Anti-CLU (C-terminal) polyclonal antibody

Introduction. - Allergic contact dermatitis around chronic leg ulcers (CLU) is a common complication in patients presenting CLU and prolongs healing times. The aim of this study was to describe the rate of sensitization to modern dressings (MD) used in these patients and to assess whether there is a relation between the number of sensitizations and ulcer type, the time from onset of the ulcer, and patient age and gender. Patients and methods. - We conducted a retrospective study at Reims University Hospital between 2010 and 2014 that included all patients with CLU of vascular etiology surrounded by eczematous lesions, and who had one of the patch-tests in the following 3 series: European baseline +/- leg ulcers +/- corticosteroids. Results. - Among the 73 patients included, 43 % were polysensitized. Thirty-three patients (45 %) were sensitized to MD (38 % to hydrocolloids, 18 % to hydrogels, 7 % to hydrocellular dressings, 7 % to hydrofiber dressings, 5 % to contact layers and 3 % to alginates). Median age and sex did not differ between "polysensitized" patients and "nonpolysensitized" patients (P=0.84 and P=0.25, respectively). Polysensitization was more frequent among patients presenting ulcers for more than 5 years (P=0.032). Conclusion. - Practically half of all patients presenting CLU with surrounding contact dermatitis had sensitization to modern dressings (mostly hydrocolloids and hydrogels). The rate of sensitization increased with the length of presence of CLU. (C) 2018 Elsevier Masson SAS. All rights reserved.

Dry eye is a common disorder caused by inadequate hydration of the ocular surface that results in disruption of barrier function. The homeostatic protein clusterin (CLU) is prominent at fluid-tissue interfaces throughout the body. CLU levels are reduced at the ocular surface in human inflammatory disorders that manifest as severe dry eye, as well as in a preclinical mouse model for desiccating stress that mimics dry eye. Using this mouse model, we show here that CLU prevents and ameliorates ocular surface barrier disruption by a remarkable sealing mechanism dependent on attainment of a critical all-or-none concentration. When the CLU level drops below the critical all-or-none threshold, the barrier becomes vulnerable to desiccating stress. CLU binds selectively to the ocular surface subjected to desiccating stress in vivo, and in vitro to the galectin LGALS3, a key barrier component. Positioned in this way, CLU not only physically seals the ocular surface barrier, but it also protects the barrier cells and prevents further damage to barrier structure. These findings define a fundamentally new mechanism for ocular surface protection and suggest CLU as a biotherapeutic for dry eye.