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.

The chitinase-like proteins breast regression protein-39 and YKL-40 regulate hyperoxia-induced acute lung injury

Abstract: Rationale: Prolonged exposure to 100% O2 causes hyperoxic acute lung injury (HALI), characterized by alveolar epithelial cell injury and death. We previously demonstrated that the murine chitinase-like protein, breast regression protein (BRP)–39 and its human homolog, YKL-40, inhibit cellular apoptosis. However, the regulation and roles of these molecules in hyperoxia have not been addressed.Objectives: We hypothesized that BRP-39 and YKL-40 (also called chitinase-3–like 1) play important roles in the pathogenesis of HALI.Methods: We characterized the regulation of BRP-39 during HALI and the responses induced by hyperoxia in wild-type mice, BRP-39–null (−/−) mice, and BRP-39−/− mice in which YKL-40 was overexpressed in respiratory epithelium. We also compared the levels of tracheal aspirate YKL-40 in premature newborns with respiratory failure.Measurements and Main Results: These studies demonstrate that hyperoxia inhibits BRP-39 in vivo in the murine lung and in vitro in epithelial cells. They also demon...

Hypoxia regulates gene expression of alveolar epithelial transport proteins.

Abstract: Alveolar hypoxia occurs during ascent to high altitude but is also commonly observed in many acute and chronic pulmonary disorders. The alveolar epithelium is directly exposed to decreases in O2 te...

Culture and differentiation of mouse tracheal epithelial cells.

Abstract: Airway epithelial cell biology has been greatly advanced by studies of genetically defined and modified mice; however it is often difficult to isolate, manipulate, and assay epithelial cell-specific responses in vivo. In vitro proliferation and differentiation of mouse airway epithelial cells are made possible by a high-fidelity system for primary culture of mouse tracheal epithelial cells described in this chapter. Using this method, epithelial cells purified from mouse tracheas proliferate in growth factor-enriched medium. Subsequent culture in defined medium and the use of the air-liquid interface condition result in the development of well-differentiated epithelia composed of ciliated and non-ciliated cells with characteristics of native airways. Methods are also provided for manipulation of differentiation and analysis of differentiation and gene expression. These approaches allow the assessment of global responses and those of specific cell subpopulations within the airway epithelium.

Aqueous Tear Deficiency Increases Conjunctival Interferon-γ (IFN-γ) Expression and Goblet Cell Loss.

Abstract: The number of mucin-filled conjunctival goblet cells (GC) has been found to decrease in aqueous-deficient dry eye and certain ocular surface inflammatory conditions, such as Stevens-Johnson syndrome and graft-versus-host disease (GVHD).1–4 The cause for GC loss in these dry eye/ocular surface diseases has not been established, but mouse models suggest it may be due to imbalanced expression of T helper (Th) cytokines, with increased levels of the Th1 cytokine interferon-γ (IFN-γ) and increased ratio of IFN-γ to the Th2 cytokine IL-13 (IFN-γ/IL-13).5,6 Altered ratios of these Th cytokines have been associated with hyperplasia or loss of GC in the airway and gut mucosa.7,8 Interleukin-13 has been found to promote GC differentiation in the conjunctival and airway epithelium, while IFN-γ has caused conjunctival GC loss in mice.6,7,9 Expression of these Th cytokines and their receptors in the conjunctiva and the relationship between levels of these cytokines and goblet cell density (GCD) and expression of cornified envelope precursors have not been studied in patients with tear dysfunction. The purpose of this study was to investigate the hypothesis that increased IFN-γ expression is associated with conjunctival GC loss and mucin deficiency in subjects with tear dysfunction.

Foxp1/4 control epithelial cell fate during lung development and regeneration through regulation of anterior gradient 2

Abstract: The molecular pathways regulating cell lineage determination and regeneration in epithelial tissues are poorly understood. The secretory epithelium of the lung is required for production of mucus to help protect the lung against environmental insults, including pathogens and pollution, that can lead to debilitating diseases such as asthma and chronic obstructive pulmonary disease. We show that the transcription factors Foxp1 and Foxp4 act cooperatively to regulate lung secretory epithelial cell fate and regeneration by directly restricting the goblet cell lineage program. Loss of Foxp1/4 in the developing lung and in postnatal secretory epithelium leads to ectopic activation of the goblet cell fate program, in part, through de-repression of the protein disulfide isomerase anterior gradient 2 (Agr2). Forced expression of Agr2 is sufficient to promote the goblet cell fate in the developing airway epithelium. Finally, in a model of lung secretory cell injury and regeneration, we show that loss of Foxp1/4 leads to catastrophic loss of airway epithelial regeneration due to default differentiation of secretory cells into the goblet cell lineage. These data demonstrate the importance of Foxp1/4 in restricting cell fate choices during development and regeneration, thereby providing the proper balance of functional epithelial lineages in the lung.