Psoriasis is a chronic , recurrent inflammatory skin disease, characterized by erythema, papules, plaques and scaling. The etiology of the disease is much complicated . Infections especially bacterial infections is an important factor which leads to the onset or deterioration of the disease.In recent years, many studies have proved the superantigen of Gram-positive(G~ ) bacteria is relevant to the pathogenesis of psoriasis. It's also much common that psoriatic patients have infections caused by Gram-negtive(G~-) bacteria. The most virulent agent of G" bacteria is endotoxin, also known as lipopolysaccharide(LPS). LPS has many biological effects which obviously influence the innate and adaptive immunity of the host. LPS binding to its receptor complex (CD14、 TLR4、 MD-2 ,et al) can activate a series of cellular signal transductions and the nuclear factor- κ B(NF- κB), leading to the production of cytokines, chemokines, adhesion molecules and growth factors that involve in inflammatory responses. These inflammatory factors are increased in psoriasis. We speculate that endotoxin and its signal pathway may have a relationship with the pathogenesis of psoriasis. Our experiments studied on this relationship to further elucidate the pothogenesis of psoriasis and may help make new methods for the treatment of the disease.Firstly, the plasma level of endotoxin in 33 patients with psoriasis vulgaris and28 normal controls was determined by ELISA. The endotoxin level was tested again in 18 patients when their skin lesions disappeared completely after treatment. Secondly, the plasma level of sCD14 was tested by ELISA in 19 patients and 15 normal controls. Lastly, the surface expression of CD14, TLR4 and the expression of activated NF- k B of peripheral blood leukocytes in 32 patients and 29 normal controls was determined by flow cytometry.The result of the study illustrated: (T) The plasma endotoxin level in patients with psiriasis vulgaris was significantly increased compared with that in healthy controls ( p<0.05 ) . The endotoxin level in patients recovered completely after treatment was significantly decreased compared with that before treatment ( p< 0.05 ) . (2) Significantly increased plasma level of sCD14 was observed in psoriatic patients compared with that in normal controls by ELISA ( P<0.05 ) . (3) The surface expressions of LPS receptors CD14, TLR4 of peripheral blood leukocytes in patients were significantly higher than those in normal controls ( p< 0.05 ) . ? The expression of activated NF- k B in totol blood leukocytes in patients was higher than that in normal controls, but without statistical significance. The expresson of activated NF- k B in peripheral blood mononuclear cells (PBMC) in patients was decreased compared with that in normal controls ( p<0.05 ) .Conclusion: our study first confirmed that the blood endotoxin level is increased in patients with psoriasis vulgaris. The endotoxin level decreases in accordance with the recovery of the disease , and there is a significant difference between the endotoxin levels before and after treatment. These results proved that there is an increased rate of G" bacteria infection in the pathogenesis of psoriasis .The higher plasma level of sCD14 in psoriatic patients also implied the increasd endotoxin. The higher surface expression of CD14, TLR4 of blood leukocytes in patients indicated there is an abnormal activation of LPS signal pathway in psoriasis. The decreased activated NF- k B expression in PBMC of the patients was perhaps due to the transmigration of activated T lymphocytes (such as CLA  T cell) to skin tissue which is mediated by chemokines and adhesion molecules. The higher activity of NF- tB in totol blood leukocytes in psoriatic patients compared with normal control, although without statistical significance, was much likely caused by neutrophils activation by the increased endotoxin.