Effects Of Glucocorticoid On The Mechanisms Of ALI

【Objective】To establish an animal model ofALI and to investigatethe roles of glucocorticoid and CD4+CD25+ regulatory T cells in thesystem inflammatory response syndrome of ALI.【Methods】64 male,6 to 8 weeks age,Sprague-Dawley rats weredivided into 8 groups, including Group-A,Group-B,Group-C,Group-D,Group-E,Group-F,Group-G and Group-H. Group-A: rats were madeALI by a single intratracheal instillation of 6 mg/kg body weight oflipopolysaccharide; Group-B: rats received an intratracheal instillation of1.2 ml/kg body weight of PBS; Group-C,-D,-E,-F,-G and -H receivedan intravenous dexamethasone of 2 mg/kg body weight through the tailvein of the rats 2h,30min before and 30min,1h,2h,4h after theinstillation of 6 mg/kg body weight of lipopolysaccharide separately.Total and differential leukocyte counts were carry out in blood samples24h after the operation; bronchoalveolar lavage was performed in ratfrom each group; inflammatory cells in BALF were counted andclassified; the concentration of total protein and phospholipid of BALFwere measured; the ratios of CD4+CD25+ regulatory T cells/CD4+ T cellswas measured; total lung injure score was carried out.【Results 】Group-D exhibited significantly decreased totalleucocytes (1.3316±0.4875×109/L and 0.4363±0.2004×109/L,respectively; P=0.013) ,neutro-phils(0.8976±0.2751×109/L and0.4026±0.2048×109/L, respecttively; P=0.021) and concentration of totalprotein(7.7250±1.4350 g/L and 5.5000±0.8912 g/L, respect -tively; P<0.05) in BALF,lung coefficient(0.2285±0.0565 and 0.1544±0.0588,respectively; P<0.05) and total lung injure score (6.2500±1.2817 and4.0000±1.0690, respectively; P=0.031); whereas the concentration ofBALF phospholipid (2.7493±1.5175 mmol/L and 6.9739±2.2024 mmol/L,respectively; P=0.012) and ratios of CD4+CD25+ regulatory T cells/CD4+T cells in BALF(2.3137±1.4342% and 4.3275±2.1910%, respecttively; P<0.05) increased markedly compared with Group-A. Group-E exhibitedsignifycantly increased the concentration of BALFphospholipid(2.7493±1.5175 mmol/L and 9.6446±3.0543 mmol/L,respectively; P=0.003); whereas the concentration of total protein inBALF decreased markedly (7.7250±1.4350 g/L and 4.6625±2.3567 g/L,respectively; P<0.05) compared with Group-A. Group-H exhibitedsignificantly decreased lung coefficient (0.2285±0.0565 and0.1458±0.0397, respectively; P < 0.05) compared with Group-A;Group-C,-E,-F,-G and -H exhibited no significantly differences in thetotal cells and neutrophils in BALF and total lung injure score comparedwith Group-A(P>0.05); all groups exhibited no significantly differencesin the total leucocytes,lymphocytes and monocytes in blood comparedwith Group-A; all groups except Group-D,-F and -H exhibited nosignifycantly differences in neutrophils in blood compared withGroup-A(P>0.05); all groups exhibited no significantly di-fferences inlymphocytes and macrophages in BALF compared with Group-A(P>0.05); Group-C,-F,-G and -H exhibited no significantly differences inconcentration of total protein and phospholipid in BALF compared withGroup-A (P>0.05); Group-C,-E,-F and -G exhibited no significantlydifferences in lung coefficient compared with Group-A(P > 0.05);Group-C,-E,-F,-G and -H exhibited no significantly differences in ratiosof CD4+CD25+ Regulatory T cells/CD4+ T cells in BALF compared withGroup-A(P>0.05).【Conclusions】Animal with ALI caused by lipopolysaccharidemay be benefit from an preventive glucocorticoid administered throughinhibiting system inflammatory response syndrome and decreasing thedegree of lung injury, this benefit can not achieved if you do not usecorticosteroid in the right time; the decrease of CD4+CD25+ Regulatory Tcells in BALF may be a sign of ALI; corticosteroid may inhibit ALIthrough increasing the number of CD4+CD25+ Regulatory T cells in lung.