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001-es BibID:	BIBFORM007064
Első szerző:	Halloran, Margaret M.
Cím:	The role of an epithelial neutrophil-activating peptide-78-like protein in rat adjuvant-induced arthritis / Margaret M. Halloran, James M. Woods, Robert M. Strieter, Zoltan Szekanecz, Michael V. Volin, Shigeru Hosaka, G. Kenneth Haines III, Steven L. Kunkel, Marie D. Burdick, Alfred Walz, Alisa E. Koch
Dátum:	1999
ISSN:	0022-1767 (Print)
Megjegyzések:	The chemokine, epithelial neutrophil-activating peptide-78 (ENA-78), is a potent neutrophil chemotaxin whose expression is increased in inflamed synovial tissue and fluid in human rheumatoid arthritis compared with osteoarthritis. Since ENA-78 has been implicated in the pathogenesis of RA, we examined the expression of an ENA-78-like protein during the development of rat adjuvant-induced arthritis (AIA). Using an ELISA assay, we found increased levels of antigenic ENA-78-like protein in the sera of AIA animals compared with control normal animals by day 7 postadjuvant injection. ENA-78-like protein levels continued to increase as AIA developed. ENA-78-like protein levels in joint homogenates were increased in AIA animals later in the development of the disease, by day 18 during maximal arthritis, compared with control animals. Expression of ENA-78-like protein in both the AIA serum and joint correlated with the progression of inflammation of the joints. Anti-human ENA-78 administered before disease onset modified the severity of AIA, while administration of anti-ENA-78 after clinical onset of AIA did not modify the disease. These data support a role for an ENA-78-like protein as an important chemokine in the progression and maintenance of AIA.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Animals Arthritis, Experimental Cell Movement Chemokine CXCL5 Chemokines, CXC Epithelial Cells Female Immune Sera Injections, Intraperitoneal Interleukin-8 derivatives Neutrophil Activation Neutrophils Peritoneum Rats Rats, Inbred Lew Synovial Fluid Tarsus, Animal Time Factors
Megjelenés:	The Journal of Immunology 162 : 12 (1999), p. 7492-7500. -
További szerzők:	Woods, James M. Strieter, Robert M. Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus) Volin, Michael V. Hosaka, Shigeru Haines, Kenneth G. III. Kunkel, Steven L. Burdick, Marie D. Walz, Alfred Koch, Alisa E.
Internet cím:	Szerző által megadott URL Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM018159
Első szerző:	Szekanecz Zoltán (reumatológus, belgyógyász, immunológus)
Cím:	Temporal expression of cytokines and chemokines in rat adjuvant-induced arthritis / Szekanecz, Z., Halloran, M. M., Woods, J. M., Volin, M. V., Haines, G. K., Koch, A. E.
Dátum:	2001
ISSN:	1465-9905
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idézhető absztrakt
Megjelenés:	Arthritis Research. - 3 : Suppl. A. (2001), p. 9. -
További szerzők:	Halloran, Margaret M. Woods, James M. Volin, Michael V. Haines, G. Kenneth Koch, Alisa E.
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM007107
Első szerző:	Szekanecz Zoltán (reumatológus, belgyógyász, immunológus)
Cím:	Temporal expression of inflammatory cytokines and chemokines in rat adjuvant-induced arthritis / Szekanecz, Z., Halloran, M. M., Volin, M. V., Woods, J. M., Strieter, R. M., Kenneth Haines, G. 3rd, Kunkel, S. L., Burdick, M. D., Koch, A. E.
Dátum:	2000
ISSN:	0004-3591 (Print)
Megjegyzések:	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 a (TNFalpha), interleukin-1beta (IL-1beta), and IL-6, as well as levels of the chemokines macrophage inflammatory protein 1alpha (MIP-1alpha) 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 TNFalpha, IL-1beta, MIP-1alpha, and, as determined earlier, epithelial neutrophil-activating peptide 78-like protein was abundant prior to and during the course of AIA, while that of IL-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-1beta 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.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Animals Arthritis, Experimental Chemokines Cytokines Enzyme-Linked Immunosorbent Assay Female Inflammation Mediators Joints Kinetics Rats Rats, Inbred Lew Reference Values Synovitis Time Factors
Megjelenés:	Arthritis and Rheumatism. - 43 : 6 (2000), p. 1266-1277. -
További szerzők:	Halloran, Margaret M. Volin, Michael V. Woods, James M. Strieter, Robert M. Haines, Kenneth G. III. Kunkel, Steven L. Burdick, Marie D. Koch, Alisa E.
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001-es BibID:	BIBFORM045764
Első szerző:	Volin, Michael V.
Cím:	PECAM-1 and Leukosialin (CD43) Expression Correlate with Heightened Inflammation in Rat Adjuvant-Induced Arthritis / Volin Michael V., Szekanecz Zoltan, Halloran Margaret M., Woods James M., Magua Jessenia, Damergis John A. Jr., Haines Kenneth G. III., Crocker Paul R., Koch Alisa E.
Dátum:	1999
ISSN:	0014-4800
Megjegyzések:	A hallmark of both adjuvant-induced arthritis (AIA) and rheumatoid arthritis is chronic joint inflammation characterized by ingress of leukocytes into the inflamed synovial tissue. The timing of expression of adhesion molecules, which govern the ingress of leukocytes, is important in the orchestration of an inflammatory response. We examined the expression of vascular cell adhesion molecule-1 (VCAM-1), sialo adhesin, platelet and endothelial cell adhesion molecule-1 (PECAM-1), and leukosialin (CD43) in AIA, starting at adjuvant injection (day 0), through the peak of inflammation (day 18 postadjuvant injection), until day 54. VCAM-1 is constitutively expressed on the lining layer and ECs and its expression levels do not change throughout the progression of AIA. Sialoadhesin synovial tissue lining cell expression is decreased after adjuvant injection. In contrast, PECAM-1 expression is increased on synovial tissue lining cells on day 7 and is elevated through day 54 (peaking on day 54 with six-fold more cells expressing PECAM-1). PECAM-1 expression on endothelial cells peaks on day 7 with three-fold more cells expressing it, while on macrophages expression maximizes on day 25 with six-fold more cells expressing PECAM-1. CD43 expression is increased on synovial tissue lining cells, macrophages, neutrophils, and lymphocytes on days 18 and 25, before going back to basal levels. The increased expression of PECAM-1 and CD43 on leukocytes at the height of inflammation in AIA suggests important roles for these adhesion molecules in potentially binding their EC ligands resulting in leukocyte ingress into the synovial tissue.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Experimental And Molecular Pathology. - 66 : 3 (1999), p. 211-219. -
További szerzők:	Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus) Halloran, Margaret M. Woods, James M. Magua, Jessenia Damergis, John A. jr. Haines, Kenneth G. III. Crocker, Paul R. Koch, Alisa E.
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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