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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Am+J+Respir+Crit+Care+Med
2017 ; 195
(8
): 1010-1021
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Secretory IgA Deficiency in Individual Small Airways Is Associated with
Persistent Inflammation and Remodeling
#MMPMID27911098
Polosukhin VV
; Richmond BW
; Du RH
; Cates JM
; Wu P
; Nian H
; Massion PP
; Ware LB
; Lee JW
; Kononov AV
; Lawson WE
; Blackwell TS
Am J Respir Crit Care Med
2017[Apr]; 195
(8
): 1010-1021
PMID27911098
show ga
RATIONALE: Maintenance of a surface immune barrier is important for homeostasis
in organs with mucosal surfaces that interface with the external environment;
however, the role of the mucosal immune system in chronic lung diseases is
incompletely understood. OBJECTIVES: We examined the relationship between
secretory IgA (SIgA) on the mucosal surface of small airways and parameters of
inflammation and airway wall remodeling in chronic obstructive pulmonary disease
(COPD). METHODS: We studied 1,104 small airways (<2 mm in diameter) from 50
former smokers with COPD and 39 control subjects. Small airways were identified
on serial tissue sections and examined for epithelial morphology, SIgA, bacterial
DNA, nuclear factor-?B activation, neutrophil and macrophage infiltration, and
airway wall thickness. MEASUREMENTS AND MAIN RESULTS: Morphometric evaluation of
small airways revealed increased mean airway wall thickness and inflammatory cell
counts in lungs from patients with COPD compared with control subjects, whereas
SIgA level on the mucosal surface was decreased. However, when small airways were
classified as SIgA intact or SIgA deficient, we found that pathologic changes
were localized almost exclusively to SIgA-deficient airways, regardless of study
group. SIgA-deficient airways were characterized by (1) abnormal epithelial
morphology, (2) invasion of bacteria across the apical epithelial barrier, (3)
nuclear factor-?B activation, (4) accumulation of macrophages and neutrophils,
and (5) fibrotic remodeling of the airway wall. CONCLUSIONS: Our findings support
the concept that localized, acquired SIgA deficiency in individual small airways
of patients with COPD allows colonizing bacteria to cross the epithelial barrier
and drive persistent inflammation and airway wall remodeling, even after smoking
cessation.
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