scholarly journals Autophagy Is Required for Maturation of Surfactant-Containing Lamellar Bodies in the Lung and Swim Bladder

Cell Reports ◽  
2020 ◽  
Vol 33 (10) ◽  
pp. 108477
Author(s):  
Hideaki Morishita ◽  
Yuki Kanda ◽  
Takeshi Kaizuka ◽  
Haruka Chino ◽  
Kazuki Nakao ◽  
...  
Keyword(s):  
Swim Bladder ◽  
Lamellar Bodies

Swim bladder gas gland cells produce surfactant: in vivo and in culture

2000 ◽  
Vol 279 (6) ◽  
pp. R2336-R2343 ◽  
Author(s):  
C. Prem ◽  
W. Salvenmoser ◽  
J. Würtz ◽  
B. Pelster
Keyword(s):  
Surfactant Protein ◽  
Cross Reaction ◽  
Tissue Homogenate ◽  
European Eel ◽  
Microscopical Examination ◽  
Swim Bladder ◽  
Lamellar Bodies ◽  
Bladder Tissue ◽  
Gland Cells ◽  
Gas Gland

Electron microscopical examination of gas gland cells of the physostome European eel ( Anguilla anguilla) and of the physoclist perch ( Perca fluviatilis) revealed the presence of significant numbers of lamellar bodies, which are known to be involved in surfactant secretion. In the perch, in which the gas gland is a compact structure and gas gland cells are connected to the swim bladder lumen via small canals, lamellar bodies were also found in flattened cells forming the swim bladder epithelium. Flat epithelial cells are absent in the eel swim bladder, in which the whole epithelium consists of cuboidal gas gland cells. In both species, Western blot analysis using specific antibodies to human surfactant protein A (SP-A) showed a cross-reaction with swim bladder tissue homogenate proteins of ∼65 kDa and in the eel occasionally of ∼120 kDa, probably representing SP-A-like proteins in a dimeric and a tetrameric state. An additional band was observed at ∼45 kDa. Western blots using antibodies to rat SP-D again resulted in a single band at ∼45 kDa in both species, suggesting that there might be a cross-reaction of the antibody to human SP-A with an SP-D-like protein of the swim bladder tissue. To localize the surfactant protein, eel gas gland cells were cultured on permeable supports. Under these conditions, the gas gland cells regain their characteristic polarity. Electron microscopy confirmed the presence of lamellar bodies in cultured cells, and occasionally, exocytotic events were observed. Immunohistochemical staining using an antibody to human SP-A demonstrated the presence of surfactant protein only in luminal membranes and in adjacent lateral membranes. Only occasionally, evidence was found for the presence of surfactant protein in lamellar bodies.

Swim bladder mycosis in farmed rainbow trout Oncorhynchus mykiss caused by Phoma herbarum and experimental verification of pathogenicity

2020 ◽  
Vol 138 ◽  
pp. 237-246 ◽  
Author(s):  
J Řehulka ◽  
A Kubátová ◽  
V Hubka
Keyword(s):  
Rainbow Trout ◽  
Histopathological Examination ◽  
Periodic Acid ◽  
Bladder Wall ◽  
Swim Bladder ◽  
Cell Reactivity ◽  
Periodic Acid Schiff ◽  
Posterior Portion ◽  
Hepatic Congestion ◽  
Phoma Herbarum

In this study, spontaneous swim bladder mycosis was documented in a farmed fingerling rainbow trout from a raceway culture system. At necropsy, the gross lesions included a thickened swim bladder wall, and the posterior portion of the swim bladder was enlarged due to massive hyperplasia of muscle. A microscopic wet mount examination of the swim bladder contents revealed abundant septate hyphae, and histopathological examination showed periodic acid-Schiff-positive mycelia in the lumen and wall of the swim bladder. Histopathological examination of the thickened posterior swim bladder revealed muscle hyperplasia with expansion by inflammatory cells. The causative agent was identified as Phoma herbarum through morphological analysis and DNA sequencing. The disease was reproduced in rainbow trout fingerlings using intraperitoneal injection of a spore suspension. Necropsy in dead and moribund fish revealed extensive congestion and haemorrhages in the serosa of visceral organs and in liver and abdominal serosanguinous fluid. Histopathological examination showed severe hepatic congestion, sinusoidal dilatation, Kupffer cell reactivity, leukostasis and degenerative changes. Fungi were disseminated to the liver, pyloric caeca, kidney, spleen and heart. Although infections caused by Phoma spp. have been repeatedly reported in fish, species identification has been hampered by extensive taxonomic changes. The results of this study confirmed the pathogenicity of P. herbarum in salmonids by using a reliably identified strain during experimental fish infection and provides new knowledge regarding the course of infection.

Detection of intracellular lamellar bodies as a screening marker for fibrotic lesions

2021 ◽  
pp. 115501
Author(s):  
Eun-Jung Park ◽  
Min-Sung Kang ◽  
Hyun-Ji Lim ◽  
Tae Kyu Kang ◽  
Seung-Woo Jin ◽  
...  
Keyword(s):  
Lamellar Bodies ◽  
Screening Marker

Giant Lamellar Bodies in Alveolar Type II Cells of Rats Exposed to a Low Concentration of Ozone

Respiration ◽  
1984 ◽  
Vol 46 (3) ◽  
pp. 303-309 ◽  
Author(s):  
Sanae Shimura ◽  
Shinsaku Maeda ◽  
Tamotsu Takismima
Keyword(s):  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Lamellar Bodies ◽  
Alveolar Type Ii Cells ◽  
Low Concentration

Influence of cycloheximide on the lung

1975 ◽  
Vol 38 (4) ◽  
pp. 623-629 ◽  
Author(s):  
D. B. Gail ◽  
G. D. Massaro ◽  
D. Massaro
Keyword(s):  
Oxygen Consumption ◽  
Surface Density ◽  
Time Course ◽  
Lamellar Body ◽  
Lamellar Bodies ◽  
Cytoplasmic Area ◽  
The Right

We examined the time course of the influence of cycloheximide on descending pressure-volume curves of excised lungs and on protein and lecithin synthesis and oxygen consumption by lung slices. We also looked at the influence of cycloheximide on granular pneumocyte ultrastructure. Excised lungs from cycloheximide-treated animals are more compliant than controls. After ventilation with air, lungs from control and cycloheximide animals show increased retractive forces and a shift to the right of the deflation P-V curve. Incubation at 38 degrees C for 30 min reverses these changes in control lungs, but not in lungs from cycloheximide-treated rabbits. There is no change in liquid delfation P-V curves after cycloheximide. Cycloheximide causes an immediate decrease of 50% in incorporation of radioactive leucine into protein by lung slices. Incorporation of radioactive palmitate into lecithin and oxygen consumption are also decreased by 50% 6 h after cycloheximide. Lamellar bodies in granular pneumocytes are smaller after cycloheximide. Cycloheximide causes a significant increase in the surface density of the lamellar body envelope. Cytoplasmic area of granular pneumocytes is increased after cycloheximide.

scholarly journals Control of Mucosal Candidiasis in the Zebrafish Swim Bladder Depends on Neutrophils That Block Filament Invasion and Drive Extracellular-Trap Production

2017 ◽  
Vol 85 (9) ◽  
Author(s):  
Remi L. Gratacap ◽  
Allison K. Scherer ◽  
Brittany G. Seman ◽  
Robert T. Wheeler
Keyword(s):  
Invasive Disease ◽  
Extracellular Dna ◽  
Epithelial Barrier ◽  
Infection Model ◽  
Swim Bladder ◽  
Spatiotemporal Resolution ◽  
Zebrafish Model ◽  
Content Type ◽  
Mucosal Candidiasis ◽  
Disease Pressure

ABSTRACT Candida albicans is a ubiquitous mucosal commensal that is normally prevented from causing acute or chronic invasive disease. Neutrophils contribute to protection in oral infection but exacerbate vulvovaginal candidiasis. To dissect the role of neutrophils during mucosal candidiasis, we took advantage of a new, transparent zebrafish swim bladder infection model. Intravital microscopic tracking of individual animals revealed that the blocking of neutrophil recruitment leads to rapid mortality in this model through faster disease progression. Conversely, artificial recruitment of neutrophils during early infection reduces disease pressure. Noninvasive longitudinal tracking showed that mortality is a consequence of C. albicans breaching the epithelial barrier and invading surrounding tissues. Accordingly, we found that a hyperfilamentous C. albicans strain breaches the epithelial barrier more frequently and causes mortality in immunocompetent zebrafish. A lack of neutrophils at the infection site is associated with less fungus-associated extracellular DNA and less damage to fungal filaments, suggesting that neutrophil extracellular traps help to protect the epithelial barrier from C. albicans breach. We propose a homeostatic model where C. albicans disease pressure is balanced by neutrophil-mediated damage of fungi, maintaining this organism as a commensal while minimizing the risk of damage to host tissue. The unequaled ability to dissect infection dynamics at a high spatiotemporal resolution makes this zebrafish model a unique tool for understanding mucosal host-pathogen interactions.

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