Increased abnormal erythrocytes caused by spleen filtration deficiency provide a hypoxic environment for the occurrence of psoriasis

Abstract

Abstract Background Psoriasis is a chronic autoimmune disease with a long disease course and frequent relapse characteristics, however, its pathogenesis is still not completely clear. Clinical study indicated that blood state is abnormal in psoriasis and seems related with the severity of psoriasis. However, whether this is true and which constituents of blood play the key role and its mechanism behind is not clear. Methods Effect of blood constituents on the psoriasis development was determined by comparing serum, red cells, and leukocytes of psoriasis on the onset of psoriasis of NOG mice, using samples of healthy people as the control. The effect of red cell on psoriasis was further demonstrated by splenectomy using Kunming mice. Red cell morphology and spleen histopathology were studied by microscope. IL-6, IL-17A, IL-23, VEGF, IL-22, MDA, NO and HIF were determined by Elisa kits, and q-PCR was used to detect the mRNA of IL-6, IL-22, and IL-23, and western blot was used to detect CD-11b, SPIC, SIPR-α, TSP-1, and CD47. Results The hemorheology of psoriatic patients to be abnormal, and aging and deformed erythrocytes increased in the blood. Red cell and leukocyte from psoriasis were more likely to induce psoriasis when comparing with that of from the healthy volunteers, and the effect of red cell was more strong. When splenectomy, mice were also easy to induce psoriasis, demonstrating by the skin lesion, inflammatory factors and histopathology which all similar with psoriasis patients. Psoriasis spleen showed an increased red pulp and white pulp, and increased CD-11b, SPIC, TSP-1 and decreased SPRP-α, CD47 showed marginal change, indicated that the weakening of the “eat me” function of spleen macrophages phagocytizing aging and deformed erythrocytes, resulting in the dysfunction of spleen filtration and the increase of aging and deformed erythrocytes in the body. Additionally, the decreased oxygen-carrying capacity and the declined antioxidant capacity of those erythrocytes led to the hypoxia environment, making psoriasis more likely to be induced. Conclusion These findings demonstrate that spleen filtration dysfunction contributes to the pathogenesis of psoriasis and suggest that improving it may be an effective therapy for psoriasis and control its relapse.