A Related Study Between Pathogenesis Of Pityriasis Rosea And Hypersensitivity Reaction Mediated By Immunoglobin E

Objective: Pityriasis rosea (PR) is an acute inflammation skin disease, which is common in the Department of Dermatology. The etiology and pathogenesis of PR remain unkown. Now many people consider that it is related with infection, hypersensitivity reaction, cell-mediated immunity, autoimmunity, hereditary susceptibility and so on. There is not yet reported about the relation between Pathogenesis of PR and hypersensitivity reaction mediated by Immunoglobin E (IgE) in domestic and abroad. IgE and mast cell (MC) are main cell-affinitied antibody and the primary effectors cell of typeⅠhypersensitivity. IgE is combined together with IgE Fc high affinity acceptor on the surface of mast cell and basophilic leukocyte, mast cell as well as basophilic leukocyte degranulates and releases multiple mediators of inflammation and cell factors which mediated inflammation reaction and induced tissue damage. Furthermore,IgE is combined together with IgE Fc high affinity acceptor on the surface of langerhans cell and macrophage, which mediated antigen presentation. MC not only has the ability of saving tumor necrosis factor-α(TNF-α) that is synthesized in advance, but also releasing immediately. TNF-αbelongs to a kind of pro-inflammation factor, which is synthesized and secreted by many activated immunocytes. It takes part in mediating inflammation reaction and the process of immunological regulation. At the same time, it can promote the production of many cell factors and promote the development of inflammation. Under the circumstances of stress, tissue cells can express a protective protein, which is also named heat shock protein-70 (HSP-70), HSP-70 is able to protect organism from avoiding harmful stimulus. It also can evaluate the stress ability of body and confine the inducible expression of inflammation factors. This study proposed to explain the relation between pathogenesis of PR and hypersensitivity reaction mediated by IgE and provided educational proof through detecting the serum concentration of IgE, the number of mast cell (MC) and the expressions of tumor necrosis factor (TNF-α), heat shock prorein (HSP-70) in PR lesions.Materials and Methods: Sixty sera cases diagnosed as PR clinically were collected from the dermatological department of the Fourth Affiliated Hospital of Hebei Medical University during Jan. 2006 to Oct. 2006, who had no other IgE novel diseases (for example bronchial asthma, allergic diseases, atopic dermatitis) and so on, and had no systematic mediation history as well as swim history (to exclude drug eruption and PR-type secondary syphilis) within one month , had not taken immunodepressants or anti-histamine drugs within one month .These cases included 25 male and 35 female ,age ranged from 12 to 47 years (mean26.45±9.33 ); Course from 2 days to 2 months (mean16.70±13.38 days) .The twenty-eight normal controls were from healthy volunteers, and had no significant difference in sex and age between patients and controls .Twenty lesion cases diagnosed as PR clinically and histopathologically were collected from the dermatological department of the Fourth Affiliated Hospital of Hebei Medical University during Oct. 2002 to Apr. 2006, who had no other systemic diseases or skin diseases, and had not received any treatment since they were attracted. These cases included 8 males and 12 females, age arranged from 15 to 50 years (mean 31.80±1.94), course arranged from 3 to 21 days (mean 10.36±4.31). The ten normal controls were healthy volunteers in the hospital, and had no significant difference in sex, age and position between patients and controls.The sera concentration of IgE were measured by enzyme linked immunosorbent assay (ELISA), the result were analyzed by 2-independent sample compared T test. The result of gender was analyzed by2-independent sample compared T test and the results of different age and pruritus degree were analyzed by one-factor analysis of variance. The lesion samples were investigated with histopathological method, and the number of MC was measured by toluidine blue special staining (TB) whose results were analyzed by 2-independent sample compared T test, the levels of TNF-αand HSP-70 expressions were measured by immunohistochemical method. HE- staining was used in histopathology and histostain-SP in immuno-histochemistry. The results were analyzed by Mann-whitney U rand sum test and Spearman's rank correlation test.Results1 ELISA results1.1 The mean concentrations of sera IgE of PR patients and normal controls were 2.09±0.44 and 1.75±0.46, compared with each other, there was statistal significance (p<0.01).1.2 The mean concentrations of sera IgE of PR patients, which compared from gender, age phases and pruritus degrees, there were no statistal significance (p>0.05).2 Toluidine blue special staining (TB) results The endochylema grains of MC were stained prunosus, and the nucleus submitted blue.The mean number of MC of PR patients and normal controls were (31.95±9.65) piece/HP and (20.00±3.83) piece/HP respectively. Compared with each other, there was statistal significance (p<0.01).3 Immunohistochemistry resultsPositive staining was submitted Buffy grains.3.1 TNF-αstained on cell membranes and cytoplasm of full epidermis cell and periphery of blood vessel in dermis superficial layer. Among these positive cells, 4 cases (+++), 8 cases (++), 8 cases (+), 0 case (-).The level of its expression was markedly increased comparing with the controls (p<0.01).3.2 HSP-70 stained on cell membranes and cytoplasm of full epidermis cell and periphery of blood vessel in dermis superficial layer. Among these positive cells, 15 cases (+++), 2 cases (++), 3 cases (+), 0 case (-).The level of its expression was markedly increased comparing with the controls (p<0.01).3.3 There was significant correlation between the expression degree of HSP-70 and TNF-α(p>0.05).Conclusion1 In this study, the concentration of serum IgE of PR patients is significantly increased. The result demonstrates that the pathogenesis of PR possibly is concerned with the hypersensitivity reaction that is mediated by IgE which generated by the stimulatation of a certain antigen (for example virus, et al).On the first aspect, IgE produces the inflammation by mast cell's degranultion to mediate inflammation relation; at the other aspect, IgE mediatd the antigen presetntion of APC to promote inflammation relation.2 The number of MC in the lesions of PR is obviously increased and many MCs have degranulation phenomena. We can see that MCs as an important effective cell perhaps take part in the pathogenesis of PR; moreover, MCs release mediators of inflammation and cell factors to promote the inflammation reaction.3 The expression of TNF-αin the lesions is stronger than that of controls that lead to the immnunol damage of the body. It perhaps explains that TNF-αnot only takes part in the form of rash inflammation, but inducing releasing more cell factors and mediators of inflammation that aggravate part inflammation reaction.4 The expression of HSP-70 in the lesions is stronger than that of controls; it explains that PR patients are under a stress station, which can help to resist maximatily infringing of outside harmful stimulation. Further more, HSP-70 as an anti-inflammatory factor confines further damage from inflammation factors and accelerates the repair of rash through confining the expression of inflammation factors.