CC16 Regulates Inflammation, ROS Generation and Apoptosis in Bronchial Epithelial Cells during <i>Klebsiella pneumoniae</i> Infection

Gram-negative (G-) bacteria are the leading cause of hospital-acquired pneumonia in the United States. The devastating damage caused by G- bacteria results from the imbalance of bactericidal effects and overwhelming inflammation. Despite decades of research, the underlying mechanisms by which runawa...

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Autores principales:	Sultan Almuntashiri, Yohan Han, Yin Zhu, Saugata Dutta, Sara Niazi, Xiaoyun Wang, Budder Siddiqui, Duo Zhang
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	SCGB1A1 bacterial pneumonia lung injury cell death innate immunity NF-κB pathway Biology (General) QH301-705.5 Chemistry QD1-999
Acceso en línea:	https://doaj.org/article/049b254359db4a1fbcaf47112b9f9c85
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spelling	oai:doaj.org-article:049b254359db4a1fbcaf47112b9f9c852021-11-11T16:55:23ZCC16 Regulates Inflammation, ROS Generation and Apoptosis in Bronchial Epithelial Cells during <i>Klebsiella pneumoniae</i> Infection10.3390/ijms2221114591422-00671661-6596https://doaj.org/article/049b254359db4a1fbcaf47112b9f9c852021-10-01T00:00:00Zhttps://www.mdpi.com/1422-0067/22/21/11459https://doaj.org/toc/1661-6596https://doaj.org/toc/1422-0067Gram-negative (G-) bacteria are the leading cause of hospital-acquired pneumonia in the United States. The devastating damage caused by G- bacteria results from the imbalance of bactericidal effects and overwhelming inflammation. Despite decades of research, the underlying mechanisms by which runaway inflammation is developed remain incompletely understood. Clara Cell Protein 16 (CC16), also known as uteroglobin, is the major protein secreted by Clara cells and the most abundant protein in bronchoalveolar lavage fluid (BALF). However, the regulation and functions of CC16 during G- bacterial infection are unknown. In this study, we aimed to assess the regulation of CC16 in response to <i>Klebsiella pneumoniae</i> (<i>K. pneu</i>) and to investigate the role of CC16 in bronchial epithelial cells. After <i>K. pneu</i> infection, we found that CC16 mRNA expression was significantly decreased in bronchial epithelial cells. Our data also showed that <i>K. pneu</i> infection upregulated cytokine and chemokine genes, including IL-1β, IL-6, and IL-8 in BEAS-2B cells. Endogenously overexpressed CC16 in BEAS-2B cells provided an anti-inflammatory effect by reducing these markers. We also observed that endogenous CC16 can repress NF-κB reporter activity. In contrast, the recombinant CC16 (rCC16) did not show an anti-inflammatory effect in <i>K. pneu-</i>infected cells or suppression of NF-κB promoter activity. Moreover, the overexpression of CC16 reduced reactive oxygen species (ROS) levels and protected BEAS-2B cells from <i>K. pneu</i>-induced apoptosis.Sultan AlmuntashiriYohan HanYin ZhuSaugata DuttaSara NiaziXiaoyun WangBudder SiddiquiDuo ZhangMDPI AGarticleSCGB1A1bacterial pneumonialung injurycell deathinnate immunityNF-κB pathwayBiology (General)QH301-705.5ChemistryQD1-999ENInternational Journal of Molecular Sciences, Vol 22, Iss 11459, p 11459 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	SCGB1A1 bacterial pneumonia lung injury cell death innate immunity NF-κB pathway Biology (General) QH301-705.5 Chemistry QD1-999
spellingShingle	SCGB1A1 bacterial pneumonia lung injury cell death innate immunity NF-κB pathway Biology (General) QH301-705.5 Chemistry QD1-999 Sultan Almuntashiri Yohan Han Yin Zhu Saugata Dutta Sara Niazi Xiaoyun Wang Budder Siddiqui Duo Zhang CC16 Regulates Inflammation, ROS Generation and Apoptosis in Bronchial Epithelial Cells during <i>Klebsiella pneumoniae</i> Infection
description	Gram-negative (G-) bacteria are the leading cause of hospital-acquired pneumonia in the United States. The devastating damage caused by G- bacteria results from the imbalance of bactericidal effects and overwhelming inflammation. Despite decades of research, the underlying mechanisms by which runaway inflammation is developed remain incompletely understood. Clara Cell Protein 16 (CC16), also known as uteroglobin, is the major protein secreted by Clara cells and the most abundant protein in bronchoalveolar lavage fluid (BALF). However, the regulation and functions of CC16 during G- bacterial infection are unknown. In this study, we aimed to assess the regulation of CC16 in response to <i>Klebsiella pneumoniae</i> (<i>K. pneu</i>) and to investigate the role of CC16 in bronchial epithelial cells. After <i>K. pneu</i> infection, we found that CC16 mRNA expression was significantly decreased in bronchial epithelial cells. Our data also showed that <i>K. pneu</i> infection upregulated cytokine and chemokine genes, including IL-1β, IL-6, and IL-8 in BEAS-2B cells. Endogenously overexpressed CC16 in BEAS-2B cells provided an anti-inflammatory effect by reducing these markers. We also observed that endogenous CC16 can repress NF-κB reporter activity. In contrast, the recombinant CC16 (rCC16) did not show an anti-inflammatory effect in <i>K. pneu-</i>infected cells or suppression of NF-κB promoter activity. Moreover, the overexpression of CC16 reduced reactive oxygen species (ROS) levels and protected BEAS-2B cells from <i>K. pneu</i>-induced apoptosis.
format	article
author	Sultan Almuntashiri Yohan Han Yin Zhu Saugata Dutta Sara Niazi Xiaoyun Wang Budder Siddiqui Duo Zhang
author_facet	Sultan Almuntashiri Yohan Han Yin Zhu Saugata Dutta Sara Niazi Xiaoyun Wang Budder Siddiqui Duo Zhang
author_sort	Sultan Almuntashiri
title	CC16 Regulates Inflammation, ROS Generation and Apoptosis in Bronchial Epithelial Cells during <i>Klebsiella pneumoniae</i> Infection
title_short	CC16 Regulates Inflammation, ROS Generation and Apoptosis in Bronchial Epithelial Cells during <i>Klebsiella pneumoniae</i> Infection
title_full	CC16 Regulates Inflammation, ROS Generation and Apoptosis in Bronchial Epithelial Cells during <i>Klebsiella pneumoniae</i> Infection
title_fullStr	CC16 Regulates Inflammation, ROS Generation and Apoptosis in Bronchial Epithelial Cells during <i>Klebsiella pneumoniae</i> Infection
title_full_unstemmed	CC16 Regulates Inflammation, ROS Generation and Apoptosis in Bronchial Epithelial Cells during <i>Klebsiella pneumoniae</i> Infection
title_sort	cc16 regulates inflammation, ros generation and apoptosis in bronchial epithelial cells during <i>klebsiella pneumoniae</i> infection
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/049b254359db4a1fbcaf47112b9f9c85
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CC16 Regulates Inflammation, ROS Generation and Apoptosis in Bronchial Epithelial Cells during <i>Klebsiella pneumoniae</i> Infection

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