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2008 ; 130
(5
): 979-92
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TLR9 is expressed in idiopathic interstitial pneumonia and its activation
promotes in vitro myofibroblast differentiation
#MMPMID18633634
Meneghin A
; Choi ES
; Evanoff HL
; Kunkel SL
; Martinez FJ
; Flaherty KR
; Toews GB
; Hogaboam CM
Histochem Cell Biol
2008[Nov]; 130
(5
): 979-92
PMID18633634
show ga
Infectious diseases can be cofactors in idiopathic interstitial pneumonias (IIP)
pathogenesis; recent data suggests that toll-like receptors 9 (TLR9) ligands
contribute to experimental chronic tissue remodeling. Real-time TAQMAN and
immunohistochemical analysis of IIP normal surgical lung biopsies (SLBs), primary
fibroblast lines grown from both IIP and normal SLBs indicate that TLR9 is
prominently and differentially expressed in a disease-specific manner. TLR9
expression was increased in biopsies from patients with IIP compared with normal
lung biopsies and its expression is localized to areas of marked interstitial
fibrosis. TLR9 in fibroblasts appeared to be increased by profibrotic Th2
cytokines (IL-4 and IL-13) and this was true in fibroblasts cultured from the
most severe form of IIP, idiopathic pulmonary fibrosis (IPF) SLBs, in
non-specific interstitial pneumonia fibroblast lines, and in normal fibroblasts.
Finally, confocal microscopy studies have shown that TLR9 activation by its
synthetic agonist CpG-ODN significantly increased the expression of alpha smooth
muscle actin, the main marker of myofibroblast differentiation. These data
indicate that TLR9 expression may drive the abnormal tissue healing response in
severe forms of IIP and its activation can have a key role in myofibroblast
differentiation promoting the progression of disease during the terminal phase of
IPF.
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