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Host defesen effects of vitamin D

ABSTRACT: To study the pleiotropic effects of vitamin D in airway host defense, we use airway epithelial organoids cultured on air-liquid interface (ALI), originating from three chronic rhinosinusitis patients, marking as N66, N67 and N69, respectively. 24 hours prior to infection of Staphylococcus Aureus or influenza virus H1N1, 10nM and 100nM 1,25(OH)2D3 were added respectively to the medium in the lower chamber of Transwells with organoids. 24 hours post infection, 100μl DPBS were added to the apical surface of organoids for 20 minutes and then cellular secretion diluted in the DPBS were collected for proteomics analysis. The control groups without 1,25(OH)2D3 treatment were denoted as ND and those without infection were denoted as C. We applied a mass spectrometry-based tandem mass tag quantitative proteomics to analyze the cellular secretion from airway epithelial organoids, so as to study the host defense effects of vitamin D against pathogen infection.

ORGANISM(S): Homo Sapiens

SUBMITTER: Liang li

PROVIDER: PXD031956 | iProX | Mon Feb 28 00:00:00 GMT 2022

REPOSITORIES: iProX

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Vitamin D promotes epithelial tissue repair and host defense responses against influenza H1N1 virus and Staphylococcus aureus infections.

Liao Shumin S Huang Yanhong Y Zhang Jinxiu J Xiong Qinglan Q Chi Mengshi M Yang Liang L Zhang Junhang J Li Liang L Fan Yunping Y

Respiratory research 20230705 1

<h4>Background</h4>Early studies indicated that vitamin D (VD) exerted pleiotropic extra-skeletal effects in the airway, but the definite linkage between VD deficiency and airway host responses remains unclear.<h4>Methods</h4>142 cases of clinical data from Department of Otolaryngology, the Seventh Affiliated Hospital of Sun Yat-sen University, were collected to characterize the relationship between VD deficiency and chronic rhinosinusitis (CRS). Based on the clinical observations, 2.5-D airway ...[more]

PMID: 37407993

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Project description:In the process of seeking novel lung host defense regulators by analyzing genome-wide RNA sequence data from normal human airway epithelium, we detected expression of POU2AF1, a known transcription co-factor previously thought to be expressed only in lymphocytes. Lymphocyte contamination of human airway epithelial samples obtained by bronchoscopy and brushing was excluded by immunohistochemistry staining, the observation of up-regulation of POU2AF1 in purified airway basal stem/progenitor cells undergoing differentiation and analysis of differentiating single basal cell clones. Lentivirus-mediated up-regulation of POU2AF1 in airway basal cells induced up-regulation of host defense genes, including MX1, IFIT3, IFITM and known POU2AF1 downstream genes HLA-DRA, ID2, ID3, IL6, BCL6. Interestingly, expression of these genes paralleled changes of POU2AF1 expression during airway epithelium differentiation in vitro, suggesting POU2AF1 helps to maintain a "host defense tone" even in pathogen-free condition. Cigarette smoke, a known risk factor for airway infection, suppressed POU2AF1 expression both in vivo in humans and in vitro in human airway epithelial cultures, accompanied by deregulation of POU2AF1 downstream genes. Finally, enhancing POU2AF1 expression in human airway epithelium attenuated the suppression of host defense genes by smoking. Together, these findings suggest a novel function of POU2AF1 as a potential regulator of host defense genes in the human airway epithelium. Methods: Massive parallel RNA sequencing was used to compare the transcriptome of lentivirus mediated POU2AF1 or RFP (control) gene expression in human primary airway epithelial cells (3 samples per group). Uninfected basal cell was used as a further control. Conclusions: The genes up-regulated by POU2AF1 in human airway epithelial cells are mainly related to the intracellular or extracellular anti-pathogen response, suggesting POU2AF1 plays a role in airway epithelial host defense. This Series represents samples complementary to those in GSE60989.

Project description:In the process of seeking novel lung host defense regulators by analyzing genome-wide RNA sequence data from normal human airway epithelium, we detected expression of POU2AF1, a known transcription co-factor previously thought to be expressed only in lymphocytes. Lymphocyte contamination of human airway epithelial samples obtained by bronchoscopy and brushing was excluded by immunohistochemistry staining, the observation of up-regulation of POU2AF1 in purified airway basal stem/progenitor cells undergoing differentiation and analysis of differentiating single basal cell clones. Lentivirus-mediated up-regulation of POU2AF1 in airway basal cells induced up-regulation of host defense genes, including MX1, IFIT3, IFITM and known POU2AF1 downstream genes HLA-DRA, ID2, ID3, IL6, BCL6. Interestingly, expression of these genes paralleled changes of POU2AF1 expression during airway epithelium differentiation in vitro, suggesting POU2AF1 helps to maintain a "host defense tone" even in pathogen-free condition. Cigarette smoke, a known risk factor for airway infection, suppressed POU2AF1 expression both in vivo in humans and in vitro in human airway epithelial cultures, accompanied by deregulation of POU2AF1 downstream genes. Finally, enhancing POU2AF1 expression in human airway epithelium attenuated the suppression of host defense genes by smoking. Together, these findings suggest a novel function of POU2AF1 as a potential regulator of host defense genes in the human airway epithelium. Methods: Massive parallel RNA sequencing was used to compare the transcriptome of lentivirus mediated POU2AF1 or RFP (control) gene expression in human primary airway epithelial cells (3 samples per group). Uninfected basal cell was used as a further control. Conclusions: The genes up-regulated by POU2AF1 in human airway epithelial cells are mainly related to the intracellular or extracellular anti-pathogen response, suggesting POU2AF1 plays a role in airway epithelial host defense. By genome-wide-based screening, POU2AF1, a known lymphocyte transcription co-factor, was found to be expressed in human airway epithelium and regulate host defense genes. It might be a drug target as smoking-compromised host defense is associated with down-regulation of POU2AF1. In this Series, human airway epithelial cell transcriptomes (3 uninfected without treatment, 3 infected with lenti-RFP virus and 3 infected with lenti-POU2AF1 virus) were compared using massive parallel RNA sequencing (Illumina HiSeq 2000).

Dataset Information

Host defesen effects of vitamin D

Publications

Vitamin D promotes epithelial tissue repair and host defense responses against influenza H1N1 virus and Staphylococcus aureus infections.

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