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Inactivation of the gene encoding procalcitonin prevents antibody-mediated arthritis

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Inactivation of the gene encoding procalcitonin prevents antibody-mediated arthritis. / Maleitzke, Tazio; Dietrich, Tamara; Hildebrandt, Alexander; Weber, Jérôme; Appelt, Jessika; Jahn, Denise; Otto, Ellen; Zocholl, Dario; Jiang, Shan; Baranowsky, Anke; Duda, Georg N; Tsitsilonis, Serafeim; Keller, Johannes.

In: Inflammation research : official journal of the European Histamine Research Society ... [et al.], Vol. 72, No. 5, 05.2023, p. 1069-1081.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Maleitzke, T, Dietrich, T, Hildebrandt, A, Weber, J, Appelt, J, Jahn, D, Otto, E, Zocholl, D, Jiang, S, Baranowsky, A, Duda, GN, Tsitsilonis, S & Keller, J 2023, 'Inactivation of the gene encoding procalcitonin prevents antibody-mediated arthritis', Inflammation research : official journal of the European Histamine Research Society ... [et al.], vol. 72, no. 5, pp. 1069-1081. https://doi.org/10.1007/s00011-023-01719-x

APA

Maleitzke, T., Dietrich, T., Hildebrandt, A., Weber, J., Appelt, J., Jahn, D., Otto, E., Zocholl, D., Jiang, S., Baranowsky, A., Duda, G. N., Tsitsilonis, S., & Keller, J. (2023). Inactivation of the gene encoding procalcitonin prevents antibody-mediated arthritis. Inflammation research : official journal of the European Histamine Research Society ... [et al.], 72(5), 1069-1081. https://doi.org/10.1007/s00011-023-01719-x

Vancouver

Maleitzke T, Dietrich T, Hildebrandt A, Weber J, Appelt J, Jahn D et al. Inactivation of the gene encoding procalcitonin prevents antibody-mediated arthritis. Inflammation research : official journal of the European Histamine Research Society ... [et al.]. 2023 May;72(5):1069-1081. https://doi.org/10.1007/s00011-023-01719-x

Bibtex

@article{00599827090341fd9fa7cf0f2d025b8a,
title = "Inactivation of the gene encoding procalcitonin prevents antibody-mediated arthritis",
abstract = "BACKGROUND: Procalcitonin (PCT) is applied as a sensitive biomarker to exclude bacterial infections in patients with rheumatoid arthritis (RA) flare-ups. Beyond its diagnostic value, little is known about the pathophysiological role of PCT in RA.METHODS: Collagen antibody-induced arthritis (CAIA) was induced in Calca-deficient mice (Calca-/-), lacking PCT (n = 15), and wild-type (WT) mice (n = 13), while control (CTRL) animals (n = 8 for each genotype) received phosphate-buffered saline. Arthritis severity and grip strength were assessed daily for 10 or 48 days. Articular inflammation, cartilage degradation, and bone lesions were assessed by histology, gene expression analysis, and µ-computed tomography.RESULTS: Serum PCT levels and intra-articular PCT expression increased following CAIA induction. While WT animals developed a full arthritic phenotype, Calca-deficient mice were protected from clinical and histological signs of arthritis and grip strength was preserved. Cartilage turnover markers and Tnfa were exclusively elevated in WT mice. Calca-deficient animals expressed increased levels of Il1b. Decreased bone surface and increased subchondral bone porosity were observed in WT mice, while Calca-deficiency preserved bone integrity.CONCLUSION: The inactivation of Calca and thereby PCT provided full protection from joint inflammation and arthritic bone loss in mice exposed to CAIA. Together with our previous findings on the pathophysiological function of Calca-derived peptides, these data indicate an independent pro-inflammatory role of PCT in RA.",
author = "Tazio Maleitzke and Tamara Dietrich and Alexander Hildebrandt and J{\'e}r{\^o}me Weber and Jessika Appelt and Denise Jahn and Ellen Otto and Dario Zocholl and Shan Jiang and Anke Baranowsky and Duda, {Georg N} and Serafeim Tsitsilonis and Johannes Keller",
note = "{\textcopyright} 2023. The Author(s), under exclusive licence to Springer Nature Switzerland AG.",
year = "2023",
month = may,
doi = "10.1007/s00011-023-01719-x",
language = "English",
volume = "72",
pages = "1069--1081",
journal = "INFLAMM RES",
issn = "1023-3830",
publisher = "Birkhauser Verlag Basel",
number = "5",

}

RIS

TY - JOUR

T1 - Inactivation of the gene encoding procalcitonin prevents antibody-mediated arthritis

AU - Maleitzke, Tazio

AU - Dietrich, Tamara

AU - Hildebrandt, Alexander

AU - Weber, Jérôme

AU - Appelt, Jessika

AU - Jahn, Denise

AU - Otto, Ellen

AU - Zocholl, Dario

AU - Jiang, Shan

AU - Baranowsky, Anke

AU - Duda, Georg N

AU - Tsitsilonis, Serafeim

AU - Keller, Johannes

N1 - © 2023. The Author(s), under exclusive licence to Springer Nature Switzerland AG.

PY - 2023/5

Y1 - 2023/5

N2 - BACKGROUND: Procalcitonin (PCT) is applied as a sensitive biomarker to exclude bacterial infections in patients with rheumatoid arthritis (RA) flare-ups. Beyond its diagnostic value, little is known about the pathophysiological role of PCT in RA.METHODS: Collagen antibody-induced arthritis (CAIA) was induced in Calca-deficient mice (Calca-/-), lacking PCT (n = 15), and wild-type (WT) mice (n = 13), while control (CTRL) animals (n = 8 for each genotype) received phosphate-buffered saline. Arthritis severity and grip strength were assessed daily for 10 or 48 days. Articular inflammation, cartilage degradation, and bone lesions were assessed by histology, gene expression analysis, and µ-computed tomography.RESULTS: Serum PCT levels and intra-articular PCT expression increased following CAIA induction. While WT animals developed a full arthritic phenotype, Calca-deficient mice were protected from clinical and histological signs of arthritis and grip strength was preserved. Cartilage turnover markers and Tnfa were exclusively elevated in WT mice. Calca-deficient animals expressed increased levels of Il1b. Decreased bone surface and increased subchondral bone porosity were observed in WT mice, while Calca-deficiency preserved bone integrity.CONCLUSION: The inactivation of Calca and thereby PCT provided full protection from joint inflammation and arthritic bone loss in mice exposed to CAIA. Together with our previous findings on the pathophysiological function of Calca-derived peptides, these data indicate an independent pro-inflammatory role of PCT in RA.

AB - BACKGROUND: Procalcitonin (PCT) is applied as a sensitive biomarker to exclude bacterial infections in patients with rheumatoid arthritis (RA) flare-ups. Beyond its diagnostic value, little is known about the pathophysiological role of PCT in RA.METHODS: Collagen antibody-induced arthritis (CAIA) was induced in Calca-deficient mice (Calca-/-), lacking PCT (n = 15), and wild-type (WT) mice (n = 13), while control (CTRL) animals (n = 8 for each genotype) received phosphate-buffered saline. Arthritis severity and grip strength were assessed daily for 10 or 48 days. Articular inflammation, cartilage degradation, and bone lesions were assessed by histology, gene expression analysis, and µ-computed tomography.RESULTS: Serum PCT levels and intra-articular PCT expression increased following CAIA induction. While WT animals developed a full arthritic phenotype, Calca-deficient mice were protected from clinical and histological signs of arthritis and grip strength was preserved. Cartilage turnover markers and Tnfa were exclusively elevated in WT mice. Calca-deficient animals expressed increased levels of Il1b. Decreased bone surface and increased subchondral bone porosity were observed in WT mice, while Calca-deficiency preserved bone integrity.CONCLUSION: The inactivation of Calca and thereby PCT provided full protection from joint inflammation and arthritic bone loss in mice exposed to CAIA. Together with our previous findings on the pathophysiological function of Calca-derived peptides, these data indicate an independent pro-inflammatory role of PCT in RA.

U2 - 10.1007/s00011-023-01719-x

DO - 10.1007/s00011-023-01719-x

M3 - SCORING: Journal article

C2 - 37039837

VL - 72

SP - 1069

EP - 1081

JO - INFLAMM RES

JF - INFLAMM RES

SN - 1023-3830

IS - 5

ER -