To explore the effects of lipopolysaccharide binding protein (LBP) on toll like receptor 4 (TLR4) pathway in alveolar macrophages of acute lung injury induced by lipopolysaccharide (LPS) in rats. The TNF ?concentration, IL 1? and IL 18 mRNA expression in alveolar macrophages (AM?) from rats challenged with LPS or LPS + LBP or LPS+LBP+multi LBP antibody (mLBPab) were measured with ELISA and semi quantative reverse transcription polymerase chain reaction (RT PCR) respectively. The expression of TLR4 was determined with RT PCR and Western blot. The results showed that: the TNF ? concentration ,IL 1?, IL 18 mRNA expressions and TLR4 expression were increased significantly in the AM? stimulated with LPS +LBP compared with single LPS stimulation group. However, mLBPab blocked these effects. It is suggested that LBP could enhance the trans membrane transduction function of LPS via TLR4 in rat AM? and these might be the main reason that LBP could enhance the inflammatory activity of LPS, and LBP antibody could be used to alleviate such morbid conditions such as SIRS, acute lung injury, ARDS, and septic syndrome.

Objective To study the role of pro inflammatory cytokines tumor necrosis factor?(TNF ?),interleukin 1beta(IL 1?),interleukin 6(IL 6) and anti inflammatory cytokines interleukin 4(IL 4),interleukin 10(IL 10),interleukin 13(IL 13) in acute lung injury(ALI). Methods Wistar Rats (200?50g) were randomly divided into the oleic acid(OA) and Lipoplysaccharide(LPS) induced lung injury experimental group and the only OA induced lung injury control group. The LPS(2mg/kg) was injected in rat's tail vein at the 1, 4, 12 and 24 hours after administration of OA(0.2ml/kg, iv). Reverse transcription polymerase chain reaction(RT PCR) were used to detecting the expression of TNF ?, IL 1?, IL 6 and IL 4, IL 10, IL 13 mRNA in the lung tissue of rats in two groups. Results The results showed that the peak expression of TNF ? and IL 1? mRNA at one hour after first hit by oleic acid, and IL 6 mRNA at four hours were observed. Others, such as IL 4, IL 10 and IL 13 mRNA, the highest levels in lung tissue at four hours after lung injury induced by oleic acid. Conclusions The results suggested that TNF ? and IL 1? are presenting early phase of ALI, and that IL 6 played its important role in delayed development. The over expression of anti inflammatory cytokines IL 4, IL 10 and IL 13 may be as a promoters rather than protectors in inflammatory amplification.

Objective　To study the effect of IFN-γ inhalation via aerosol on cytokines of the immunocompromised rats. Methods　Immunocomprised rat model was established with cortisol acetate injection for 14 d and then Candida albicans fluid was injected by tracheal for establishing am immuno comprised with pulmonary infection model. IFN-γ was inhaled with aerosol 1 d before the bacterium injection and then for 1, 3 and 7 d respectively. The activity of TNF-α, and the levels of IL-1β and IL-6 in the supernatant of the cultured alveolar macrophage(AM), the activity of IFN-γ and TNF-α in bronchial alveolar lavage fluid (BALF), the expressions of IFN-γ,TNF-α, IL-1β, and IL-6 of the lung tissues, the level of IFN-γ,IL-1β, and IL-6 in the serum were investigated. Results　The activity of TNF-α, and the levels of IL-1β and IL-6 in the culture supernatant of the AM of the rats treated with IFN-γ were significantly higher than those of the control. The activity of IFN-γ and TNF-α in BALF was higher in the IFN-γ inhaled rats than in the control (except the activity of TNF-α on the 7th day). The expressions of IFN-γ and IL-1β in lung tissues was higher in the rats treated with IFN-γ than in the control. The expression of TNF-α in the rats treated with IFN-γ was less than that in the control rats. The expression of IL-6 had no difference between 2 groups. And no difference was found in the activity of IFN-γ, and the levels of IL-1β and IL-6 in the serum between 2 groups(except IL-1β on the 3rd day). Conclusion　Administration of IFN-γ via aerosol can obviously increase the activity or levels of some cytokines in the lung of the immunocompromised rats, but has no effect on them in serum of the immunocompromised rats.