Interleukin-8 response in an intestinal HCT-8 cell line infected with enteroaggregative and enterotoxigenic Escherichia coli
Interleukin-8 response in an intestinal HCT-8 cell line infected with enteroaggregative and enterotoxigenic Escherichia coli
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DOI：
10.1128/cdli.11.3.548-551.2004
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发表时间：
2004-05-01
期刊：
影响因子：
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通讯作者：
Okhuysen, PC
中科院分区：
文献类型：
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作者：
Huang, DB;DuPont, HL;Okhuysen, PC
本研究检测了白细胞介素-8（IL-8）的肠腺癌HCT-8细胞系感染肠聚集性和肠致病性大肠杆菌致病型分离的旅行者腹泻患者的反应。单孢E.大肠杆菌菌株（肠聚集性E. coli [EAEC]; n = 30）、产耐热肠毒素（ST）的肠毒素E.大肠埃希菌（ETEC ST; n = 11）、产不耐热肠毒素（LT）的产肠毒素E.大肠埃希菌（ETEC LT; n = 10）和产ST和LT的产肠毒素E. coli（ETEC ST：LT; n = 8）与HCT-8细胞共孵育3 h。通过酶联免疫吸附测定法测定组织培养上清液中IL-8的含量。50%的EAEC（72%的EAEC携带毒力因子aggR、aggA和aspU，40%的EAEC不携带毒力因子）和64%的ETEC ST诱导产生IL-8。相比之下，10%的ETEC LT引起IL-8的产生高于基线。这些结果表明：（i）HCT-8细胞系感染模型可用作区分促炎性E.（ii）EAEC具有诱导IL-8产生的异质性能力，这可能与毒力因子的存在有关;和（iii）ETEC ST可引起炎症反应，有助于解释我们早期发现的ETEC腹泻患者粪便中IL-8升高。8细胞系感染从旅行者腹泻患者中分离的肠聚集性和产肠球菌性大肠杆菌致病型。单孢E.大肠杆菌菌株（肠聚集性E. coli [EAEC]; n = 30）、产耐热肠毒素（ST）的肠毒素E.大肠埃希菌（ETEC ST; n = 11）、产不耐热肠毒素（LT）的产肠毒素E.大肠埃希菌（ETEC LT; n = 10）和产ST和LT的产肠毒素E. coli（ETEC ST：LT; n = 8）与HCT-8细胞共孵育3 h。通过酶联免疫吸附测定法测定组织培养上清液中IL-8的含量。50%的EAEC（72%的EAEC携带毒力因子aggR、aggA和aspU，40%的EAEC不携带毒力因子）和64%的ETEC ST诱导产生IL-8。相比之下，10%的ETEC LT引起IL-8的产生高于基线。这些结果表明：（i）HCT-8细胞系感染模型可用作区分促炎性大肠杆菌的工具。来自非炎症分离株的大肠杆菌;（ii）EAEC具有诱导IL-8产生的异质性能力，这可能与病毒因子的存在有关;（iii）ETEC ST可以引起炎症反应，并有助于解释我们早期发现的ETEC腹泻患者粪便IL-8增加。
This study examined the interleukin-8 (IL-8) response of the intestinal adenocarcinoma HCT-8 cell line to infection with enteroaggregative and enterotoxigenic Escherichia coli pathotypes isolated from patients with travelers' diarrhea. Individual diarrheagenic E. coli strains (enteroaggregative E. coli [EAEC]; n = 30), heat-stable enterotoxin (ST)-producing enterotoxigenic E. coli (ETEC ST; n = 11), heat-labile enterotoxin (LT)-producing enterotoxigenic E. coli (ETEC LT; n = 10), and ST- and LT-producing enterotoxigenic E. coli (ETEC ST:LT; n = 8) were coincubated with HCT-8 cells for 3 h. Tissue culture supernatants were assayed for IL-8 content by enzyme-linked immunosorbent assay. Fifty percent of EAEC (72% of those EAEC carrying the virulence factors aggR, aggA, and aspU and 40% of those EAEC not carrying virulence factors) and 64% of ETEC ST elicited IL-8 production. In contrast, 10% of ETEC LT elicited the production of IL-8 above baseline. These results suggest that (i) the HCT-8 cell line infection model can be used as a tool to differentiate proinflammatory E. coli from noninflammatory isolates; (ii) EAEC has a heterogeneous ability to induce the production of IL-8, and this may be associated with the presence of virulence factors; and (iii) ETEC ST can elicit an inflammatory response and helps explain our earlier findings of increased fecal IL-8 in patients with ETEC diarrhea.This study examined the interleukin-8 (IL-8) response of the intestinal adenocarcinoma HCT-8 cell line to infection with enteroaggregative and enterotoxigenic Escherichia coli pathotypes isolated from patients with travelers' diarrhea. Individual diarrheagenic E. coli strains (enteroaggregative E. coli [EAEC]; n = 30), heat-stable enterotoxin (ST)-producing enterotoxigenic E. coli (ETEC ST; n = 11), heat-labile enterotoxin (LT)-producing enterotoxigenic E. coli (ETEC LT; n = 10), and ST- and LT-producing enterotoxigenic E. coli (ETEC ST:LT; n = 8) were coincubated with HCT-8 cells for 3 h. Tissue culture supernatants were assayed for IL-8 content by enzyme-linked immunosorbent assay. Fifty percent of EAEC (72% of those EAEC carrying the virulence factors aggR, aggA, and aspU and 40% of those EAEC not carrying virulence factors) and 64% of ETEC ST elicited IL-8 production. In contrast, 10% of ETEC LT elicited the production of IL-8 above baseline. These results suggest that (i) the HCT-8 cell line infection model can be used as a tool to differentiate pro-inflammatory E. coli from noninflammatory isolates; (ii) EAEC has a heterogeneous ability to induce the production of IL-8, and this may be associated with the presence of virullence factors; and (iii) ETEC ST can elicit an inflammatory response and helps explain our earlier findings of increased fecal IL-8 in patients with ETEC diarrhea.