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Moraxella catarrhalis-induced innate...

Chen, Miao.

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Moraxella catarrhalis-induced innate immune responses in human pulmonary epithelial cells and monocytes.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Moraxella catarrhalis-induced innate immune responses in human pulmonary epithelial cells and monocytes./
Author:	Chen, Miao.
Description:	118 p.
Notes:	Source: Dissertation Abstracts International, Volume: 71-03, Section: B, page: 1608.
Contained By:	Dissertation Abstracts International71-03B.
Subject:	Health Sciences, Immunology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3399811
ISBN:	9781109657869

Moraxella catarrhalis-induced innate immune responses in human pulmonary epithelial cells and monocytes.
Chen, Miao.

Moraxella catarrhalis-induced innate immune responses in human pulmonary epithelial cells and monocytes. - 118 p.

Source: Dissertation Abstracts International, Volume: 71-03, Section: B, page: 1608.

Thesis (Ph.D.)--The University of Toledo, 2010.

COPD is characterized by chronic inflammation in the lung, and its severe stage exacerbation is one of the major burdens of healthcare, causing diminished quality of life and highly increased mortality rate. Most common treatments for COPD could only improve the symptoms, but do not suppress the undergoing inflammations. Our study based on understanding the molecular basis of M. catarrhalis-induced innate immune responses on pulmonary epithelial cells and monocytes would help to identify new therapeutic target for COPD. M. catarrhalis has been proved to be the third leading cause of COPD. We found that M. catarrhalis could induce CCL20/MIP-3alpha expression mainly through TLR2-MyD88-TRAF-6-NF-kappaB/MAPK signaling pathway on pulmonary epithelial cells. Only TLR2, but not TLR4 signaling pathway can be activated on those cells during M. catarrhalis infection. Study on stable transfected HEK293 cells suggested that CD14 and MD2 are critical to activate TLR4 signaling; and sCD14 could enhance TLR2-mediated inflammatory responses. Thus our hypothesis is that lack of CD14 and MD2 might contribute to the silence of TLR4 signaling; and sCD14 released from monocytes could modulate TLR2- and TLR4-mediated inflammatory responses on airway epithelial cells. Both mCD14 and sCD14 expression levels are very low on naive monocytic THP1 cells. 1alpha, 25-dihydroxy VD3 and specific ligands of TLR2 and TLR4 could increase mCD14 and sCD14 expression, which up-regulates both TLR2- and TLR4-mediated inflammatory responses on THP1 cells. Meanwhile, conditioned media from 1alpha, 25-dihydroxy VD3 primed THP1 cells could activate TLR4 signaling pathway and enhance TLR2-mediated inflammatory responses on pulmonary epithelial cells under M. catarrhalis infection. Such amplified inflammatory responses could be abolished by CD14 antibody. All these data suggest that sCD14 could mediate a crosstalk between monocytes and pulmonary epithelial cells to mount an amplification loop through TLR2 and TLR4 during bacteria-induced inflammatory responses. Thus CD14 could be a potential therapeutic target to inhibit the abnormal inflammation during the pathogenesis of COPD or development of exacerbation.

ISBN: 9781109657869Subjects--Topical Terms:

1017716
Health Sciences, Immunology.

Moraxella catarrhalis-induced innate immune responses in human pulmonary epithelial cells and monocytes.
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502 $a Thesis (Ph.D.)--The University of Toledo, 2010.
520 $a COPD is characterized by chronic inflammation in the lung, and its severe stage exacerbation is one of the major burdens of healthcare, causing diminished quality of life and highly increased mortality rate. Most common treatments for COPD could only improve the symptoms, but do not suppress the undergoing inflammations. Our study based on understanding the molecular basis of M. catarrhalis-induced innate immune responses on pulmonary epithelial cells and monocytes would help to identify new therapeutic target for COPD. M. catarrhalis has been proved to be the third leading cause of COPD. We found that M. catarrhalis could induce CCL20/MIP-3alpha expression mainly through TLR2-MyD88-TRAF-6-NF-kappaB/MAPK signaling pathway on pulmonary epithelial cells. Only TLR2, but not TLR4 signaling pathway can be activated on those cells during M. catarrhalis infection. Study on stable transfected HEK293 cells suggested that CD14 and MD2 are critical to activate TLR4 signaling; and sCD14 could enhance TLR2-mediated inflammatory responses. Thus our hypothesis is that lack of CD14 and MD2 might contribute to the silence of TLR4 signaling; and sCD14 released from monocytes could modulate TLR2- and TLR4-mediated inflammatory responses on airway epithelial cells. Both mCD14 and sCD14 expression levels are very low on naive monocytic THP1 cells. 1alpha, 25-dihydroxy VD3 and specific ligands of TLR2 and TLR4 could increase mCD14 and sCD14 expression, which up-regulates both TLR2- and TLR4-mediated inflammatory responses on THP1 cells. Meanwhile, conditioned media from 1alpha, 25-dihydroxy VD3 primed THP1 cells could activate TLR4 signaling pathway and enhance TLR2-mediated inflammatory responses on pulmonary epithelial cells under M. catarrhalis infection. Such amplified inflammatory responses could be abolished by CD14 antibody. All these data suggest that sCD14 could mediate a crosstalk between monocytes and pulmonary epithelial cells to mount an amplification loop through TLR2 and TLR4 during bacteria-induced inflammatory responses. Thus CD14 could be a potential therapeutic target to inhibit the abnormal inflammation during the pathogenesis of COPD or development of exacerbation.
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