Interleukin‐1: The Pros and Cons of Its Clinical Relevance

Shaldon, Stanley; Dinarello, C. A.; Port, F. K.; Kluger, Matthew J.

doi:10.1111/j.1525-1594.1988.tb02759.x

Cited by 6 publications

(5 citation statements)

References 0 publications

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“…The present findings lend further strength to the hypothesis that pro-inflammatory cytokines are induced by haemodialysis treatment and account for the acute and chronie innammatory symptomatology in dialysed patients [9]. They hnplicate a direct contact of blood monocytes with dialysis membrane as the primary cause of long-lasting TNF-a generation in haemodiaiysis patients.…”

Section: Discussionsupporting

confidence: 78%

Alterations in mononuclear cell tumour necrosis factor-alpha (TNF-a) response in patients on long term cuprophane haemodialysis

Annenkov

Строков

Baranova

1992

Clinical and Experimental Immunology

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SUMMARYWe have investigated TNF-a secretory response of peripheral blood mononuclear eells (PBMC) from 13 uraemic patients undergoing regular haemodiaiysis with cuprophane membrane (CM). Sixteen healthy subjects and five uraemic patients under conservative therapy were also studied as controls. Cells ofhacmodialy.sis patients exhibited increa.sed TNF-a release//irf/rrnn the absence of activating siimuli other than culture conditions, as compared with normal and uraemic controls. In contrast to normal cells, this spontaneous secretion of TNF-i Irom dialysis PBMC could not be significantly reduced by addition of polymyxin B to culture medium, thus indicating its mdependence of trace amount of lipopoiysaccharide (LPS) present in the medium as contaminant. Furlhcrmorc. predialysis PBMC were considerably more sensitive to stimulation with 10'pg/ml of LPS under in vitro culture conditions than normal and uraemic controls. To elucidate a role of direct contact with CM in stimulation of TNF'-j release from monoeytes, PBMC were cultured on CM in vitro. Contact with CM stimulated TNF-::( secretion from PBMC above the level ofcells cultured on tis,sue culture plastic. This response persisted with time in culture in contrast to a transient LPS-induced TNF-x release. Furthermore. PBMC stimulated by contact with CM for 2 days did not lose the capacity to secrete TNF-a in response to a subsequent LPS stimulation, while a 2-day treatment ofceils with LPS was followed by LPS refractory state. Therefore, direct conuici with CM induces in PBMC a long-lasting TNF-2 response which is not down-regutated by the acquisition ofrefractorincss in a manner similar to that which occurs in the case of LPS stimulation. These in vitro findings provide a possible explanation ofthe observalion ihat predialysis PBMC exhibit elevated TNF'-a secretory capacity.

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Section: Discussionsupporting

confidence: 78%

Alterations in mononuclear cell tumour necrosis factor-alpha (TNF-a) response in patients on long term cuprophane haemodialysis

Annenkov

Строков

Baranova

1992

Clinical and Experimental Immunology

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“…It must be stressed, however, that the interpretation of plasma and intracellular I L-I values is still difficult, owing to several methodological problems [51]. Therefore, the precise role played by different types of membranes in the stimula tion of IL-1 production is far from being fully under stood.…”

Section: The Monokine Hypothesismentioning

confidence: 99%

“…The consequences of repeated in ductions of an acute-phase response by IL-1 and TNF are undesirable, and may consist of a large spectrum of complications including muscle wasting, osteopenia, bone cysts, fibrosis of joints and the carpal tunnel syn drome [53]. However, even though the monokine hypo thesis is very attractive on theoretical grounds, there is no clear-cut evidence at present of the clinical consequences resulting from stimulation of 1 L-l and TNF secretion during dialysis [51].…”

Section: The Monokine Hypothesismentioning

confidence: 99%

Dialysis Membrane Biocompatibility

Basile¹,

Drüeke²

1989

Nephron

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“…Complement activation induced by the conventional cellulosic dialysis membrane [4], acetate buffer in the dialysis fluid, and last but not least, a contamination of the dialysis fluid by organic chemicals or heavy metals and later also by bacterial endotoxins have been considered as reasons for such febrile reactions. Discussions during scientific conferences did not yield clear conclusions and remained controversial [5]. The problem was also addressed by Jürgen Bommer and E. Ritz in a publication in Nephron in 1987 entitled: "Water quality, a neglected problem in hemodialysis" [6].…”

mentioning

confidence: 99%