service from Galicia), Division of Orthopaedics Surgery and Traumatology, Santiago University Clinical Hospital, Santiago de Compostela, Spain.
Department of Surgery and Medical-Surgery Specialities, University of Santiago de Compostela, Santiago de Compostela, Spain.

Oreste Gualillo (O)

SERGAS (Health Service from Galicia) and IDIS (Health Research Institute of Santiago de Compostela), The NEIRID Lab (Neuroendocrine Interactions in Rheumatology and Inflammatory Diseases), Research Laboratory 9, Santiago University Clinical Hospital, Santiago de Compostela, Spain.

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Classifications MeSH