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001-es BibID:BIBFORM046367
Első szerző:Halloran, Margaret M.
Cím:Cellular adhesion molecules in rat adjuvant arthritis / Halloran M. M., Szekanecz Z., Barquin N., Haines G. K., Koch A. E.
Dátum:1996
ISSN:0004-3591
Megjegyzések:To examine adhesion molecule expression during the progression of inflammation in a rheumatoid arthritis model of adjuvant-induced arthritis (AIA) in rats. METHODS: Immunohistochemical analysis was used to determine the distribution of the following adhesion molecules: lymphocyte function-associated antigen 1 (LFA-1; CD11a/CD18), Mac-1 and p150/95 (CD11bc/CD18), intercellular adhesion molecule 1 (ICAM-1), and CD44 in tissue sections from the ankle joints of rats with AIA. Control animals and those with AIA were killed at intervals over a 54-day period after injection with mineral oil and Mycobacterium butyricum, respectively. RESULTS: CD44 and LFA-1 were expressed on lymphocytes, macrophages, and synovial (ST) lining cells. CD44 expression on macrophages was found to be increased compared with control animals by day 18, and was significantly increased by day 41. CD44 expression on lymphocytes significantly increased earlier, on days 11-18. Increased LFA-1 expression on macrophages occurred late, on day 41. LFA-1 expression on lymphocytes was significantly increased on days 25, 47, and 54. ST lining cells exhibited two distinct periods of increased expression, one early, on days 11-25 and one later, on days 41-54. CD11b/c was expressed on macrophages and ST lining cells, showing a significant increase on AIA rat ST lining cells compared with control animals on day 4. No differences in ICAM-1 expression on endothelial cells between rats with AIA and controls were found on any of the days examined. CONCLUSION: CD44 expression is up-regulated on macrophages and lymphocytes during the early development of AIA, while LFA-1 expression is up-regulated later in the development of AIA. The up-regulation of CD44 and LFA-1 at different times in the development of AIA suggests an important role for these adhesion molecules in establishing and sustaining an inflammatory response in the AIA joint.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Arthritis and Rheumatism. - 39 : 5 (1996), p. 810-819. -
További szerzők:Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus) Barquin, Nora Haines, G. Kenneth Koch, Alisa E.
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2.

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.
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3.

001-es BibID:BIBFORM034670
Első szerző:Szekanecz Zoltán (reumatológus, belgyógyász, immunológus)
Cím:Mediators of angiogenesis : the role of cellular adhesion molecules / Szekanecz Zoltán, Halloran, M. M., Haskell, C. J., Shah, M. R., Polverini, P. J., Koch, Alicia E.
Dátum:1999
Megjegyzések:Angiogenesis, the production of new blood vessels, plays an important role in a number of physiological and pathological processes, such as development, tissue repair, inflammation, atherosclerosis and tumor progression. A number of mediators including cytokines, growth factors and others, have been implicated in angiogenesis. During tissue neovascularization, endothelial cells(EC) adhere to extracellular matrix(ECM) components and other ECs, which is an essential process in angiogenesis. Thus, in addition to soluble mediators mentioned above, ECM macromolecules and cellular adhesion molecules(CAMs) may also act as angiogenic factors. Among CAMs, E-selectin, vascular cell adhesion molecule(VCAM)-1, CD31, and some integrins may facilitate capillary formation both in vivo and in vitro. CAMs, as well as other angiogenic mediators may play a role in the pathogenesis of "angiogenic diseases". Targeting of any of these factors may have potential therapeutic relevance in such disorders. (author abst.)
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Angiogenesis
Cellular Adhesion Molecules
külföldön készült közlemény
Megjelenés:Trends in Glycoscience and Glycotechnology. - 11 : 58 (1999), p. 73-93. -
További szerzők:Halloran, Margaret M. Haskell, C. J. Shah, M. R. Polverini, P. J. Koch, Alisa E.
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4.

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.
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DOI
Intézményi repozitóriumban (DEA) tárolt változat
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5.

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.
Internet cím:elektronikus változat
elektronikus változat
Szerző által megadott URL
DOI
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6.

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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