Sepsis by Gram-negative bacteria infection leads to further increase in procalcitonin (PCT). Herein, we examined the expression of PCT after 24 h in rats by injecting Escherichia coli (E. coli) or Staphylococcus aureus (SA). Healthy male SD rats were divided into six groups (n = 8): (1) Control group: no treatment; (2) SA group: injected with 106CFU/ml SA suspension 0.1 ml in the tail vein; (3) SA and antibiotics group: injected with 106/ml SA bacterial suspension 0.1 ml and 4 mg/kg Cefotaxime sodium, q8h in the tail vein; (4) E. coli group: injected with 106CFU/ml E. coli suspension 0.1 ml in the tail vein; (5) E. coli and antibiotics group: injected with 106/ml E. coli bacterial suspension 0.1 ml and 4 mg/kg Cefotaxime sodium, q8h in the tail vein; and (6) Endotoxin group: injected with 5 mg/kg endotoxin in the tail vein. Expression of PCT was significantly increased in the E. coli, SA or endotoxin-induced bacteremia rats than in the control rats. Compared with SA, PCT was more significantly increased in E. coli rats. NF-κB changes were in line with PCT. Next, we investigated whether the expression of PCT decreased when TLR4 or NF-κB were inhibited after injecting E. coli in rats. A total of 40 healthy male SD rats were divided into five groups (n = 8): (1) Control group: no treatment; (2) E. coli group: injected with 106CFU/ml E. coli suspension 0.1 ml in the tail vein. (3) E. coli and PBS group: injected with 106CFU/ml E. coli suspension 0.1 ml and PBS 0.1 ml in the tail vein. (4) E. coli and TAK242: injected with 106CFU/ml E. coli suspension 0.1 ml and 3 mg/kg TAK242 in the tail vein. (5) E. coli and BAY-11-7082: injected with 106/ml E. coli suspension 0.1 ml and 25 mg/kg BAY-11-7082 in the tail vein. A marked increase of TLR4, NF-κB, LPS and PCT expression was observed in the lungs after E. coli induced bacteremia. Expressions of TLR4, NF-κB, and PCT proteins were decreased in the lungs at 24 h after injection of TAK-242 or BAY-11-7082. In summary, this study suggested that LPS is the key factor for differential expression of PCT between E. coli and SA bacteremia. E. coli induces PCT elevation via the TLR4/NF-κB pathway.

中文翻译：

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LPS通过TLR-4/NF-кB通道诱导PCT产生：与G−/G+菌血症大鼠的差异


革兰氏阴性菌感染引起的败血症导致降钙素原（PCT）进一步增加。在此，我们通过注射大肠杆菌（E. coli）或金黄色葡萄球菌（SA）24小时后检测大鼠体内PCT的表达。健康雄性SD大鼠分为6组（n=8）：（1）对照组：不处理； (2)SA组：尾静脉注射106CFU/ml SA混悬液0.1ml； (3)SA+抗生素组：尾静脉注射106/ml SA菌悬液0.1ml和4mg/kg头孢噻肟钠，q8h； (4)大肠杆菌组：尾静脉注射106CFU/ml大肠杆菌悬液0.1ml； (5)大肠杆菌和抗生素组：尾静脉注射106/ml大肠杆菌菌悬液0.1ml和4mg/kg头孢噻肟钠，q8h； (6)内毒素组：尾静脉注射内毒素5mg/kg。大肠杆菌、SA或内毒素诱导的菌血症大鼠中PCT的表达较对照大鼠显着增加。与SA相比，大肠杆菌大鼠中PCT的升高更为显着。 NF-κB变化与PCT一致。接下来，我们研究了向大鼠注射大肠杆菌后，当 TLR4 或 NF-κB 受到抑制时，PCT 的表达是否下降。健康雄性SD大鼠40只，随机分为5组（n=8）：（1）对照组：不处理； (2)大肠杆菌组：尾静脉注射106CFU/ml大肠杆菌悬液0.1ml。 (3)大肠杆菌和PBS组：尾静脉注射106CFU/ml大肠杆菌悬液0.1ml和PBS 0.1ml。 (4)大肠杆菌和TAK242：尾静脉注射106CFU/ml大肠杆菌悬液0.1ml和3mg/kg TAK242。 (5)大肠杆菌和BAY-11-7082：尾静脉注射106/ml大肠杆菌悬液0.1ml和25mg/kg BAY-11-7082。 大肠杆菌诱导菌血症后，肺部 TLR4、NF-κB、LPS 和 PCT 表达显着增加。注射 TAK-242 或 BAY-11-7082 后 24 小时，肺部 TLR4、NF-κB 和 PCT 蛋白的表达下降。综上所述，本研究提示LPS是大肠杆菌和SA菌血症PCT差异表达的关键因素。大肠杆菌通过 TLR4/NF-κB 途径诱导 PCT 升高。