A Morphometric Study on the Thickness of the Pulmonary Air-Blood Barrier

Weibel, Ewald R.; Knight, Bruce W.

doi:10.1083/jcb.21.3.367

Cited by 339 publications

(173 citation statements)

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“…The lamellae's water-blood barrier thickness (τ h ) were calculated from the harmonic mean intercept length (l h ) of random probing lines crossing the barrier, according to the equation τ h = 2/ 3 l h (Weibel & Knight, 1964). The l values were determined by superimposing a grid for layered structure (Gundersen et al, 1988) on randomized electron micrographs (magnified x 3000) of lamellar cross sections.…”

Section: Methodsmentioning

confidence: 99%

Epithelial gill cells in the armored catfish, Hypostomus cf. plecostomus (Loricariidae)

Fernandes

Perna-Martins

2001

Rev. Bras. Biol.

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Epithelial gill cell morphology and distribution were investigated in the armored catfish, Hypostomus cf. plecostomus, which lives in soft ion-poor Brazilian freshwaters. Pavement cells are the most abundant type of cell on both filament and lamellar epithelia and there are a great number of mucous and chloride cells between them. Mucous cells are almost covered by adjacent pavement cells and have large packed granules showing electrondense differences. No mucous cells were found on the lamellar epithelium. Chloride cell were distributed throughout both epithelia and usually have large apical surface facing the external medium and may exhibit short and sparsely distributed microvilli. The presence of chloride cells on the lamellar epithelium may be an adaptation to low ion concentrations in the water, allowing for improved ion-transport capacity of the gill. The large size of these cells increases the water-blood barrier and may affect the transference of respiratory gases. However, the negative effect on the respiratory process may be minimized by this species' ability to resort to atmospheric air to fulfill its oxygen requirements.Key words: gills, epithelium, teleost, loricariid, Hypostomus cf. plecostomus. RESUMOEpitélio branquial de cascudo, Hypostomus cf. plecostomus (Loricariidae)

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Section: Methodsmentioning

confidence: 99%

Epithelial gill cells in the armored catfish, Hypostomus cf. plecostomus (Loricariidae)

Fernandes

Perna-Martins

2001

Rev. Bras. Biol.

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“…The average thickness of the alveolar capillary membrane is just over 1 m, which includes a single layer of alveolar epithelium, wisps of interstitial tissue, and a single layer of lung microvascular endothelium (11). In some areas, the membrane is as thin as 200 nm (11). Thus, the death of infected epithelial cells will create gaps in the monolayer and give newly released virions access to the endothelium (10,12), even in the absence of frank viremia.…”

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confidence: 99%

“…However, in primary viral pneumonia, the virus also infects the distal lung, particularly type I pneumocytes and ciliated bronchiolar epithelium, leading to alveolar damage and frank alveolar denudement (10). The average thickness of the alveolar capillary membrane is just over 1 m, which includes a single layer of alveolar epithelium, wisps of interstitial tissue, and a single layer of lung microvascular endothelium (11). In some areas, the membrane is as thin as 200 nm (11).…”

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confidence: 99%

Influenza Virus Infection Induces Platelet-Endothelial Adhesion Which Contributes to Lung Injury

Sugiyama

Gamage

Zyla

et al. 2016

J Virol

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Lung injury after influenza infection is characterized by increased permeability of the lung microvasculature, culminating in acute respiratory failure. Platelets interact with activated endothelial cells and have been implicated in the pathogenesis of some forms of acute lung injury. Autopsy studies have revealed pulmonary microthrombi after influenza infection, and epidemiological studies suggest that influenza vaccination is protective against pulmonary thromboembolism; however, the effect of influenza infection on platelet-endothelial interactions is unclear. We demonstrate that endothelial infection with both laboratory and clinical strains of influenza virus increased the adhesion of human platelets to primary human lung microvascular endothelial cells. Platelets adhered to infected cells as well as to neighboring cells, suggesting a paracrine effect. Influenza infection caused the upregulation of von Willebrand factor and ICAM-1, but blocking these receptors did not prevent platelet-endothelial adhesion. Instead, platelet adhesion was inhibited by both RGDS peptide and a blocking antibody to platelet integrin ␣ 5 ␤ 1 , implicating endothelial fibronectin. Concordantly, lung histology from infected mice revealed viral dose-dependent colocalization of viral nucleoprotein and the endothelial marker PECAM-1, while platelet adhesion and fibronectin deposition also were observed in the lungs of influenza-infected mice. Inhibition of platelets using acetylsalicylic acid significantly improved survival, a finding confirmed using a second antiplatelet agent. Thus, influenza infection induces platelet-lung endothelial adhesion via fibronectin, contributing to mortality from acute lung injury. The inhibition of platelets may constitute a practical adjunctive strategy to the treatment of severe infections with influenza. Here, we show that this infection causes platelets to adhere to the lung endothelium. Importantly, blocking platelets using two distinct antiplatelet drugs improved survival in a mouse model of severe influenza infection. Thus, platelet inhibition may constitute a novel therapeutic strategy to improve the host response to severe infections with influenza.

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“…This criterion has been adhered to here . Also, to prevent undue changes in tissue volume during subsequent processing stages, dehydration was started in ethanol : water 3 :1 v :v (13) . In view of these precautions, the lack of obvious signs of swelling or extraction and the consistency of the estimates of the areas, volumes, and sizes of cell compo-…”

Section: Discussionmentioning

confidence: 99%