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首页> 外文期刊>Applied Microbiology and Biotechnology >Intranasal delivery of Duox2 DNA using cationic polymer can prevent acute influenza A viral infection in vivo lung
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Intranasal delivery of Duox2 DNA using cationic polymer can prevent acute influenza A viral infection in vivo lung

机译：使用阳离子聚合物的Duox2 DNA的鼻内递送可以防止急性流感体内肺的病毒感染

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摘要

We studied the contribution of Duox2 in mucosal host defense against influenza A virus (IAV) infection in in vivo lung. We found that Duox2 was required for the induction of type I and III interferon (IFN)s and transient Duox2 overexpression using cationic polymer polyethyleneimine (PEI) leads to suppression of IAV infection in in vivo lung. Twenty mice (C57BL/6J) were anesthetized and challenged by intranasal administration of 213 pfu/30 mu l of IAV (WS/33/H1N1), and IAV-infected mice were euthanized at 1, 3, 5, 7, 10, 14 days post infection (dpi). Duox2 small hairpin RNA (shRNA) and pCMV-Duox2 formulated with PEI were inoculated to mice to assess the regulatory mechanism between Duox2 and IFN secretion. Following intranasal IAV inoculation, viral infection was significantly aggravated from 3 dpi in in vivo lung and viral titer was highest at 7 dpi. Consistent with this, Duox2 messenger RNA (mRNA) and protein expressions were significantly induced from 3 dpi in the lung tissue of IAV-infected mice. Viral titer was much higher in IAV-infected mice that were inoculated with Duox2 shRNA accompanied with lower survival rate and extensive lung pathologies. Interestingly, severe lung pathologies in IAV-infected mice were not observed and viral titer was significantly reduced in mice with pulmonary administration of pCMV-Duox2 formulated with PEI before IAV inoculation. Both mRNA and secreted protein levels of IFN-beta and IFN-lambda(2/3) were highly elevated in IAV-infected mice with pCMV-Duox2 formulated with PEI. Duox2 is necessary for the regulation of IFN secretion in in vivo lung, and pulmonary administration of Duox2 DNA using cationic polymer triggers the induction of type I and III IFNs resulting in more complete suppression of IAV infection.
机译：我们研究了Duox2在体内肺部对乳腺宿主防御的粘膜宿主防御的贡献。我们发现，使用阳离子聚合物聚乙烯亚胺（PEI）诱导I和III型干扰素（IFN）S和瞬时DUOX2过表达诱导DUOX2，导致体内肺的IAV感染抑制IAV感染。通过Intranisal施用213pfu /30μl的IAV（WS / 33 / H1N1）麻醉和攻击，在1,3,5,7,10,14，1,3,5,7,11，14感染后天（DP​​I）。 Duox2用PEI配制的Duox2小发夹RNA（ShRNA）和PCMV-Duox2接种小鼠，以评估Duox2和IFN分泌之间的调节机制。 intranasal Iav接种后，在体内肺的3 dpi中显着加剧病毒感染，病毒滴度在7 dpi中最高。符合此，在IAV感染的小鼠的肺组织中显着诱导Duox2信使RNA（mRNA）和蛋白质表达。 IAV感染小鼠的病毒滴度高得多，该小鼠与Duox2 shRNA接种，伴随着降低的存活率和广泛的肺病理。有趣的是，未观察到IAV感染的小鼠的严重肺病理，并且在IAV接种前用PEI配制的PCMV-DUOX2小鼠中的病毒滴度显着降低。 IFN-β和IFN-Lambda（2/3）的mRNA和分泌的蛋白水平在IAV感染的小鼠中高度升高，所述小鼠用PEI配制PCMV-DUOX2。 Duox2对于在体内肺的IFN分泌中调节IFOX2，并且使用阳离子聚合物的Duox2 DNA的肺部施用触发I型和III IFNS的诱导导致IAV感染更完全抑制IAV感染。

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