Temporal expression of inflammatory cytokines and chemokines in rat adjuvant-induced arthritis

Z. Szekanecz, Margaret M. Halloran, Michael V. Volin, James M. Woods, Robert M. Strieter, G. Kenneth Haines, Steven L. Kunkel, Marie D. Burdick, Alisa E. Koch

Research output: Contribution to journalArticle

137 Citations (Scopus)

Abstract

Objective. To examine cytokine and chemokine production during the evolution of rat adjuvant-induced arthritis (AIA), a model of rheumatoid arthritis. Methods. Clinical and laboratory assessment of the course of AIA was performed over a 47-day period. Levels of the cytokines tumor necrosis factor α (TNFα), interleukin-1β (IL-1β), and IL-6, as well as levels of the chemokines macrophage inflammatory protein 1α (MIP,1α) and JE, the murine homolog of monocyte chemoattractant protein 1, were determined by enzyme-linked immunosorbent assay in the sera and joints of AIA and control rats. Synovia from AIA rats were (immuno)histochemically analyzed. Results of cytokine and chemokine measurements were correlated with clinical and laboratory markers of inflammation and histology. Results. Early (before day 14 post adjuvant injection) and later phases of AIA could be distinguished. Cytokine and chemokine production was increased in AIA versus control rats. The production of TNFα, IL-1β, MIP-1α, and, as determined earlier, epithelial neutrophil-activating peptide 78-like protein was abundant prior to and during the course of AIA, while that of 1L-6 and JE was elevated in the late phase of AIA. Cytokine and chemokine levels were correlated with the clinical symptoms of arthritis and blood neutrophil counts. Joint levels of IL-1β showed correlation with synovial lining proliferation and neutrophil ingress into AIA synovium. Conclusion. Cytokines and chemokines are involved in the clinical, laboratory, and histologic changes underlying AIA. The production of these mediators may be temporally and spatially regulated. These findings may be important for the optimal timing of cytokine and chemokine targeting.

Original languageEnglish
Pages (from-to)1266-1277
Number of pages12
JournalArthritis and Rheumatism
Volume43
Issue number6
DOIs
Publication statusPublished - Jun 2000

Fingerprint

Experimental Arthritis
Chemokines
Cytokines
Interleukin-1
Neutrophils
Tumor Necrosis Factor-alpha
Joints
Biomarkers
Macrophage Inflammatory Proteins
Synovial Membrane
Chemokine CCL2
Synovial Fluid
Arthritis
Interleukin-6
Rheumatoid Arthritis
Histology
Enzyme-Linked Immunosorbent Assay
Inflammation
Injections

ASJC Scopus subject areas

  • Immunology
  • Rheumatology

Cite this

Temporal expression of inflammatory cytokines and chemokines in rat adjuvant-induced arthritis. / Szekanecz, Z.; Halloran, Margaret M.; Volin, Michael V.; Woods, James M.; Strieter, Robert M.; Haines, G. Kenneth; Kunkel, Steven L.; Burdick, Marie D.; Koch, Alisa E.

In: Arthritis and Rheumatism, Vol. 43, No. 6, 06.2000, p. 1266-1277.

Research output: Contribution to journalArticle

Szekanecz, Z, Halloran, MM, Volin, MV, Woods, JM, Strieter, RM, Haines, GK, Kunkel, SL, Burdick, MD & Koch, AE 2000, 'Temporal expression of inflammatory cytokines and chemokines in rat adjuvant-induced arthritis', Arthritis and Rheumatism, vol. 43, no. 6, pp. 1266-1277. https://doi.org/10.1002/1529-0131(200006)43:6<1266::AID-ANR9>3.0.CO;2-P
Szekanecz, Z. ; Halloran, Margaret M. ; Volin, Michael V. ; Woods, James M. ; Strieter, Robert M. ; Haines, G. Kenneth ; Kunkel, Steven L. ; Burdick, Marie D. ; Koch, Alisa E. / Temporal expression of inflammatory cytokines and chemokines in rat adjuvant-induced arthritis. In: Arthritis and Rheumatism. 2000 ; Vol. 43, No. 6. pp. 1266-1277.
@article{a39c5946773d4ab883b4b8903446d61e,
title = "Temporal expression of inflammatory cytokines and chemokines in rat adjuvant-induced arthritis",
abstract = "Objective. To examine cytokine and chemokine production during the evolution of rat adjuvant-induced arthritis (AIA), a model of rheumatoid arthritis. Methods. Clinical and laboratory assessment of the course of AIA was performed over a 47-day period. Levels of the cytokines tumor necrosis factor α (TNFα), interleukin-1β (IL-1β), and IL-6, as well as levels of the chemokines macrophage inflammatory protein 1α (MIP,1α) and JE, the murine homolog of monocyte chemoattractant protein 1, were determined by enzyme-linked immunosorbent assay in the sera and joints of AIA and control rats. Synovia from AIA rats were (immuno)histochemically analyzed. Results of cytokine and chemokine measurements were correlated with clinical and laboratory markers of inflammation and histology. Results. Early (before day 14 post adjuvant injection) and later phases of AIA could be distinguished. Cytokine and chemokine production was increased in AIA versus control rats. The production of TNFα, IL-1β, MIP-1α, and, as determined earlier, epithelial neutrophil-activating peptide 78-like protein was abundant prior to and during the course of AIA, while that of 1L-6 and JE was elevated in the late phase of AIA. Cytokine and chemokine levels were correlated with the clinical symptoms of arthritis and blood neutrophil counts. Joint levels of IL-1β showed correlation with synovial lining proliferation and neutrophil ingress into AIA synovium. Conclusion. Cytokines and chemokines are involved in the clinical, laboratory, and histologic changes underlying AIA. The production of these mediators may be temporally and spatially regulated. These findings may be important for the optimal timing of cytokine and chemokine targeting.",
author = "Z. Szekanecz and Halloran, {Margaret M.} and Volin, {Michael V.} and Woods, {James M.} and Strieter, {Robert M.} and Haines, {G. Kenneth} and Kunkel, {Steven L.} and Burdick, {Marie D.} and Koch, {Alisa E.}",
year = "2000",
month = "6",
doi = "10.1002/1529-0131(200006)43:6<1266::AID-ANR9>3.0.CO;2-P",
language = "English",
volume = "43",
pages = "1266--1277",
journal = "Arthritis and Rheumatology",
issn = "2326-5191",
publisher = "John Wiley and Sons Ltd",
number = "6",

}

TY - JOUR

T1 - Temporal expression of inflammatory cytokines and chemokines in rat adjuvant-induced arthritis

AU - Szekanecz, Z.

AU - Halloran, Margaret M.

AU - Volin, Michael V.

AU - Woods, James M.

AU - Strieter, Robert M.

AU - Haines, G. Kenneth

AU - Kunkel, Steven L.

AU - Burdick, Marie D.

AU - Koch, Alisa E.

PY - 2000/6

Y1 - 2000/6

N2 - Objective. To examine cytokine and chemokine production during the evolution of rat adjuvant-induced arthritis (AIA), a model of rheumatoid arthritis. Methods. Clinical and laboratory assessment of the course of AIA was performed over a 47-day period. Levels of the cytokines tumor necrosis factor α (TNFα), interleukin-1β (IL-1β), and IL-6, as well as levels of the chemokines macrophage inflammatory protein 1α (MIP,1α) and JE, the murine homolog of monocyte chemoattractant protein 1, were determined by enzyme-linked immunosorbent assay in the sera and joints of AIA and control rats. Synovia from AIA rats were (immuno)histochemically analyzed. Results of cytokine and chemokine measurements were correlated with clinical and laboratory markers of inflammation and histology. Results. Early (before day 14 post adjuvant injection) and later phases of AIA could be distinguished. Cytokine and chemokine production was increased in AIA versus control rats. The production of TNFα, IL-1β, MIP-1α, and, as determined earlier, epithelial neutrophil-activating peptide 78-like protein was abundant prior to and during the course of AIA, while that of 1L-6 and JE was elevated in the late phase of AIA. Cytokine and chemokine levels were correlated with the clinical symptoms of arthritis and blood neutrophil counts. Joint levels of IL-1β showed correlation with synovial lining proliferation and neutrophil ingress into AIA synovium. Conclusion. Cytokines and chemokines are involved in the clinical, laboratory, and histologic changes underlying AIA. The production of these mediators may be temporally and spatially regulated. These findings may be important for the optimal timing of cytokine and chemokine targeting.

AB - Objective. To examine cytokine and chemokine production during the evolution of rat adjuvant-induced arthritis (AIA), a model of rheumatoid arthritis. Methods. Clinical and laboratory assessment of the course of AIA was performed over a 47-day period. Levels of the cytokines tumor necrosis factor α (TNFα), interleukin-1β (IL-1β), and IL-6, as well as levels of the chemokines macrophage inflammatory protein 1α (MIP,1α) and JE, the murine homolog of monocyte chemoattractant protein 1, were determined by enzyme-linked immunosorbent assay in the sera and joints of AIA and control rats. Synovia from AIA rats were (immuno)histochemically analyzed. Results of cytokine and chemokine measurements were correlated with clinical and laboratory markers of inflammation and histology. Results. Early (before day 14 post adjuvant injection) and later phases of AIA could be distinguished. Cytokine and chemokine production was increased in AIA versus control rats. The production of TNFα, IL-1β, MIP-1α, and, as determined earlier, epithelial neutrophil-activating peptide 78-like protein was abundant prior to and during the course of AIA, while that of 1L-6 and JE was elevated in the late phase of AIA. Cytokine and chemokine levels were correlated with the clinical symptoms of arthritis and blood neutrophil counts. Joint levels of IL-1β showed correlation with synovial lining proliferation and neutrophil ingress into AIA synovium. Conclusion. Cytokines and chemokines are involved in the clinical, laboratory, and histologic changes underlying AIA. The production of these mediators may be temporally and spatially regulated. These findings may be important for the optimal timing of cytokine and chemokine targeting.

UR - http://www.scopus.com/inward/record.url?scp=0034125853&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034125853&partnerID=8YFLogxK

U2 - 10.1002/1529-0131(200006)43:6<1266::AID-ANR9>3.0.CO;2-P

DO - 10.1002/1529-0131(200006)43:6<1266::AID-ANR9>3.0.CO;2-P

M3 - Article

C2 - 10857785

AN - SCOPUS:0034125853

VL - 43

SP - 1266

EP - 1277

JO - Arthritis and Rheumatology

JF - Arthritis and Rheumatology

SN - 2326-5191

IS - 6

ER -