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- 저자 : Kolliputi, Narasaiah (검색결과 3 건)
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Lee, Kyung Sun,Jeong, Jae Seok,Kim, So Ri,Cho, Seong Ho,Kolliputi, Narasaiah,Ko, Yun Hee,Lee, Kyung Bae,Park, Suk Chul,Park, Hae Jin,Lee, Yong Chul BMJ Publishing Group 2016 Thorax Vol.71 No.1
<P><B>Background</B></P><P>Sensitisation with <I>Aspergillus fumigatus</I> (<I>Af</I>) is known to be associated with severe allergic lung inflammation, but the mechanism remains to be clarified. Phosphoinositide 3-kinase (PI3K)-δ and endoplasmic reticulum (ER) stress are suggested to be involved in steroid-resistant lung inflammation. We aimed to elucidate the role of PI3K-δ and its relationship with ER stress in fungus-induced allergic lung inflammation.</P><P><B>Methods</B></P><P>Using <I>Af</I>-exposed in vivo and in vitro experimental systems, we examined whether PI3K-δ regulates ER stress, thereby contributing to steroid resistance in fungus-induced allergic lung inflammation. Moreover, we checked expression of an ER stress marker in lung tissues isolated from patients with allergic bronchopulmonary aspergillosis.</P><P><B>Results</B></P><P><I>Af</I>-exposed mice showed that ER stress markers, unfolded protein response (UPR)-related proteins, phosphorylated Akt, generation of mitochondrial reactive oxygen species (mtROS), eosinophilic allergic inflammation, and airway hyperresponsiveness (AHR) were increased in the lung. Similarly, glucose-regulated protein 78 was increased in lung tissues of patients with ABPA. A PI3K-δ inhibitor reduced <I>Af</I>-induced increases in ER stress markers, UPR-related proteins, allergic inflammation and AHR in mice. However, dexamethasone failed to reduce <I>Af</I>-induced allergic inflammation, AHR and elevation of ER stress. Administration of an ER stress inhibitor or a mtROS scavenger improved <I>Af</I>-induced allergic inflammation. The PI3K-δ inhibitor reduced <I>Af</I>-induced mtROS generation and the mtROS scavenger ameliorated ER stress. In primary cultured tracheal epithelial cells, <I>Af</I>-induced ER stress was inhibited by blockade of PI3K-δ.</P><P><B>Conclusions</B></P><P>These findings suggest that PI3K-δ regulates <I>Af</I>-induced steroid-resistant eosinophilic allergic lung inflammation through ER stress.</P>
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Jeong, Jae Seok,Lee, Kyung Bae,Kim, So Ri,Kim, Dong Im,Park, Hae Jin,Lee, Hern-Ku,Kim, Hyung Jin,Cho, Seong Ho,Kolliputi, Narasaiah,Kim, Soon Ha,Lee, Yong Chul BMJ Publishing Group 2018 Thorax Vol.73 No.8
<P><B>Background</B></P><P>Respiratory fungal exposure is known to be associated with severe allergic lung inflammation. Airway epithelium is an essential controller of allergic inflammation. An innate immune recognition receptor, nucleotide-binding domain, leucine-rich-containing family, pyrin-domain-containing-3 (NLRP3) inflammasome, and phosphoinositide 3 kinase (PI3K)-δ in airway epithelium are involved in various inflammatory processes.</P><P><B>Objectives</B></P><P>We investigated the role of NLRP3 inflammasome in fungi-induced allergic lung inflammation and examined the regulatory mechanism of NLRP3 inflammasome, focusing on PI3K-δ in airway epithelium.</P><P><B>Methods</B></P><P>We used two in vivo models induced by exposure to <I>Aspergillus fumigatus</I> (<I>Af</I>) and <I>Alternaria alternata</I> (<I>Aa</I>), as well as an <I>Af</I>-exposed in vitro system. We also checked NLRP3 expression in lung tissues from patients with allergic bronchopulmonary aspergillosis (ABPA).</P><P><B>Results</B></P><P>Assembly/activation of NLRP3 inflammasome was increased in the lung of <I>Af</I>-exposed mice. Elevation of NLRP3 inflammasome assembly/activation was observed in <I>Af</I>-stimulated murine and human epithelial cells. Similarly, pulmonary expression of NLRP3 in patients with ABPA was increased. Importantly, neutralisation of NLRP3 inflammasome derived IL-1β alleviated pathophysiological features of <I>Af</I>-induced allergic inflammation. Furthermore, PI3K-δ blockade improved <I>Af</I>-induced allergic inflammation through modulation of NLRP3 inflammasome, especially in epithelial cells. This modulatory role of PI3K-δ was mediated through the regulation of mitochondrial reactive oxygen species (mtROS) generation. NLRP3 inflammasome was also implicated in <I>Aa</I>-induced eosinophilic allergic inflammation, which was improved by PI3K-δ blockade.</P><P><B>Conclusion</B></P><P>These findings demonstrate that fungi-induced assembly/activation of NLRP3 inflammasome in airway epithelium may be modulated by PI3K-δ, which is mediated partly through the regulation of mtROS generation. Inhibition of PI3K-δ may have potential for treating fungi-induced severe allergic lung inflammation.</P>
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( Shanze Yi ),( Dewei Niu ),( Fang Bai ),( Shuaiguang Li ),( Luyuan Huang ),( Wenyan He ),( Anand Prasad ),( Alexander Czachor ),( Lee Charles Tan ),( Narasaiah Kolliputi ),( Feng Wang ) 한국미생물 · 생명공학회 2016 Journal of microbiology and biotechnology Vol.26 No.11
Manganese superoxide dismutase (MnSOD) is a vital enzyme that protects cells from free radicals through eliminating superoxide radicals (O<sup>2-</sup>). Hirudin, a kind of small active peptide molecule, is one of the strongest anticoagulants that can effectively cure thrombus diseases. In this study, we fused Hirudin to the C terminus of human MnSOD with the GGGGS linker to generate a novel dual-feature fusion protein, denoted as hMnSOD-Hirudin. The hMnSOD-Hirudin gene fragment was cloned into the pET15b (SmaI, CIAP) vector, forming a recombinant pET15b-hMnSOD-Hirudin plasmid, and then was transferred into Escherichia coli strain Rosetta-gami for expression. SDS-PAGE was used to detect the fusion protein, which was expected to be about 30 kDa upon IPTG induction. Furthermore, the hMnSOD-Hirudin protein was heavily detected as a soluble form in the supernatant. The purification rate observed after Ni NTA affinity chromatography was above 95%. The hMnSOD-Hirudin protein yield reached 67.25 mg per liter of bacterial culture. The identity of the purified protein was confirmed by western blotting. The hMnSOD-Hirudin protein activity assay evinced that the antioxidation activity of the hMnSOD-Hirudin protein obtained was 2,444.0 ± 96.0 U/㎎, and the anticoagulant activity of the hMnSOD-Hirudin protein was 599.0 ± 35.0 ATU/㎎. In addition, in vitro bioactivity assay showed that the hMnSODHirudin protein had no or little cytotoxicity in H9c2, HK-2, and H9 (human CD<sub>4</sub> <sup>+</sup>, T cell) cell lines. Transwell migration assay and invasion assay showed that the hMnSOD-Hirudin protein could suppress human lung cancer 95-D cell metastasis and invasion in vitro.
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