Intranasal heparin reduces eosinophil recruitment after nasal allergen challenge in patients with allergic rhinitis

Biochemical and functional characterization of glycosaminoglycans released from degranulating rat peritoneal mast cells: Insights into the physiological role of endogenous heparin

“…These findings extend previous observations that exogenous heparin can inhibit leukocyte infiltration into a number of tissues, both experimentally (35,37) and clinically (38). Our results support the hypothesis (14) that the release of endogenous heparin in an inflammatory response may serve to act as a homeostatic braking mechanism to limit cell infiltration into tissues and by virtue of the well known ability of heparin to neutralise the actions of various cationic pro-inflammatory mediators, may also serve to limit the effects of the mediators released from infiltrating inflammatory cells.…”

Direct In Vivo Monitoring of Acute Allergic Reactions in Human Conjunctiva

“…These results argue against the direct role of local cellular inflammation in acute allergic reactions in human conjunctiva within the minutes after allergen or histamine challenge. In animal models of more chronic diseases such as delayed-type hypersensitivity, inhibition of lymphocyte, or eosinophil adhesion to the vascular endothelium has reduced inflammation (49,50). It is possible that a longer detection period of more chronic forms of allergic inflammation may also show improved clinical outcome or the differences may be due to different effector cell populations.…”

Pharmacology of Heparin and Related Drugs

“…In patients with COPD, early studies suggested that heparin may be of benefit on account of its ability to neutralize the induction of emphysema by elastase (Rao et al, 1990;Laufma et al, 1991). Treatment of patients with allergic rhinitis with topical heparin reduces eosinophil recruitment into the nose after allergen exposure (Vancheri et al, 2001). Furthermore, administration of heparin exhibits clinical benefits in the treatment of patients with inflammatory bowel disease, even in individuals known to be resistant to treatment with glucocorticosteroids (Gaffney et al, 1991(Gaffney et al, , 1995Evans et al, 1997;Michell et al, 2001), although meta-analyses of these trials concluded that there is insufficient evidence to support the use of heparin for the treatment of active ulcerative colitis (Shen et al, 2007;Chande et al, 2008).…”

“…Heparin has been shown to inhibit the adhesion of leukocytes to endothelium both in vitro (Bazzoni et al, 1993;Silvestro et al, 1994;Lever et al, 2000;Smailbegovic et al, 2001) and in vivo (Ley et al, 1991;Tangelder and Arfors, 1991;Nelson et al, 1993;Xie et al, 1997;Salas et al, 2000;Johnson et al, 2004;Lever et al, 2010). Furthermore, the ultimate accumulation of cells in inflamed tissue sites, in response to both allergic (Sasaki et al, 1993;Seeds et al, 1995;Seeds and Page, 2001;Vancheri et al, 2001) and nonallergic (Nelson et al, 1993;Teixeira and Hellewell, 1993;Yanaka and Nose, 1996;Johnson et al, 2004;Lever et al, 2010) stimuli, is inhibited by heparin.…”