Nontypeable Haemophilus influenzae (NTHi) directly interfere with the regulation of E-cadherin in lung epithelial cells

Inga Kaufhold; Sünja Osbahr; Kensuke Shima; Sebastian Marwitz; Kristina Rohmann; Daniel Drömann; Torsten Goldmann; Klaus Dalhoff; Jan Rupp

doi:10.1016/j.micinf.2017.07.002

Nontypeable Haemophilus influenzae (NTHi) directly interfere with the regulation of E-cadherin in lung epithelial cells

Inga Kaufhold^*, Sünja Osbahr, Kensuke Shima, Sebastian Marwitz, Kristina Rohmann, Daniel Drömann, Torsten Goldmann, Klaus Dalhoff, Jan Rupp

^*Corresponding author for this work

Abstract

Loss of epithelial barriers characterized by reduction of E-cadherin is a hallmark of chronic obstructive pulmonary disease (COPD). We investigated the effects of nontypeable Haemophilus influenzae (NTHi) infections, associated with acute exacerbations of chronic bronchitis, on the regulation of E-cadherin in host cells. NTHi infection decreased E-cadherin mRNA and protein-levels in lung epithelial cells. E-cadherin reduction was mediated by activation of the fibroblast growth factor 2 (FGF2), the mammalian target of rapamycin (mTOR) and Slug. These data indicate that epithelial integrity and barrier function is disturbed by NTHi infection. Mainly, the destruction of cell–cell contacts is a prominent feature in NTHi infection.

Original language	English
Journal	Microbes and Infection
Volume	19
Issue number	11
Pages (from-to)	560-566
Number of pages	7
ISSN	1286-4579
DOIs	https://doi.org/10.1016/j.micinf.2017.07.002
Publication status	Published - 01.11.2017

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Academic Focus: Center for Infection and Inflammation Research (ZIEL)

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10.1016/j.micinf.2017.07.002

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title = "Nontypeable Haemophilus influenzae (NTHi) directly interfere with the regulation of E-cadherin in lung epithelial cells",

abstract = "Loss of epithelial barriers characterized by reduction of E-cadherin is a hallmark of chronic obstructive pulmonary disease (COPD). We investigated the effects of nontypeable Haemophilus influenzae (NTHi) infections, associated with acute exacerbations of chronic bronchitis, on the regulation of E-cadherin in host cells. NTHi infection decreased E-cadherin mRNA and protein-levels in lung epithelial cells. E-cadherin reduction was mediated by activation of the fibroblast growth factor 2 (FGF2), the mammalian target of rapamycin (mTOR) and Slug. These data indicate that epithelial integrity and barrier function is disturbed by NTHi infection. Mainly, the destruction of cell–cell contacts is a prominent feature in NTHi infection.",

author = "Inga Kaufhold and S{\"u}nja Osbahr and Kensuke Shima and Sebastian Marwitz and Kristina Rohmann and Daniel Dr{\"o}mann and Torsten Goldmann and Klaus Dalhoff and Jan Rupp",

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language = "English",

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TY - JOUR

T1 - Nontypeable Haemophilus influenzae (NTHi) directly interfere with the regulation of E-cadherin in lung epithelial cells

AU - Kaufhold, Inga

AU - Osbahr, Sünja

AU - Shima, Kensuke

AU - Marwitz, Sebastian

AU - Rohmann, Kristina

AU - Drömann, Daniel

AU - Goldmann, Torsten

AU - Dalhoff, Klaus

AU - Rupp, Jan

PY - 2017/11/1

Y1 - 2017/11/1

N2 - Loss of epithelial barriers characterized by reduction of E-cadherin is a hallmark of chronic obstructive pulmonary disease (COPD). We investigated the effects of nontypeable Haemophilus influenzae (NTHi) infections, associated with acute exacerbations of chronic bronchitis, on the regulation of E-cadherin in host cells. NTHi infection decreased E-cadherin mRNA and protein-levels in lung epithelial cells. E-cadherin reduction was mediated by activation of the fibroblast growth factor 2 (FGF2), the mammalian target of rapamycin (mTOR) and Slug. These data indicate that epithelial integrity and barrier function is disturbed by NTHi infection. Mainly, the destruction of cell–cell contacts is a prominent feature in NTHi infection.

AB - Loss of epithelial barriers characterized by reduction of E-cadherin is a hallmark of chronic obstructive pulmonary disease (COPD). We investigated the effects of nontypeable Haemophilus influenzae (NTHi) infections, associated with acute exacerbations of chronic bronchitis, on the regulation of E-cadherin in host cells. NTHi infection decreased E-cadherin mRNA and protein-levels in lung epithelial cells. E-cadherin reduction was mediated by activation of the fibroblast growth factor 2 (FGF2), the mammalian target of rapamycin (mTOR) and Slug. These data indicate that epithelial integrity and barrier function is disturbed by NTHi infection. Mainly, the destruction of cell–cell contacts is a prominent feature in NTHi infection.

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U2 - 10.1016/j.micinf.2017.07.002

DO - 10.1016/j.micinf.2017.07.002

M3 - Journal articles

AN - SCOPUS:85027964181

SN - 1286-4579

VL - 19

SP - 560

EP - 566

JO - Microbes and Infection

JF - Microbes and Infection

IS - 11

ER -

Nontypeable Haemophilus influenzae (NTHi) directly interfere with the regulation of E-cadherin in lung epithelial cells

Abstract

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UN SDGs

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