Expression of neutrophil activation markers and neutrophil adhesion to chondrocytes in rheumatoid arthritis patients: relationship with disease activity

Clerck, Luc S. De; Gendt, C.M. De; Bridts, Chris H.; Osselaer, Nancy Van; Stevens, W. J.

doi:10.1016/0923-2494(96)80241-0

Cited by 32 publications

(24 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…CD62L in particular showed a clear reduction below 50% on SFGs of all patients, as could be expected from earlier studies [23,24]. Besides the strong up-regulation of CD66 molecules on SFG in the majority of patients, we found only marginal changes in the expression of CD66b in two patients and CD66c in one patient (Fig.…”

Section: Discussionsupporting

confidence: 68%

Synovial PMN show a coordinated up-regulation of CD66 molecules

Hönig

Peter

Jantscheff

et al. 1999

Journal of Leukocyte Biology

View full text Add to dashboard Cite

Changes in the expression of various activation-dependent surface markers have been reported for polymorphonuclear neutrophils (PMN) isolated from synovial fluid of patients with inflammatory joint diseases. We extend these findings to the expression of CD66 molecules and several other surface markers. Three members of the CD66 family, namely CD66a, CD66b, and CD66c, showed an up to fourfold up-regulation on synovial fluid PMN compared with peripheral blood PMN (PBG) of the same patients; CD59 was increased twofold, the expression of CD16 did not change, whereas CD62L was reduced by more than 50% on synovial fluid PMN. It is interesting that CD66a, CD66b, and CD66c showed a coordinated expression on PBG of patients and controls and a coordinated up-regulation on synovial neutrophils. In contrast, after in vitro stimulation of peripheral blood PMN with phorbol myristate acetate, CD66c was much less up-regulated compared with CD66a and CD66b. All samples of synovial fluid PMN exhibited an additional increase in the expression of CD66a, CD66b, and CD66c when stimulated with phorbol myristate acetate in vitro. Prostaglandins are known to inhibit various responses of neutrophils to inflammatory stimuli. We could show that prostaglandins inhibit N-formyl-methionylleucyl-phenylalanine-induced up-regulation of CD66 on peripheral blood PMN in a concentrationdependent manner. J. Leukoc. Biol. 66: 429-436; 1999.

show abstract

Section: Discussionsupporting

confidence: 68%

Synovial PMN show a coordinated up-regulation of CD66 molecules

Hönig

Peter

Jantscheff

et al. 1999

Journal of Leukocyte Biology

View full text Add to dashboard Cite

show abstract

“…3D). Neutrophil markers (Ela2, Itgb2, Ltf, and Fcgr1) (16,31,41,54) were upregulated only in Wakullainfected livers (Fig. 3D), in agreement with a large number of infiltrating neutrophils in the liver tissues (Fig.…”

Section: Vol 77 2009 Liver Microarray Of E Chaffeensis-infected MIsupporting

confidence: 66%

Liver Transcriptome Profiles Associated with Strain-SpecificEhrlichia chaffeensis-Induced Hepatitis in SCID Mice

Miura

Rikihisa

2009

Infect Immun

View full text Add to dashboard Cite

Infection of humans with Ehrlichia chaffeensis, the etiologic agent of human monocytic ehrlichiosis, can cause hepatitis of various levels of severity. When the three human isolates of E. chaffeensis, each belonging to a different genogroup, are inoculated into severe combined immunodeficiency mice, the order of severity of clinical signs and bacterial burden detected in the liver is as follows (from greatest to least severity and highest to lowest burden): strain Wakulla, followed by strain Liberty, followed by strain Arkansas. In this article, we used microarray analysis to define transcriptional profiles characteristic of the histopathological features in the mouse liver. Cytokine and chemokine profiles and their receptor profiles were strikingly different among the three strains of E. chaffeensis: gamma interferon, CCL5, CXCL1, CXCL2, CXCL7, CXCL9, interleukin 2 receptor gamma (IL2R␥), IL21R, CCR2, and CXCR6 were highly upregulated with strain Arkansas; and tumor necrosis factor (TNF), CCL2, CCL3, CCL5, CCL6, CCL12, CCL20, CXCL2, CXCL7, CXCL9, CXCL13, TNF receptor superfamily 9 (TNFRSF9), TNFRSF13␤, IL1R2, IL2R␥, IL20R␤, IL21R, CCR1, CCR2, and CXCR4 were highly upregulated with strain Wakulla. With strain Liberty, only CXCL13 was highly upregulated, and IL13R␣2 was downregulated. In livers infected with the Arkansas strain, monocytes/macrophages and NK cells were enriched in the granulomas and an increase in NK cell marker mRNAs was detected. Livers infected with the Wakulla strain displayed infiltration of significantly more neutrophils and an increase in neutrophil marker mRNAs. Genes commonly upregulated in liver tissue infected with the three strains are other host innate immune and inflammatory response genes, including those encoding several acute-phase proteins. Genes downregulated commonly are related to host physiologic functions. The results suggest that marked modulation of host cytokine and chemokine profiles by E. chaffeensis strains underlies the distinct host liver disease.Human monocytic ehrlichiosis (HME) was discovered in 1986 (34), and the etiologic agent, a monocyte-tropic Ehrlichia species, was isolated several years later and named Ehrlichia chaffeensis (15). HME is one of the most prevalent life-threatening tick-borne zoonoses in North America and was designated a nationally notifiable disease in 1998 (35). HME is an acute febrile illness characterized by headache, malaise, nausea, and myalgia and/or arthralgia and frequently accompanied by leukopenia, thrombocytopenia, anemia, and elevation of hepatic transaminase levels (43). The severity of HME, however, varies from subclinical infection to death. A previous investigation of the pathology of injury in liver tissues from five immunocompetent patients, one human immunodeficiency virus (HIV)-infected patient, and one monoclonal gammopathy patient with laboratory-confirmed HME revealed scattered lobular lymphohistiocytic foci and diffuse lymphohistiocytic infiltration and Kupffer cell hyperplasia with moderate cholestasis (cholestasis w...

show abstract

“…Neutrophils are considered important in the pathogenesis of arthritis, for example, because of their ability to destroy cartilage [42][43][44][45]. In the human system, IL-8 is the most potent, neutrophil-activating chemokine, whereas other Glu-Leu-Arg (ELR) ϩ CXC chemokines, such as GCP-2/CXCL6, are weaker Blocking experiments were performed as described in Materials and Methods.…”

Section: Discussionmentioning

confidence: 99%