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Human nasal epithelial cell, Influenza virus, iTRAQ

ABSTRACT: Few studies have examined the local surface remodeling of primary human nasal epithelial cells (HNECs) during viral infection. Hence, the full range of upregulated adhesion molecules during respiratory viral infections that facilitate bacterial attachment and entry remain unknown. Accordingly, the current study provides a comprehensive view of HNEC responses to influenza virus pH1N1 infection, via global proteome profiling of uninfected (Mock, n = 4) and influenza-infected (Virus-only, n = 4) HNECs with isobaric tags using relative and absolute quantitation (iTRAQ) technique. A total of 3583 proteins were detected, 89 of which were significantly increased (52 proteins) or decreased (37 proteins) in the virus-infected HNECs compared to mock-infected controls (p < 0.05).

INSTRUMENT(S): LTQ Orbitrap Velos

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Primary Cell, Epithelial Cell

DISEASE(S): Influenza

SUBMITTER: Youn Wook Chung

LAB HEAD: Ji-Hwan Ryu

PROVIDER: PXD042618 | Pride | 2024-05-08

REPOSITORIES: Pride

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Project description:E2 exposure significantly decreased peak viral titer in hNECs from female donors. We used microarray analyses to identify global gene expression patterns between E2 and vehicle exposed hNECs from female donors Influenza causes an acute infection characterized by virus replication in respiratory epithelial cells. The severity of influenza and other respiratory diseases changes over the life course and during pregnancy in women, suggesting that sex steroid hormones, such as estrogens, may be involved. Using primary, differentiated human nasal epithelial cell (hNEC) cultures from adult male and female donors, we exposed cultures to the endogenous 17Î²-estradiol (E2) or select estrogen receptor modulators (SERMs), then infected cultures with a seasonal influenza A virus (IAV) to determine whether estrogenic signaling could affect the outcome of IAV infection and whether these effects where sex-dependent. Estradiol, raloxifene, and bisphenol A decreased IAV titers in hNECs from female, but not male, donors. The estrogenic decrease in viral titer was dependent on the genomic estrogen receptor- 2 (ESR2) as neither genomic ESR1 nor non- genomic GPR30 were expressed in hNEC cultures and addition of the genomic ER antagonist ICI 182,780 reversed the antiviral effects of E2. Treatment of hNECs with E2 had no effect on interferon or chemokine secretion, but significantly downregulated cell metabolic processes, including genes that encode for zinc finger proteins, many of which contain estrogen response elements in their promoters. These data provide novel insights into the cellular and molecular mechanisms of how natural and synthetic estrogens impact IAV infection in respiratory epithelial cells derived from humans. Primary human nasal epithelial cells from females were exposed to E2 for 24h prior to infection, then infected with an H3N2 strain of influenza a virus for 2 hours. At 24 and 48h post infection, hNECs were collected in Trizol for RNA extraction and hybridization on Affymetrix Human Gene ST 2.0 microarrays.

			Action	DRS
	H7-iTRAQ-Wook-1-24.msf	Msf
	H7-iTRAQ-Wook-1.raw	Raw
	H7-iTRAQ-Wook-10.raw	Raw
	H7-iTRAQ-Wook-11.raw	Raw
	H7-iTRAQ-Wook-12.raw	Raw

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Human nasal epithelial cell, Influenza virus, iTRAQ

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