scholarly journals Interactions of nasal epithelium with macrophages and dendritic cells variously alter urban PM-induced inflammation in healthy, asthma and COPD

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Magdalena Paplinska-Goryca ◽  
Paulina Misiukiewicz-Stepien ◽  
Malgorzata Proboszcz ◽  
Patrycja Nejman-Gryz ◽  
Katarzyna Gorska ◽  
...  

AbstractUrban particulate matter (UPM) is an important trigger of airway inflammation. The cross-talk between the external and internal matrix in the respiratory tract occurs due to the transepithelial network of macrophages/dendritic cells. This study characterized the immune processes induced by the epithelium after UPM exposure in special regard to interactions with monocyte-derived dendritic cells (moDCs) and monocyte-derived macrophages (moMφs) in obstructive lung diseases. A triple-cell co-culture model (8 controls, 10 asthma, and 8 patients with COPD) utilized nasal epithelial cells, along with moMφs, and moDCs was exposed to UPM for 24 h. The inflammatory response of nasal epithelial cells to UPM stimulation is affected differently by cell–cell interactions in healthy people, asthma or COPD patients of which the interactions with DCs had the strongest impact on the inflammatory reaction of epithelial cells after UPM exposure. The epithelial remodeling and DCs dysfunction might accelerate the inflammation after air pollution exposure in asthma and COPD.

Cells ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 1944
Author(s):  
Magdalena Paplinska-Goryca ◽  
Paulina Misiukiewicz-Stepien ◽  
Malgorzata Proboszcz ◽  
Patrycja Nejman-Gryz ◽  
Katarzyna Gorska ◽  
...  

Background. The cross-talk between the external and internal environment in the respiratory tract involves macrophage/dendritic cell (DC) transepithelial network. Epithelium triggers dendritic cell-mediated inflammation by producing thymic stromal lymphopoietin (TSLP), IL-33, and IL-17A. The study aimed to evaluate the expression of TSLP, IL-33, and IL-17A in human monocyte derived dendritic cells (moDCs) co-cultured with respiratory epithelium and monocyte derived macrophages (moMφs) in asthma, chronic obstructive pulmonary disease (COPD) and healthy controls. Methods. The study used a triple-cell co-culture model, utilizing nasal epithelial cells, along with moMφs and moDCs. Cells were cultured in mono-, di-, and triple-co-cultures for 24 h. Results. Co-culture with epithelium and moMφs significantly increased TSLP in asthma and did not change IL-33 and IL-17A mRNA expression in moDCs. moDCs from asthmatics were characterized by the highest TSLP mRNA expression and the richest population of TSLPR, ST2, and IL17RA expressed cells. A high number of positive correlations between the assessed cytokines and CHI3L1, IL-12p40, IL-1β, IL-6, IL-8, TNF in moDCs was observed in asthma and COPD. Conclusion. TSLP, IL-33, and IL-17A expression in moDCs are differently regulated by epithelium in asthma, COPD, and healthy subjects. These complex cell–cell interactions may impact airway inflammation and be an important factor in the pathobiology of asthma and COPD.


2009 ◽  
Vol 131 (1) ◽  
pp. 40-51 ◽  
Author(s):  
Georgia Zoumpopoulou ◽  
Effie Tsakalidou ◽  
Joelle Dewulf ◽  
Bruno Pot ◽  
Corinne Grangette

2021 ◽  
Author(s):  
Nicole C. Shaw ◽  
Anthony Kicic ◽  
Sue Fletcher ◽  
Stephen D. Wilton ◽  
Stephen M. Stick ◽  
...  

Abstract ATP Binding Cassette Subfamily A Member 3 (ABCA-3) is a lipid transporter protein highly expressed in type-II alveolar (AT-II) cells. Mutations in ABCA3 can result in severe respiratory disease in infants and children. To study ABCA-3 deficiency in vitro, primary AT-II cells would be the cell culture of choice although sample accessibility is limited. Our aim was to investigate the suitability of primary nasal epithelial cells, as a surrogate culture model for AT-II cells, to study ABCA-3 deficiency. Expression of ABCA3, and surfactant protein genes, SFTPB and SFTPC, was detected in primary nasal epithelial cells but at a significantly lower level than in AT-II cells. ABCA-3, SP-B and SP-C were detected by immunofluorescence microscopy in primary nasal epithelial cells. However, SP-B and SP-C were undetectable in primary nasal epithelial cells using western blot. Structurally imperfect lamellar bodies were observed in primary nasal epithelial cells using transmission electron microscopy. Functional assessment of the ABCA-3 protein demonstrated that higher concentrations of doxorubicin reduced cell viability in ABCA-3 deficient nasal epithelial cells compared to controls in an assay-dependent manner. Our results indicate that there may be a role for primary nasal epithelial cell cultures to model ABCA-3 deficiency in vitro although additional cell culture models that more effectively recapitulate the AT-II phenotype may be required.


Author(s):  
Silvano Dragonieri ◽  
Donato Lacedonia ◽  
Grazia Pia Palladino ◽  
Giulia Scioscia ◽  
Giovanna Elisiana Carpagnano ◽  
...  

2020 ◽  
Vol 56 (4) ◽  
pp. 214-217 ◽  
Author(s):  
Silvano Dragonieri ◽  
Donato Lacedonia ◽  
Giulia Scioscia ◽  
Grazia Pia Palladino ◽  
Vitaliano Nicola Quaranta ◽  
...  

2019 ◽  
Vol 20 (6) ◽  
pp. 1379 ◽  
Author(s):  
Emilie Bequignon ◽  
Christine Dhommée ◽  
Christelle Angely ◽  
Lucie Thomas ◽  
Mathieu Bottier ◽  
...  

Monoclonal antibodies (mAbs) are promising therapies to treat airway chronic inflammatory disease (asthma or nasal polyps). To date, no study has specifically assessed, in vitro, the potential function of neonatal Fc receptor (FcRn) in IgG transcytosis through the human nasal airway epithelium. The objective of this study was to report the in vitro expression and function of FcRn in nasal human epithelium. FcRn expression was studied in an air–liquid interface (ALI) primary culture model of human nasal epithelial cells (HNEC) from polyps. FcRn expression was characterized by quantitative RT-PCR, western blot, and immunolabeling. The ability of HNECs to support mAb transcytosis via FcRn was assessed by transcytosis assay. This study demonstrates the expression of FcRn mRNA and protein in HNEC. We report a high expression of FcRn in the cytosol of ciliated, mucus, and basal cells by immunohistochemistry with a higher level of FcRn proteins in differentiated HNEC. We also proved in vitro transepithelial delivery of an IgG1 therapeutic mAb with a dose–response curve. This is the first time that FcRn expression and mAb transcytosis has been shown in a model of human nasal respiratory epithelium in vitro. This study is a prerequisite for FcRn-dependent nasal administration of mAbs.


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