人源乳酸杆菌对幽门螺杆菌诱导胃上皮细胞炎症反应的调节及可能通路

Human-derived lactobacillus Lac15 inhibits Helicobacter pylori-induced p38 mitogenactivated protein kinase phosphorylation and interleukin-8 secretion in human gastric cancer SGC7901 cells

目的:探讨人源乳酸杆菌对Hpylori诱导SGC7901细胞分泌IL-8及p38MAPK磷酸化水平的影响.方法:实验分为空白对照组、Hpylori刺激组、SB203580干预Hpylori刺激组和Lac15干预Hpylori刺激组.采用免疫细胞化学法观察该人源乳酸杆菌Lac15对Hpylori致SGC7901细胞p38MAPK磷酸化的影响.ELISA法观察该人源乳酸杆菌对Hpylori致SGC7901细胞分泌IL-8的影响.结果:Hpylori能诱导细胞的p38MAPK磷酸化水平增高(IA:1.90±0.36vs14.01±1.12,P<0.01)以及IL-8分泌量明显增高(27.2616±0.27ng/Lvs46.3691±0.33ng/L,P<0.01).预先使用一定浓度(3.0×1011cfu/L,3.0×1010cfu/L,3.0×109cfu/L)的人源乳酸杆菌Lac15干预后,p38MAPK磷酸化水平明显降低(IA:4.61±1.13,6.11±0.19,8.25±0.56vs14.01±1.12,均P<0.01),IL-8分泌量明显降低(42.3209±0.24ng/L,42.1046±0.23ng/L,43.4636±0.25ng/Lvs46.3691±0.33ng/L,均P<0.05或0.01),与Hpylori刺激组比较,具有统计学意义.结论:p38MAPK磷酸化参与Hpylori诱导的SGC7901细胞分泌IL-8,人源乳酸杆菌Lac15可能通过抑制p38MAPK磷酸化途径抑制IL-8的分泌,从而抑制炎症反应.

AIM： To investigate the effects of human-derived lactobacillus Lac15 on p38 mitogen-activated protein kinase （MAPK） phosphorylation and interleukin-8 （IL-8） secretion in human gastric cancer SGC7901 cells infected with Helicobacter pylori （H pylori）. METHODS： SGC7901 cells were divided into four groups： normal control group, H pylori infection group, SB203580 intervention group, and lactobacillus intervention group. The phos-phorylation level of p38 MAPK in SGC7901 cells infected with H pylori was evaluated by immunocytochemistry. The release of IL-8 in SGC7901 cells was detected by enzyme-linked immunosorbent assay （ELISA）. RESULTS： The phosphorylation level of p38 MAPK （IA： 1.90 ± 0.36 vs 14.01 ± 1.12, P〈0.01） and IL-8 secretion （27.2616 ± 0.27 ng/L vs 46.3691 ± 0.33 ng/L, P〈0.01） were signifi cantly higher in SGC7901 cells infected with H pylori than in normal control cells. After intervention with lactobacillus Lac15 at doses of 3×1011, 3× 1010 and 3×109 cfu/L, both the phosphorylation level of p38 MAPK （IA： 4.61 ± 1.13, 6.11 ± 0.19 and 8.25 ± 0.56 vs 14.01 ± 1.12, respectively; all P〈0.01） and IL-8 secretion （42.3209 ± 0.24 ng/L, 42.1046 ± 0.23 ng/L and 43.4636 ± 0.25 ng/L vs 46.3691 ± 0.33 ng/L, respectively; all P〈0.05 or P〈0.01） decreased signifi cantly in SGC7901 cells infected with H pylori. CONCLUSION： H pylori infection can induce IL-8 secretion perhaps via a mechanism associated with promoting p38MAPK phosphorylation. Human-derived lactobacillus Lac15 can inhibit p38MAPK phosphorylation and thus decrease IL-8 secretion.