Defective release of C5a related chemo-attractant activity from complement in Crohn's disease.

Elmgreen, J; Berkowicz, Adela; Sørensen, H.

doi:10.1136/gut.24.6.525

Cited by 21 publications

(6 citation statements)

References 24 publications

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“…Activated plasma was fractionated on a column of Sephadex G 75 with Gey's solution including EDTA (10 mM) as previously described. 5 Fractions, with chemoattractant activity eluated in the MW 15 000 region, were pooled, dialysed against Gey's solution, frozen in liquid nitrogen, and kept at -70°C until analysis. Low molecular weight fractions prepared identically, except for the use of non-activated plasma, showed no chemoattractant activity.…”

mentioning

confidence: 99%

Subnormal activation of phagocytes by complement in chronic inflammatory bowel disease? Neutrophil chemotaxis to complement split product C5a.

Elmgreen¹

1984

Gut

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confidence: 99%

Subnormal activation of phagocytes by complement in chronic inflammatory bowel disease? Neutrophil chemotaxis to complement split product C5a.

Elmgreen¹

1984

Gut

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“…Activation of serum complement by cobra venom led to diminished consumption of complement 3 (C3) to C9 in Crohn's disease and in a subgroup of ulcerative colitis patients with extraintestinal complications (1). In Crohn's disease there is a decreased release of C5a by the alternative pathway (2). Inappropriate activation of phagocytic cells by complement split products like C5a may delay the clearance of foreign macromolecules penetrating the gut mucosa (2).…”

mentioning

confidence: 99%

Hypercatabolism of Complement in Crohn's Disease—Assessment of Circulating C3c

Elmgreen

Berkowicz

Sørensen

1983

Journal of Internal Medicine

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“…Elmgreen el al. reported a decreased serum chemo-attraetant activity in CD patients after in vitro activation of the alternative pathway [3).…”

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confidence: 95%

Humoral Inhibition of Neutrophil Chemotaxis in Crohn's Disease

D’Amelio¹,

Pallone²,

Moli³

et al. 1985

Scand J Immunol

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In patients with Crohn's disease (CD) we investigated the C3 conversion of zymosan-activated serum (ZAS) and looked for the occurrence of chemotactic factor inactivation (CFI). We also studied the cell-directed inhibitory effect (CDI) of the CD patients' plasma and, in the same group, complement activation and complement-mediated deactivation. The mean value of ZAS C3 conversion in CD was no different from that of healthy controls, but in steroid-treated patients it was lower than in untreated CD. CFI occurred in 1 of the 23 CD sera tested, and CDI was observed in 6 out of the 22 patients tested. EDTA C3 conversion was present in 12 patients, and complement-mediated deactivation was associated with high values of EDTA C3 conversion. Our findings indicate that complement dysfunction and inhibitory factors of neutrophil chemotaxis are present in CD. These findings could explain the defective neutrophil migration into skin windows. Whether they are relevant to the pathogenesis of tissue injury or of infectious complications and are specific for CD, however, remains to be established.

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Defective release of C5a related chemo-attractant activity from complement in Crohn's disease.

Cited by 21 publications

References 24 publications

Subnormal activation of phagocytes by complement in chronic inflammatory bowel disease? Neutrophil chemotaxis to complement split product C5a.

Subnormal activation of phagocytes by complement in chronic inflammatory bowel disease? Neutrophil chemotaxis to complement split product C5a.

Hypercatabolism of Complement in Crohn's Disease—Assessment of Circulating C3c

Humoral Inhibition of Neutrophil Chemotaxis in Crohn's Disease

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