The Effect of Some Anti-inflammatory Agents on Elastase Release From Neutrophils In-vitro

Adeyemi, Edward O.; Chadwick, V. S.; Hodgson, H. J. F.

doi:10.1111/j.2042-7158.1990.tb06601.x

Cited by 15 publications

(7 citation statements)

References 18 publications

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“…In particular, non-steroidal anti-inflammatory drugs at therapeutic levels may inhibit elastase release [7]. Consistently, at day 2 we observed a decrease in elastase-aAT levels; in one of the four patients this dropped to one third of the value on day 1.…”

supporting

confidence: 66%

Neutrophil activation in ivermectin-treated onchocerciasis patients

Njoo

Hack

Oosting

et al. 1993

Clinical and Experimental Immunology

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SUMMARY Invermectin is a safe and effective drug for onchocerciasis treatment. In certain individuals, however, therapy is accompanied by adverse reactions. The mechanisms underlying these reactions are not yet known. The aim of the present study was to investigate whether neutrophils are involved in the development of these adverse reactions. Elastase and lactoferrin, two markers for the release of neutrophil azurophilic and specific granule contents respectively, were measured by radioimmunoassays in plasma of onchocerciasis patients with varying degrees of side effects, as well as in control subjects before and 1 and 2 days after ivermectin treatment. A considerable increase of elastase levels after treatment was observed, whereas lactoferrin levels did not change. The percentage of patients with elevated elastase levels was significantly correlated with the degree of side effects. These findings suggest that neutrophil activation may be involved in the development of adverse reactions in these patients.

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supporting

confidence: 66%

Neutrophil activation in ivermectin-treated onchocerciasis patients

Njoo

Hack

Oosting

et al. 1993

Clinical and Experimental Immunology

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“…As shown in Table 2, although prednisolone therapy had little effect on the tissue MPO activity, the NE activity of the prednisolone-treated group was significantly decreased compared with that of the colitis control group. Since it has been reported that the release of NE is inhibited by prednisolone in vitro [1], the decrease of luminal NE activity caused by prednisolone in our colitis model may have been due to blocking the release of NE by infiltrating neutrophils. Furthermore, although prednisolone did not significantly decrease the ulcer area, a tendency toward decrease was noted.…”

Section: Discussionmentioning

confidence: 70%

Colonic Ulceration and Increase of Neutrophil Elastase Activity in the Acetic Acid-Induced Colitis Model in Syrian Hamsters

Hirota

Suzuki

Yamaguchi

et al. 2004

The Journal of Veterinary Medical Science

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ABSTRACT. A novel colitis model using Syrian hamsters was developed. Colitis was induced by intracolonic administration of 1% acetic acid, and the ulcer area, tissue myeloperoxidase (MPO) activity, and luminal neutrophil elastase (NE) activity of the colon were determined at 1, 3, 8, 24 and 48 hr after colitis induction. The histopathological changes of the colon were also examined in this m odel. An increase of tissue MPO activity and NE activity was evident at 3 hr after induction of colitis, peaked at 24 hr, and decreased subsequently. The increase of luminal NE activity was well correlated with the colonic ulcer area. In histopathological examination, ulceration, erosion, crypt abscesses, neutrophil infiltration, hemorrhage, and edema were seen. The effects of prednisolone were examined to evaluate the adequacy of our colitis model. Syrian hamsters were treated orally with prednisolone at 18 and 1 hr before and at 6 hr after induction of colitis, and the ulcer area, tissue MPO activity, and luminal NE activity were evaluated at 24 hr after colitis induction. Prednisolone therapy had little effect on the tissue MPO activity. However, the NE activity of the prednisolone-treated group was significantly decreased. In addition, although prednisolone did not significantly decrease the ulcer area, a tendency toward decrease was noted. We conclude that this new model of experimental colitis in Syrian hamsters is useful for investigating the pathophysiology of colitis, especially useful for studying the relationship between colitis and NE activity. KEY WORDS: acetic acid, colitis model, neutrophil elastase, Syrian hamster.J. Vet. Med. Sci. 66(4): 417-422, 2004 Inflammatory bowel disease (IBD) is a general term for a group of chronic inflammatory conditions of the gastrointestinal tract, including ulcerative colitis and Crohn's disease. These are intractable inflammatory diseases of unknown etiology that are characterized by repeated exacerbations and remissions. The symptoms include diarrhea, bloody stools, and abdominal pain, while the histological findings are ulceration, inflammatory cell infiltration, and accumulation of neutrophils in the intestinal crypts (socalled crypt abscesses) [3,5]. Although numerous authors have discussed the pathogenesis of IBD, the precise mechanisms of onset and exacerbation have not been clarified. Recently, toxic products of neutrophils such as reactive oxygen species (ROS) and proteases, including cathepsin and elastase, have been suggested to play an important role in the pathogenesis of IBD [10,13,[19][20][21].Neutrophil elastase (NE) is a protease found in neutrophil granules that is known to have a broad-spectrum proteolytic activity against various proteins, such as elastin and type I-IV collagen. Release of NE during inflammation is related to degradation of connective tissues and an increase of vascular permeability, thus causing tissue damage and organ failure [6,7]. It has been reported that α1-protease inhibitor (α1-PI), an endogenous inhibitor of NE, is inactivated by...

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“…Lysosomal stabilisation by CQ and other anti-malarials Therapy and pharmacological properties of hydroxychloroquine and chloroquine could conceivably be a major site of action of these drugs in controlling degradation of connective tissues in arthritic conditions (Whitehouse and Cowley 1966). Several studies have shown that CQ inhibits degradation of proteoglycans in vitro and has direct effects on elastase and other enzymes released from macrophages (Whitehouse and Boström 1965;Cowey and Whitehouse 1966;Fulkerson et al 1979;Famaey and Fontaine 1980;Ackerman et al 1981;Tauber et al 1985;Bartholomew and Lowther 1987;Adeyemi et al 1990;Kamal and Bassiouni 1992;Schug and Kalbhen 1995;Lullmann-Rauch et al 1996). The central role of the destruction of cartilage (and bone) by pro-inflammatory cytokines (IL-1, TNFa) in arthritic conditions has been well recognised for several decades (Etherington et al 1981;Cox and Duff 1996).…”

Section: Cartilage Metabolism and Degradationmentioning

confidence: 96%

Therapy and pharmacological properties of hydroxychloroquine and chloroquine in treatment of systemic lupus erythematosus, rheumatoid arthritis and related diseases

et al. 2015

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HCQ and CQ have a good reputation for being effective and relatively safe treatments in SLE, mild-moderate RA and Sjøgren's syndrome. There is need for (a) more information on their mode of action in relation to the control of these diseases, (b) scope for developing formulations that have improved pharmacokinetic and therapeutic properties and safety, and (c) further exploring their use in drug combinations not only with other disease modifying agents but also with biologics.

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The Effect of Some Anti-inflammatory Agents on Elastase Release From Neutrophils In-vitro

Cited by 15 publications

References 18 publications

Neutrophil activation in ivermectin-treated onchocerciasis patients

Neutrophil activation in ivermectin-treated onchocerciasis patients

Colonic Ulceration and Increase of Neutrophil Elastase Activity in the Acetic Acid-Induced Colitis Model in Syrian Hamsters

Therapy and pharmacological properties of hydroxychloroquine and chloroquine in treatment of systemic lupus erythematosus, rheumatoid arthritis and related diseases

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