Abstract

Pressure ulcers represent most common surgical pathology in the pattern of nosocomial complications. However, no unified mechanism leading to development of pressure ulcers has been proposed yet despite the lead role played by compression and immobilization. In this regard, examining immune system as the main component maintaining integrity of anatomical barriers in the skin and mucous membranes seems highly promising for creating new methods to prevent and treat pressure ulcers. Our study was aimed at investigating phenotypic profile of peripheral blood B cells in patients with pressure ulcers. There were enrolled 67 patients complicated with pressure ulcers at the Department of Surgery. Examination of pressure ulcers included determining anatomical localization, investigating depth (degree) and size of the lesion (by measuring wound area), skin color and assessing nature of pressure ulcer edges and edema, wound bottom, presence of cavity with tendons and/or bone formations may be recognized therein, characteristics of exudate (smell, color), pain sensation. In control group there were included 81 apparently healthy subjects. All groups contained age- and sex-matched subjects. Phenotyping of peripheral blood B cells was performed by using flow cytometry with panel of monoclonal antibodies. It was found that count of B cells in patients did not change in parallel with increased total lymphocyte count, but was associated with their functional activity (increased percentage of CD23- and CD38-positive B cells). Moreover, percentage of B1 and naive B2 cells declined in patients with pressure ulcers that seemed to be associated with the premorbid background of the main disease, lack of adequate wound healing process coupled to tissue necrosis and damage to skin capillaries. The more severe the clinical course of pressure ulcers (regarding area and stage of development), the smaller percentage of B2 cells (both naive and memory B cell subsets) was detected in the patient peripheral blood. At the same time, changes in the B cell phenotypic profile from patients are associated with the area of lesion, but not with the stage of developing pressure ulcers evidencing that B cells affect healing of pressure ulcers. The features of B cell phenotype promote unfavorable disease outcome evidenced by the lack of quantitative differences in B cell lineage composition or level of surface expression for activation markers.

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