胞漿識別受體NODs及其信號通路在侵襲性肺曲霉病中的作用
發(fā)布時間：2018-09-07 14:37
【摘要】：【目的】研究天然免疫系統(tǒng)中胞漿識別受體NODs及其信號通路在小鼠侵襲性肺曲霉病(IPA)中的作用�！痉椒ā啃∈箅S機分為正常對照組、正常+接種煙曲霉菌組(正常感染組)和免疫抑制+接種煙曲霉菌組(IPA組),經(jīng)鼻吸入煙曲霉孢子后在不同時相點處死小鼠,無菌取肺組織分別進行病理切片,煙曲霉菌落計數(shù),RT-PCR法、Western blot法動態(tài)檢測小鼠感染煙曲霉菌過程中肺組織NOD1、NOD2、RIP2 mRNA表達,促炎細胞因子TNF-α含量的變化規(guī)律。【結果】鼻吸入煙曲霉菌后72 h時,IPA組肺組織出現(xiàn)嚴重炎癥反應,并有大量的菌絲生成,同時各時相點的煙曲霉菌負荷均高于正常感染組;與正常感染組比較,IPA組NOD1、RIP2 mRNA持續(xù)低表達,而NOD2 mRNA則在感染最早期(24 h)異常高表達,而在隨后的感染過程中一直處于低表達狀態(tài);正常小鼠感染煙曲霉菌后,肺組織中促炎細胞因子TNF-α在感染前期皆呈高表達,且最高表達量均出現(xiàn)在48 h或72 h,之后下降并恢復至正常水平。而IPA小鼠促炎癥細胞因子TNF-α緩慢且低水平釋放�！窘Y論】NOD1、RIP2的表達受到長期抑制,NOD2在感染最早期的過度激活以及隨后的抑制表達,引起促炎細胞因子低表達,可能導致了侵襲性肺曲霉的發(fā)生發(fā)展。
[Abstract]:[objective] to study the role of cytoplasmic recognition receptor (NODs) and its signal pathway in murine invasive pulmonary aspergillosis (IPA) in innate immune system. [methods] mice were randomly divided into normal control group. Normal inoculated aspergillus fumigatus group (normal infection group) and immunosuppressive inoculated aspergillus fumigatus group (IPA group). After nasal inhalation of aspergillus fumigatus spores, the mice were killed at different time points. The expression of NOD1,NOD2,RIP2 mRNA in lung tissue of mice infected with Aspergillus fumigatus was detected by RT-PCR and Western blot. [results] at 72 h after nasal inhalation of Aspergillus fumigatus, severe inflammatory reaction occurred in lung tissue and a large amount of mycelium was produced in IPA-treated group, and the load of Aspergillus fumigatus at each time point was higher than that in normal infection group. Compared with the normal infection group, the expression of NOD1,RIP2 mRNA in the IPA group continued to be low, while the expression of NOD2 mRNA was abnormally high in the early stage of infection (24 h), and remained in a low expression state during the subsequent infection, and the normal mice were infected with Aspergillus fumigatus. The expression of proinflammatory cytokine TNF- 偽 in lung tissue was high in the preinfection stage, and the highest expression occurred at 48 h or 72 h, then decreased and returned to normal level. However, IPA mice promote the slow and low release of inflammatory cytokine TNF- 偽. [conclusion] the expression of NOD1,RIP2 was inhibited by the excessive activation of NOD2 in the early stage of infection and the subsequent inhibition of the expression of NOD1,RIP2, which resulted in the low expression of proinflammatory cytokines. This may lead to the development of invasive pulmonary aspergillus.
【作者單位】： 江西中醫(yī)學院現(xiàn)代中藥制劑教育部重點實驗室;湖南中醫(yī)藥大學藥學院;江西中醫(yī)學院藥學院;南昌大學醫(yī)學院微生物學教研室;
【基金】：國家自然科學基金項目(No.30560147,30760236)
【分類號】：R563
[Abstract]:[objective] to study the role of cytoplasmic recognition receptor (NODs) and its signal pathway in murine invasive pulmonary aspergillosis (IPA) in innate immune system. [methods] mice were randomly divided into normal control group. Normal inoculated aspergillus fumigatus group (normal infection group) and immunosuppressive inoculated aspergillus fumigatus group (IPA group). After nasal inhalation of aspergillus fumigatus spores, the mice were killed at different time points. The expression of NOD1,NOD2,RIP2 mRNA in lung tissue of mice infected with Aspergillus fumigatus was detected by RT-PCR and Western blot. [results] at 72 h after nasal inhalation of Aspergillus fumigatus, severe inflammatory reaction occurred in lung tissue and a large amount of mycelium was produced in IPA-treated group, and the load of Aspergillus fumigatus at each time point was higher than that in normal infection group. Compared with the normal infection group, the expression of NOD1,RIP2 mRNA in the IPA group continued to be low, while the expression of NOD2 mRNA was abnormally high in the early stage of infection (24 h), and remained in a low expression state during the subsequent infection, and the normal mice were infected with Aspergillus fumigatus. The expression of proinflammatory cytokine TNF- 偽 in lung tissue was high in the preinfection stage, and the highest expression occurred at 48 h or 72 h, then decreased and returned to normal level. However, IPA mice promote the slow and low release of inflammatory cytokine TNF- 偽. [conclusion] the expression of NOD1,RIP2 was inhibited by the excessive activation of NOD2 in the early stage of infection and the subsequent inhibition of the expression of NOD1,RIP2, which resulted in the low expression of proinflammatory cytokines. This may lead to the development of invasive pulmonary aspergillus.
【作者單位】： 江西中醫(yī)學院現(xiàn)代中藥制劑教育部重點實驗室;湖南中醫(yī)藥大學藥學院;江西中醫(yī)學院藥學院;南昌大學醫(yī)學院微生物學教研室;
【基金】：國家自然科學基金項目(No.30560147,30760236)
【分類號】：R563
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