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Respiratory epithelium

About: Respiratory epithelium is a research topic. Over the lifetime, 5048 publications have been published within this topic receiving 222304 citations. The topic is also known as: respiratory tract epithelium & Respiratory Mucosa.


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Journal Article
TL;DR: Human bronchial epithelium has been maintained in organ culture in serum-supplemented medium for 4 months, and the basal lamina was frequently covered by 2 or 3 layers of epithelial cells consisting of nonkeratinizing squamous cells with short microvilli and small mucous granules.
Abstract: Summary Human bronchial epithelium has been maintained in organ culture in serum-supplemented medium for 4 months. After 4 to 6 weeks in culture, various changes in morphology were apparent. There was an increase in autophagic vacuoles in mucous, ciliated, and basal cells, a reduction in the height of the columnar cells, a decrease in the number of goblet mucous cells, and an increase in cells with small mucous granules. After 3 months in culture, the basal lamina was frequently covered by 2 or 3 layers of epithelial cells consisting of nonkeratinizing squamous cells with short microvilli and small mucous granules. Less frequently, keratinizing squamous cells were seen. Differentiated epithelium incorporated precursors into macromolecules in serum-free medium, supplemented with vitamin A, at 1 week of culture. These explants exhibited changed epithelium by 2 weeks, similar to that described for epithelium in serum-supplemented medium after 4 to 6 weeks.

80 citations

Journal ArticleDOI
TL;DR: In the airway epithelium apoptosis serves three main roles: to eliminate damaged cells; to restore homeostasis following hyperplastic changes; and to control inflammation, and thereby support the barrier and anti-inflammatory functions.
Abstract: The airway epithelium functions primarily as a barrier to foreign particles and as a modulator of inflammation. Apoptosis is induced in airway epithelial cells (AECs) by viral and bacterial infections, destruction of the cytoskeleton, or by exposure to toxins such as high oxygen and polycyclic hydrocarbons. Various growth factors and cytokines including TGF-β, IFN-γ, or the activators of the death receptors, TNF-α and FasL, also induce apoptosis in AECs. However, cell death is observed in maximally 15% of AECs after 24 h of treatment. Preincubation with IFN-γ or a zinc deficiency increases the percentage of apoptotic AECs in response to TNF-α or FasL, suggesting that AECs have mechanisms to protect them from cell death. Apoptosis of AECs is a major mechanism in reducing cell numbers after hyperplastic changes in airway epithelia that may arise due to major injuries in response to LPS or allergen exposures. Resolution of hyperplastic changes or changes during prolonged exposure to an allergen is primarily ...

80 citations

Journal ArticleDOI
TL;DR: Investigation of defensin expression at transcriptional and post-transcriptional levels demonstrated the requirement of transcription as well as new protein synthesis during A. fumigatusdefensin induction, providing evidence that respiratory epithelium might play an important role in the immune response during Aspergillus infection.
Abstract: Aspergillus fumigatus, a saprophytic mould, is responsible for life-threatening, invasive pulmonary diseases in immunocompromised hosts. The role of the airway epithelium involves a complex interaction with the inhaled pathogen. Antimicrobial peptides with direct antifungal and chemotactic activities may boost antifungal immune response. The inducible expression of defensins by human bronchial epithelial 16HBE cells and A549 pneumocyte cells exposed to A. fumigatus was investigated. Using RT-PCR and real time PCR, we showed an activation of hBD2 and hBD9 defensin genes: the expression was higher in cells exposed to swollen conidia (SC), compared to resting conidia (RC) or hyphal fragments (HF). The kinetics of defensin expression was different for each one, evoking a putative distinct function for each investigated defensin. The decrease of defensin expression in the presence of heat-inactivated serum indicated a possible link between defensins and the proteins of the host complement system. The presence of defensin peptide hBD2 was revealed using immunofluorescence that showed a punctual cytoplasmic and perinuclear staining. Quantification of the cells stained with anti hBD2 antibody demonstrated that SC induced a greater number of cells that synthesized hBD2, compared to RC or HF. Labelling of the cells with anti-hBD-2 antibody showed a positive immunofluorescence signal around RC or SC in contrast to HF. This suggests co-localisation of hBD2 and digested conidia. The HBD2 level was highest in the supernatants of cells exposed to SC, as was determined by sandwich ELISA. Experiments using neutralising anti-interleukine-1β antibody reflect the autocrine mechanism of defensin expression induced by SC. Investigation of defensin expression at transcriptional and post-transcriptional levels demonstrated the requirement of transcription as well as new protein synthesis during A. fumigatus defensin induction. Finally, induced defensin expression in primary culture of human respiratory cells exposed to A. fumigatus points to the biological significance of described phenomena. Our findings provide evidence that respiratory epithelium might play an important role in the immune response during Aspergillus infection. Understanding the mechanisms of regulation of defensin expression may thus lead to new approaches that could enhance expression of antimicrobial peptides for potential therapeutic use during aspergillosis treatment.

80 citations

BookDOI
01 Jan 1997
TL;DR: This work presents a meta-anatomy of Airway Mucus Secretion, and discusses its role in the Airway Obstruction of Asthma and Chronic Obstructive Pulmonary Disease, as well asTherapeutic Approaches to the Lung Problems in Cystic Fibrosis.
Abstract: 1. Airway Surface Liquid: Concepts and Measurements.- 2. Structure and Biochemistry of Human Respiratory Mucins.- 3. Airway Mucin Genes and Gene Products.- 4. The Microanatomy of Airway Mucus Secretion.- 5. Mechanisms Controlling Airway Ciliary Activity.- 6. Rheological Properties and Hydration of Airway Mucus.- 7. Goblet Cells: Physiology and Pharmacology.- 8. Airway Submucosal Glands: Physiology and Pharmacology.- 9. Mucus-Bacteria Interactions.- 10. Experimental Induction of Goblet Cell Hyperplasia In Vivo 227.- 11. Mucus Hypersecretion and Its Role in the Airway Obstruction of Asthma and Chronic Obstructive Pulmonary Disease.- 12. Mucus and Airway Epithelium Alterations in Cystic Fibrosis.- 13. Drug-Mucus Interactions.- 14. Therapeutic Approaches to the Lung Problems in Cystic Fibrosis.- 15. Therapeutic Approaches to Airway Mucous Hypersecretion.

80 citations

Journal ArticleDOI
TL;DR: All 3 subunits of the hENaC are low in preterm relative to full-term infants, and alpha-h ENaC mRNA in respiratory epithelium is increased by therapeutic doses of glucocorticosteroid.
Abstract: Objective. Active ion transport is critical to postnatal clearance of lung fluid. The importance of epithelial sodium channel (ENaC) in this clearance has been demonstrated in animal studies in which α-ENaC knockout mice died postnatally as a result of respiratory insufficiency. In animals, the expression of α-ENaC in respiratory epithelium is dependent on gestational age, but when assessed by in situ hybridization in the human (h), the mRNA is present from the earliest stages of pulmonary development. Therefore, the purpose of the present investigation was to quantify mRNA of the α-, β-, and γ-hENaC subunits of newborn preterm infants with respiratory distress and compare the gene expression data against those detected in healthy term infants. In addition, the effect of systemic dexamethasone therapy on the 3 hENaC subunits was studied in 4 preterm infants who received prolonged assisted ventilation. Methods. The expression of subunits of hENaC was determined in samples taken from nasal respiratory epithelium of 7 healthy term infants (gestation age: 39.3 ± 0.9 weeks [mean ± standard deviation) and 5 preterm infants (gestational age: 27.2 ± 0.9 weeks) with respiratory distress syndrome within 5 hours of birth. Betamethasone had been given to all mothers of preterm infants. In 4 additional preterm infants who still required assisted ventilation at 43 ± 6 days postnatal age, the expression of α-hENaC was determined in samples taken before and during treatment with dexamethasone. Results. Preterm infants with respiratory distress syndrome had low expression of all hENaC subunits relative to healthy term infants (α-hENaC: 5.38 ± 2.01 [amol/fmol cytokeratin 18] vs 9.13 ± 2.26; β-hENaC: 2.44 ± 1.43 vs 4.25 ± 1.10; γ-hENaC: 2.43 ± 0.11 vs 6.81 ± 3.24). Each of the 4 preterm infants who were treated with dexamethasone at ∼1 month of age showed an increase in expression of α-hENaC and β-hENaC subunit normalized to cytokeratin 18. Conclusion. All 3 subunits of the hENaC are low in preterm relative to full-term infants. α-hENaC mRNA in respiratory epithelium is increased by therapeutic doses of glucocorticosteroid. Low expression of α-hENaC in human respiratory epithelium may play a role in the pathogenesis of respiratory distress in preterm infants.

80 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
2023143
2022222
2021182
2020174
2019149
2018149