Altered expression of TIAM1 in endotoxin-challenged airway epithelial cells and rodent septic models

Jie Ma, Chuanxi Chen, Yongjun Liu, Mahendra Damarla, Becky Marie Vonakis, Xiangdong Guan, Li Gao

Research output: Contribution to journalArticle

Abstract

Background: In sepsis, reorganization of the actin cytoskeleton in the epithelium during inflammation will lead to a breakdown of epithelial barrier integrity, and contribute to the pathogenesis of sepsis, but the exact changes of various components regulating the actin cytoskeleton pathway remain unclear. Methods: We used lipopolysaccharide (LPS) challenged primary epithelial cells cultured at the airliquid interface (ALI) to mimic epithelial barrier dysfunction during sepsis. Then we detected differential expression of T-lymphoma invasion and metastasis 1 (TIAM1) gene in lung epithelial cells and septic models. Results: LPS induced barrier dysfunction in human tracheobronchial epithelial cells (HTBEs) as measured by statistically significant changes in ionic and macromolecular permeability. We observed differential expression of TIAM1 gene. The protein expression of TIAM1 was decreased after LPS challenge, in human bronchial epithelial cells. Furthermore, the expression levels of both TIAM1 mRNA and protein were decreased in lungs of septic rodent models. Conclusions: Given that expression levels of TIAM1 have been associated with mortality among sepsis patients, our findings have the potential for the development of diagnostic and treatment strategies relevant for patient management.

Original languageEnglish (US)
Pages (from-to)3187-3195
Number of pages9
JournalJournal of Thoracic Disease
Volume10
Issue number6
DOIs
StatePublished - Jun 1 2018

Fingerprint

Endotoxins
Rodentia
Lymphoma
Epithelial Cells
Neoplasm Metastasis
Sepsis
Lipopolysaccharides
Actin Cytoskeleton
Lung
Genes
Permeability
Proteins
Epithelium
Inflammation
Messenger RNA
Mortality
Therapeutics

Keywords

  • Airway epithelial cell
  • Lipopolysaccharide (LPS)
  • T-lymphoma invasion and metastasis 1 (TIAM1)

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

Cite this

Altered expression of TIAM1 in endotoxin-challenged airway epithelial cells and rodent septic models. / Ma, Jie; Chen, Chuanxi; Liu, Yongjun; Damarla, Mahendra; Vonakis, Becky Marie; Guan, Xiangdong; Gao, Li.

In: Journal of Thoracic Disease, Vol. 10, No. 6, 01.06.2018, p. 3187-3195.

Research output: Contribution to journalArticle

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AU - Ma, Jie

AU - Chen, Chuanxi

AU - Liu, Yongjun

AU - Damarla, Mahendra

AU - Vonakis, Becky Marie

AU - Guan, Xiangdong

AU - Gao, Li

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N2 - Background: In sepsis, reorganization of the actin cytoskeleton in the epithelium during inflammation will lead to a breakdown of epithelial barrier integrity, and contribute to the pathogenesis of sepsis, but the exact changes of various components regulating the actin cytoskeleton pathway remain unclear. Methods: We used lipopolysaccharide (LPS) challenged primary epithelial cells cultured at the airliquid interface (ALI) to mimic epithelial barrier dysfunction during sepsis. Then we detected differential expression of T-lymphoma invasion and metastasis 1 (TIAM1) gene in lung epithelial cells and septic models. Results: LPS induced barrier dysfunction in human tracheobronchial epithelial cells (HTBEs) as measured by statistically significant changes in ionic and macromolecular permeability. We observed differential expression of TIAM1 gene. The protein expression of TIAM1 was decreased after LPS challenge, in human bronchial epithelial cells. Furthermore, the expression levels of both TIAM1 mRNA and protein were decreased in lungs of septic rodent models. Conclusions: Given that expression levels of TIAM1 have been associated with mortality among sepsis patients, our findings have the potential for the development of diagnostic and treatment strategies relevant for patient management.

AB - Background: In sepsis, reorganization of the actin cytoskeleton in the epithelium during inflammation will lead to a breakdown of epithelial barrier integrity, and contribute to the pathogenesis of sepsis, but the exact changes of various components regulating the actin cytoskeleton pathway remain unclear. Methods: We used lipopolysaccharide (LPS) challenged primary epithelial cells cultured at the airliquid interface (ALI) to mimic epithelial barrier dysfunction during sepsis. Then we detected differential expression of T-lymphoma invasion and metastasis 1 (TIAM1) gene in lung epithelial cells and septic models. Results: LPS induced barrier dysfunction in human tracheobronchial epithelial cells (HTBEs) as measured by statistically significant changes in ionic and macromolecular permeability. We observed differential expression of TIAM1 gene. The protein expression of TIAM1 was decreased after LPS challenge, in human bronchial epithelial cells. Furthermore, the expression levels of both TIAM1 mRNA and protein were decreased in lungs of septic rodent models. Conclusions: Given that expression levels of TIAM1 have been associated with mortality among sepsis patients, our findings have the potential for the development of diagnostic and treatment strategies relevant for patient management.

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