Specific binding of lipocortin‐1 (annexin I) to monocytes and neutrophils is decreased in rheumatoid arthritis

Goulding, N J; Jefferiss, Carolyn M.; Pan, Luying; Rigby, William F.C.; Guyre, Paul M.

doi:10.1002/art.1780351126

Cited by 37 publications

(30 citation statements)

References 15 publications

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“…Blood phagocytes from patients with active rheumatoid arthritis have a binding capacity that is only 10% of that of healthy controls, or patients with psoriasis or ankylosing spondylitis. Levels of annexin-I binding return to near normal in phagocytes isolated from peripheral blood of patients with quiescent disease, who are receiving disease-modifying antirheumatic drugs [65].…”

Section: Annexin-i-binding Proteinsmentioning

confidence: 99%

Novel pathways for glucocorticoid effects on neutrophils in chronic inflammation

Goulding¹,

Euzger²,

Butt³

et al. 1998

Inflammation Research

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Neutrophils have been implicated in mediating much of the tissue damage associated with chronic inflammatory diseases such as rheumatoid arthritis, where they are involved in destruction of both cartilage and bone. Glucocorticoids are powerful anti-inflammatory agents, often used in the treatment of this autoimmune disease. They exert significant inhibitory effects on neutrophil activation and functions, such as chemotaxis, adhesion, transmigration, apoptosis, oxidative burst, and phagocytosis. The mechanisms by which glucocorticoids exert these effects on neutrophils are unclear. Evidence from studies of inflammation in human subjects and animal models suggests that annexin-I an endogenous, glucocorticoid-induced protein also known as lipocortin-1, has a pivotal role in modulating neutrophil activation, transmigratory, and phagocytic functions. Furthermore, we present evidence for altered neutrophil functions in rheumatoid arthritis that correspond to a significantly reduced capacity of these cells to bind annexin-I. A proposed novel pathway for glucocorticoid actions on neutrophils involving annexin-I could explain the development of chronic neutrophil activation in diseases such as rheumatoid arthritis.

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Section: Annexin-i-binding Proteinsmentioning

confidence: 99%

Novel pathways for glucocorticoid effects on neutrophils in chronic inflammation

Goulding¹,

Euzger²,

Butt³

et al. 1998

Inflammation Research

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“…For example, rheumatoid leukocytes exhibit reduced annexin A1 production in response to corticosteroid 7 and a reduction in the level of specific annexin A1 binding molecules on the surface ofbloodmonocytesandpolymorphonuclear cells. 8 Inaddition,previousstudieshavedemonstrated that the levels of annexin A1 in human nasal lavage fluids and bronchoalveolar lavage fluids are altered in inflammatory airway disorders.…”

Section: Arch Otolaryngol Head Neck Surg 2004;130:211-215mentioning

confidence: 97%

Expression of Annexin A1 in Normal and Chronically Inflamed Nasal Mucosa

Rodrigo¹,

García-Pedrero²,

González³

et al. 2004

Arch Otolaryngol Head Neck Surg

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Objective: To examine the expression pattern of annexin A1 in normal and chronically inflamed nasal mucosa to investigate its possible role in nasal inflammation.Design: Immunohistochemical analysis.Subjects: Samples of middle turbinates from 5 healthy subjects and 5 patients with perennial rhinitis, and samples of nasal polyps from 7 patients.Interventions: Annexin A1 expression was examined with a standard immunohistochemical protocol on paraffin-embedded sections.Results: Annexin A1 was highly expressed by ciliated cells, where it was concentrated on the apical surface and within the cilia. Goblet cells and nondifferentiated basal

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“…The molecular identity of the annexin I binding site has also not been elucidated. Flow cytometric analysis has proved invaluable in the identification of specific, saturable cell-surface annexin I binding sites on human and murine peripheral blood monocytes and neutrophils and on rat pituitary cells (1,8,9,20). This is the first report to describe annexin I binding sites on synovial cells.…”

mentioning

confidence: 91%

“…Saturable, specific binding sites for annexin I were first identified on human peripheral blood leukocytes (1). At sites of inflammation in vivo and in peripheral blood from rheumatoid arthritis (RA) patients, leukocyte annexin I binding sites are markedly reduced (8,9).…”

mentioning

confidence: 99%

“…Our finding of reduced annexin I binding sites on RA compared with OA FLS is consistent with the findings of other studies concerning the effects of inflammation on annexin I binding. Annexin I binding sites are reduced on leukocytes at sites of inflammation in vivo, and studies in RA peripheral blood have shown reduced leukocyte annexin I binding sites compared with healthy control subjects (8,9). Assuming that the numbers of annexin I binding sites are important in the antiinflammatory effects of annexin I and glucocorticoids, reduced numbers of binding sites on RA cells may contribute to incomplete control of inflammation by endogenous and therapeutic glucocorticoids in RA.…”

mentioning

confidence: 99%

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Annexin I surface binding sites and their regulation on human fibroblast-like synoviocytes

Sampey

Hutchinson

Morand

2000

Arthritis & Rheumatism

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Objective. Annexin I is a glucocorticoid-inducible protein whose expression in rheumatoid synovium and inhibitory actions in animal models of arthritis suggests its involvement in human arthritis. The present study explored the potential for annexin I to mediate its antiinflammatory actions via specific cell-surface binding sites on human fibroblast-like synoviocytes (FLS).Methods. Annexin I binding sites on cultured FLS from patients with osteoarthritis (OA) and rheumatoid arthritis (RA) were determined by ligand-binding flow cytometry. Phospholipase A 2 (PLA 2 ) activity was determined by arachidonic acid release.Results.

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Specific binding of lipocortin‐1 (annexin I) to monocytes and neutrophils is decreased in rheumatoid arthritis

Cited by 37 publications

References 15 publications

Novel pathways for glucocorticoid effects on neutrophils in chronic inflammation

Novel pathways for glucocorticoid effects on neutrophils in chronic inflammation

Expression of Annexin A1 in Normal and Chronically Inflamed Nasal Mucosa

Annexin I surface binding sites and their regulation on human fibroblast-like synoviocytes

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