scholarly journals THE DEMONSTRATION OF ACID HYDROLASE ACTIVITIES IN THE INCLUSION BODIES OF TYPE II ALVEOLAR CELLS AND OTHER LYSOSOMES IN THE RABBIT LUNG

1968 ◽  
Vol 16 (2) ◽  
pp. 102-109 ◽  
Author(s):  
SIDNEY GOLDFISCHER ◽  
YUTAKA KIKKAWA ◽  
LEE HOFFMAN
Keyword(s):  
Acid Phosphatase ◽  
Inclusion Bodies ◽  
Active Sites ◽  
Cytoplasmic Inclusion ◽  
Alveolar Epithelial Cells ◽  
Type Ii ◽  
Alveolar Cells ◽  
Rabbit Lung ◽  
Aryl Sulfatase ◽  
Alveolar Epithelial

Type II alveolar epithelial cells show high levels of acid phosphatase, aryl sulfatase B and β-glucuronidase activities. In formalin- and glutaraldehyde-fixed rabbit lung acid phosphatase and aryl sulfatase B activities were demonstrated in the cytoplasmic inclusion bodies, supporting their identification as lysosomes. Type II cells differ from alveolar macrophages in their levels of hydrolase activity and the fine structure of their active sites.

Electron Staining Characteristics of the Inclusion Bodies of Type II Alveolar Epithelial Cells

1968 ◽  
Vol 26 ◽  
pp. 46-47
Author(s):  
Yutaka Kikkawa ◽  
Ho-Soon Hahn
Keyword(s):  
Epithelial Cells ◽  
Inclusion Bodies ◽  
Alveolar Epithelial Cells ◽  
Type I ◽  
Type Ii ◽  
Colloidal Iron ◽  
Alveolar Epithelial ◽  
Mammalian Lung ◽  
First Time ◽  
Electron Lucent

The inclusion bodies of Type II epithelial cells of the mammalian lung are oval and limited by a unit membrane. They contain highly osmiophilic material. With the standard method of fixation this material is irregularly separated by a number of electron-lucent spaces (Figure 1). Because of this appearance, the inclusion bodies are often referred to as “lamellar inclusions”. Measurable periodic lamellae, however, have never been observed in the inclusions which are located intracellularly.During the course of the studies to localize acid mucopolysaccharides in the distal air way of the rabbit and rat, it is found that the alveolar surface of the cell membranes of both Type I and II cells and the inclusion bodies within Type II cells satin heavily with colloidal iron at pH 2.0 following the osmication of the tissue with phosphate-buffered solution at pH 7.4 (Figure 2). In addition, the inclusion bodies for the first time show regular periodic lamellae. Each line is granular and measures about 60 Å in width (Figure 3).

scholarly journals Alveolar Epithelial Cell Type II as main target of SARS-CoV-2 virus and COVID-19 development via NF-Kb pathway deregulation.

2020 ◽  
Author(s):  
Maurizio Carcaterra ◽  
Cristina Caruso
Keyword(s):  
Molecular Mechanisms ◽  
Virus Disease ◽  
Clinical Manifestations ◽  
Alveolar Epithelial Cells ◽  
Type Ii ◽  
Cell Type ◽  
Alveolar Cells ◽  
Alveolar Epithelial ◽  
Corona Virus ◽  
Number Of Patients

Abstract Background: The Corona Virus Disease (COVID-19) pandemic caused by Severe Acute Respiratory Syndrome Corona Virus 2 (SARS-CoV-2) requires a rapid solutionand global collaborative efforts in order to define preventive and treatment strategies.Methods: One of the major challenges of this disease is the high number of patients needing advanced respiratory support due to the Acute Respiratory Distress Syndrome (ARDS) as the lung is the major –although not exclusive-target of the virus. The molecular mechanisms, pathogenic drivers and the target cell type(s) in SARSCoV-2 infection are still poorly understood, but the development of a “hyperactive” immune response is proposed to play a role in the evolution of the disease and it is envisioned as a major cause of morbidity and mortality.Results: Here we propose a theory by which the main targets for SARS-CoV-2 are the Type II Alveolar Epithelial Cells and the clinical manifestations of the syndrome are a direct consequence of their involvement. We hypotize the existence of a vicious cycle by which once alveolar damage starts in AEC II cells, the inflammatory state is supported by macrophage proinflammatory polarization (M1), cytokines release and by the activation of the NF-κB pathway.Conclusions: If this theory is confirmed, future therapeutic efforts can be directed to target Type 2 alveolar cells and the molecular pathogenic drivers associated with their dysfunction with currently available therapeutic strategies.

Demonstration of Microtubules in Type II Alveolar Cells

1977 ◽  
Vol 35 ◽  
pp. 464-465
Author(s):  
Frederick J. Stone ◽  
Yutaka Kikkawa
Keyword(s):  
Secretory Granules ◽  
Alveolar Epithelial Cells ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Cells ◽  
Alveolar Epithelial ◽  
Type Ii Cell ◽  
Type Ii Alveolar Cells ◽  
Probable Role ◽  
Secretory Products

Two lines of evidence indicate a probable role for microtubules in the secretory processes of type II alveolar epithelial cells. These are: (1) The inhibition of the release of disaturated lecithins (the major component of putative type II cell secretory products) by lung slices pretreated and then incubated with antimicrotubular agents colchicine and vinblastine (Delahunty, J.J. and Johnston, J.M.: J. Lipid Res., 17:112,1976); and (2) The abnormality of the secretory granules, lamellar bodies, in the type II cells of beige mice (Chi, E.Y. Prueitt, J.L., and Lagunoff, D: J. Histochem. Cytochem., 23:863-869, 1975) in which microtubular function is abnormal (Oliver, J.M.: Amer. J. Pathol., 85:395, 1976). Our failure to morphologically identify the expected microtubules in type II cells from lungs prepared for electron microscopy by conventional fixations led us to attempt their visualization by the application of the tannic acid- glutaraldehyde fixative of Futaesakie, et. al. (Histochemistry and Cytochemistry, 1972.).

scholarly journals Binding of Glucuronoxylomannan to the CD14 Receptor in Human A549 Alveolar Cells Induces Interleukin-8 Production

2006 ◽  
Vol 14 (1) ◽  
pp. 94-98 ◽  
Author(s):  
Fabiane M. Barbosa ◽  
Fernanda L. Fonseca ◽  
Rodrigo T. Figueiredo ◽  
Marcelo T. Bozza ◽  
Arturo Casadevall ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Epithelial Cells ◽  
Cryptococcus Neoformans ◽  
Capsular Polysaccharide ◽  
Alveolar Epithelial Cells ◽  
Interleukin 8 ◽  
Type Ii ◽  
Alveolar Cells ◽  
Alveolar Epithelial ◽  
Human A549

ABSTRACT Glucuronoxylomannan (GXM) is the major capsular polysaccharide of Cryptococcus neoformans. GXM receptors have been characterized in phagocytes and endothelial cells, but epithelial molecules recognizing the polysaccharide remain unknown. In the current study, we demonstrate that GXM binds to the CD14 receptor in human type II alveolar epithelial cells, resulting in the production of the proinflammatory chemokine interleukin-8.

scholarly journals Role of Surfactant for the Treatment of Alveolar Cells against Coronavirus (Covid-19)

2020 ◽  
pp. 34-39
Author(s):  
Sony Ahmed ◽  
Md. Shamim Akter ◽  
Kallol Roy ◽  
Md. Shafiul Islam
Keyword(s):  
Pulmonary Surfactant ◽  
Complex Mixture ◽  
Alveolar Epithelial Cells ◽  
Type Ii ◽  
Active Components ◽  
Alveolar Cells ◽  
Epithelial Surface ◽  
Alveolar Epithelial ◽  
Susceptibility To Infection ◽  
Increased Susceptibility

Coronavirus disease (COVID-19) is an infectious disease caused by the newly discovered coronavirus. Coronavirus affects human lung tissues. Covid-19 should be infection of the lungs, the virus infects alveolar cells resulting in reduced production of pulmonary surfactant. Pulmonary surfactant is a complex of lipids and proteins that line the alveolar epithelial surface and stabilize it during respiration. The surfactant helps to reduce the surface tension on alveoli. The surface-active components of the alveoli are a complex mixture of specific lipids, proteins and carbohydrates, which is produced in the lungs by type II alveolar epithelial cells. As a result, the lungs continue to collapse, reducing its own volume, but the collapse is prevented by the muscles of inspiration, which instead increase its volume. Covid-19 allows the surfactant to maintain the correct amount of surfactant during the acute phase of infection during lung infection and allows time to resume and allow individual surfactant production for type II cells. Surfactant degradation or inactivation may contribute to increased susceptibility to pneumonia and increased susceptibility to infection. Surfactant deficiency in patients with acute respiratory syndrome in adults and surfactant administration may be a useful therapy against Covid-19.

Alveolar epithelial cells type II show a high sensitivity to cigarette smoke extract

Pneumologie ◽  
2014 ◽  
Vol 68 (06) ◽  
Author(s):  
S Seehase ◽  
B Baron-Luehr ◽  
C Kugler ◽  
E Vollmer ◽  
T Goldmann
Keyword(s):  
Epithelial Cells ◽  
Cigarette Smoke ◽  
High Sensitivity ◽  
Cigarette Smoke Extract ◽  
Alveolar Epithelial Cells ◽  
Type Ii ◽  
Alveolar Epithelial

scholarly journals Senescence associated long non-coding RNA 1 regulates cigarette smoke-induced senescence of type II alveolar epithelial cells through sirtuin-1 signaling

2021 ◽  
Vol 49 (2) ◽  
pp. 030006052098604
Author(s):  
Dong Yuan ◽  
Yuanshun Liu ◽  
Mengyu Li ◽  
Hongbin Zhou ◽  
Liming Cao ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cigarette Smoke ◽  
Alveolar Epithelial Cell ◽  
Alveolar Epithelial Cells ◽  
Lung Epithelial Cells ◽  
Sirtuin 1 ◽  
Type Ii ◽  
Alveolar Epithelial ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Objective The primary aim of our study was to explore the mechanisms through which long non-coding RNA (lncRNA)-mediated sirtuin-1 (SIRT1) signaling regulates type II alveolar epithelial cell (AECII) senescence induced by a cigarette smoke-media suspension (CSM). Methods Pharmacological SIRT1 activation was induced using SRT2104 and senescence-associated lncRNA 1 (SAL-RNA1) was overexpressed. The expression of SIRT1, FOXO3a, p53, p21, MMP-9, and TIMP-1 in different groups was detected by qRT-PCR and Western blotting; the activity of SA-β gal was detected by staining; the binding of SIRT1 to FOXO3a and p53 gene transcription promoters was detected by Chip. Results We found that CSM increased AECII senescence, while SAL-RNA1 overexpression and SIRT1 activation significantly decreased levels of AECII senescence induced by CSM. Using chromatin immunoprecipitation, we found that SIRT1 bound differentially to transcriptional complexes on the FOXO3a and p53 promoters. Conclusion Our results suggested that lncRNA-SAL1-mediated SIRT1 signaling reduces senescence of AECIIs induced by CSM. These findings suggest a new therapeutic target to limit the irreversible apoptosis of lung epithelial cells in COPD patients.

scholarly journals β-Catenin/Lin28/let-7 regulatory network determines type II alveolar epithelial stem cell differentiation phenotypes following thoracic irradiation

2020 ◽  
Vol 62 (1) ◽  
pp. 119-132
Author(s):  
Xiaozhuan Liu ◽  
Tingting Zhang ◽  
Jianwei Zhou ◽  
Ziting Xiao ◽  
Yanjun Li ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Stem Cell Differentiation ◽  
Alveolar Epithelial Cells ◽  
Type I ◽  
Type Ii ◽  
Epithelial Stem Cells ◽  
Alveolar Epithelial ◽  
Thoracic Irradiation ◽  
Radiation Induced ◽  
Differentiation Marker

Abstract The contribution of type II alveolar epithelial stem cells (AEC II) to radiation-induced lung fibrosis (RILF) is largely unknown. Cell differentiation phenotypes are determined by the balance between Lin28 and lethal-7 microRNA (let-7 miRNA). Lin28 is activated by β-catenin. The aim of this study was to track AEC II phenotypes at different phases of injury following thoracic irradiation and examine the expression of β-catenin, Lin28 and let-7 to identify their role in AEC II differentiation. Results showed that coexpression of prosurfactant protein C (proSP-C, an AEC II biomarker) and HOPX (homeobox only protein X, an AEC I biomarker) or vimentin (a differentiation marker) was detected in AEC II post-irradiation. The protein expression levels of HOPX and proSP-C were significantly downregulated, but vimentin was significantly upregulated following irradiation. The expression of E-cadherin, which prevents β-catenin from translocating to the nucleus, was downregulated, and the expression of β-catenin and Lin28 was upregulated after irradiation (P < 0.05 to P < 0.001). Four let-7 miRNA members (a, b, c and d) were upregulated in irradiated lungs (P < 0.05 to P < 0.001), but let-7d was significantly downregulated at 5 and 6 months (P < 0.001). The ratios of Lin28 to four let-7 members were low during the early phase of injury and were slightly higher after 2 months. Intriguingly, the Lin28/let-7d ratio was strikingly increased after 4 months. We concluded that β-catenin contributed to RILF by promoting Lin28 expression, which increased the number of AEC II and the transcription of profibrotic molecules. In this study, the downregulation of let-7d miRNA by Lin28 resulted in the inability of AEC II to differentiate into type I alveolar epithelial cells (AEC I).

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