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首页> 外文期刊>Infection and immunity >Helicobacter pylori Alters Exogenous Antigen Absorption and Processing in a Digestive Tract Epithelial Cell Line Model
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Helicobacter pylori Alters Exogenous Antigen Absorption and Processing in a Digestive Tract Epithelial Cell Line Model

机译：幽门螺杆菌改变消化道上皮细胞系模型中的外源性抗原吸收和加工。

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To study the influence of Helicobacter pylori on epithelial barrier function, bacteria, bacterial sonicates, or broth culture supernatants were incubated for 24 h with HT29-19A intestinal cells grown as monolayers. Subsequently, the monolayers were mounted in Ussing chambers, and electrical resistance (R), fluxes of 22Na (JNa) and14C-mannitol (JMan) (markers of the paracellular pathway), and fluxes of horseradish peroxidase (HRP) in total (J3H-HRP), intact (JHRPi), and degraded forms were measured. H. pylori did not induce any modification of the paracellular pathway (R = 148 ± 10 versus 174 ± 16 Ω · cm2; JNa = 4.16 ± 0.44 versus 3.51 ± 0.41 μEq/h · cm2; JMan = 0.081 ± 0.01 versus 0.058 ± 0.009 μmol/h · cm2), nor did it modify J3H-HRP (2,201?± 255 versus 2,110 ± 210 ng/h · cm2 forH. pylori-infected and control cells, respectively). However, in the presence of H. pylori, we observed a significant increase in JHRPi (520 ± 146 versus 171 ± 88 ng/h · cm2). This effect was not dependent of thecag status of the strain and was not reproduced by the sonicates or the culture supernatants. It was related to the presence of urease, since a urease-negative mutant of H. pylori did not induce this effect. Ammonia and bafilomycin A1, two agents known to increase the endolysosomal pH, reproduced the increase in JHRPi. In conclusion, H. pylori does not affect directly the integrity of intercellular junctions of epithelial cells in vitro, but it increases the passage of intact HRP, probably by inhibition of the intralysosomal degradation due to the release of ammonia. The increased transport of intact macromolecules may contribute to the induction and maintenance of gastric inflammation by H. pylori.
机译：为了研究幽门螺杆菌对上皮屏障功能的影响，将细菌，细菌声波或肉汤培养上清液与单层生长的HT29-19A肠细胞孵育24小时。随后，将单层膜安装在Usssing室中，并测量电阻（R）， 22 Na（JNa）和 14 C-甘露醇（JMan）的通量（测量了辣根过氧化物酶（HRP）的总量（J 3 H-HRP），完整（JHRPi）和降解形式的通量。 H。幽门螺杆菌未诱导细胞旁通路的任何改变（R = 148±10 vs 174±16Ω·cm 2 ; JNa = 4.16±0.44 vs 3.51±0.41μEq/ h·cm 2 ; JMan = 0.081±0.01对0.058±0.009μmol/ h·cm 2 ），也没有修饰J 3 H-HRP（幽门螺杆菌感染细胞和对照细胞分别为2,201？±255和2,110±210 ng / h·cm 2 。但是，在 H存在下。幽门螺杆菌，我们观察到JHRPi显着增加（520±146对171±88 ng / h·cm 2 ）。这种作用与菌株的 cag 状态无关，并且超声处理或培养物上清液也不能复制这种作用。这与脲酶的存在有关，因为 H的脲酶阴性突变体。幽门螺旋杆菌没有诱导这种作用。氨和bafilomycin A 1 是已知的两种可增加溶酶体pH值的药物，可再现JHRPi的升高。总之， H。幽门螺杆菌不会直接影响体外上皮细胞胞间连接的完整性，但它可能通过抑制由于释放氨导致的溶酶体降解而增加完整HRP的通过。完整大分子运输的增加可能有助于 H诱导和维持胃部炎症。幽门炎。

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