2018
DOI: 10.1164/rccm.201703-0561oc
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Bronchial Epithelial IgA Secretion Is Impaired in Asthma. Role of IL-4/IL-13

Abstract: This study shows impaired bronchial epithelial pIgR expression in asthma, presumably affecting secretory IgA-mediated frontline defense as a result of type 2 immune activation of the transforming growth factor pathway.

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Cited by 42 publications
(32 citation statements)
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“…A COPD-like phenotype also develops in pIgR knockout mice upon exogenous bacterial challenge (185), and it has been shown in the past that COPD patients have an impaired pIgR expression (186) and reduced sIgA levels on the airway epithelium (187). Recently a similar phenomenon was reported for asthma (188) and rhinosinusitis (189). In the study of Ladjemi et al, asthmatics show a reduced immunostaining of pIgR in airway epithelia, with IL-4 and IL-13 being the suppressors of pIgR formation in the airway epithelium.…”
Section: Siga In Chronic Inflammation Of the Lungmentioning
confidence: 68%
See 1 more Smart Citation
“…A COPD-like phenotype also develops in pIgR knockout mice upon exogenous bacterial challenge (185), and it has been shown in the past that COPD patients have an impaired pIgR expression (186) and reduced sIgA levels on the airway epithelium (187). Recently a similar phenomenon was reported for asthma (188) and rhinosinusitis (189). In the study of Ladjemi et al, asthmatics show a reduced immunostaining of pIgR in airway epithelia, with IL-4 and IL-13 being the suppressors of pIgR formation in the airway epithelium.…”
Section: Siga In Chronic Inflammation Of the Lungmentioning
confidence: 68%
“…In the study of Ladjemi et al, asthmatics show a reduced immunostaining of pIgR in airway epithelia, with IL-4 and IL-13 being the suppressors of pIgR formation in the airway epithelium. Notably, there were no significant differences in the pIgR gene expression rate among asthmatics and healthy individuals (188). Thus, a posttranslational event such as proteolytic degradation of pIgR in the epithelium may be responsible for the observed differences.…”
Section: Siga In Chronic Inflammation Of the Lungmentioning
confidence: 82%
“…A dimer of two IgA monomers linked by J("joining") chain and secretory component (SC) composes SIgA (6), which is transported across airway epithelial cells via the polymeric immunoglobulin receptor (pIgR). After transportion to the mucosal surface, pIgR is cleaved and SC remains attached to form SIgA (7). SC is an extracellular component of pIgR, which plays a role in stabilizing the structure of SIgA in the process of transportion (8).…”
Section: Introductionmentioning
confidence: 99%
“…Several factors are suspected to contribute to the increased frequency of respiratory infections/exacerbation in these patients: (i) alteration of the host immune response to respiratory pathogens through modulation of cytokines/chemokine secretion [ 30 ] and decreased production and/or activity of epithelial HDPs [ 31 ]; (ii) epithelial injury induced by chronic inflammation or direct exposure to cigarette smoke exposure, resulting in, e.g., decreased mucosal integrity and barrier activity [ 32 ]; (iii) airway epithelium remodelling resulting in impaired ciliary activity and modification of mucus secretion, composition and physical properties leading to altered mucociliary transport and deficient pathogen clearance [ 33 , 34 , 35 , 36 , 37 , 38 ]; (iv) changes in airway epithelial cell composition negatively affecting the presence of host defence proteins and peptides (HDPs) and leading to locally impaired antimicrobial defences [ 39 ]; (v) IgA/IgM transport across the airway epithelium into mucosal secretions may be impaired as a result of changes in pIgR expression in these diseases [ 40 , 41 ]. These processes and how they are affected in chronic inflammatory lung diseases are summarised in Figure 1 .…”
Section: Introductionmentioning
confidence: 99%