Morphofunctional Characteristics of Pulmonary Surfactant System and Its Effect on Immune Cells in Influenza A (H1N1) Pathogenesis

In CBA mice infected with influenza viruses A/H1N1/California/04/2009 and A/H5N1/Goose/ Krasnoozerskoye/627/05 in a dose of 10 MLD 50 , the mechanisms of death of pulmonary alveolocytes over 10 postinfection days were studied by light microscopy, immunohistochemistry, and morphometry. In mice infected with A/H1N1, alveolocytes died predominantly via necrosis, while apoptosis mostly employed the mitochondrial pathway. In mice infected with A/ H5N1, apoptosis was the dominant mechanism of alveolocyte death proceeded via membrane receptor signaling followed by switching to FAS-mediated pathway via activation of FADD, the apoptotic signal transduction protein.

show abstract

“…In infected mice, immunohistochemistry visualized the positive staining of alveolocytes for viral antigen A [3][4][5].…”

Section: Resultsmentioning

confidence: 99%

Death Mechanisms of Pulmonary Alveolocytes in Mice Infected with Influenza Viruses A/H1N1/California/04/2009 and A/H5N1/Goose/Krasnoozerskoye/627/05

Черданцева

Ковнер

Sharkova³

et al. 2019

Bull Exp Biol Med

Self Cite

View full text Add to dashboard Cite

show abstract

“…CPT plays an important role in regulating the acyl group composition of PC in the lungs and is dependent on CDP-choline availability [ 19 ]. This enzyme is able to utilize both endogenous and exogenous diacylglycerol for PC synthesis in the lungs [ 20 ].…”

Section: Discussionmentioning

confidence: 99%

Synthesis of phosphatidylcholine in rats with oleic acid-induced pulmonary edema and effect of exogenous pulmonary surfactant on its De Novo synthesis

et al. 2018

View full text Add to dashboard Cite

In mammals, oleic acid (OA) induces pulmonary edema (PE), which can initiate acute lung injury (ALI) and lead to acute respiratory distress syndrome (ARDS). Pulmonary surfactant (PS) plays a key role in a broad range of treatments for ARDS. The aim of the present investigation was to assess changes in the synthesis of phosphatidylcholine (PC) from choline and determine the effect of exogenous PS on its de novo synthesis in rats with OA-induced PE. Experimental rats were randomized into three groups, including a control group, OA-induced PE group, and OA-induced group treated with exogenous PS (OA-PS). Twenty-four rats were sacrificed 4 h after induction of the OA model, and tissue was examined by light and electron microscopy to assess the severity of ALI using an established scoring system at the end of the experiment. After 15 μCi 3H-choline chloride was injected intravenously, eight rats in each group were sacrificed at 4, 8, and 16 h. The radioactivity of 3H incorporated into total phospholipid (TPL) and desaturated phosphatidylcholine (DSPC) was measured in bronchoalveolar lavage fluid (BALF) and lung tissue (LT) using a liquid scintillation counter and was expressed as counts per minute (CPM). Results showed that TPL, DSPC, and the ratio of DSPC/total protein (TP) in lung tissue decreased 4 h after challenge with OA, but the levels recovered after 8 and 16 h. At 8 h after injection, 3H-TPL and 3H-DSPC radioactivity in the lungs reached its peak. Importantly, 3H-DSPC CPM were significantly lower in the PS treatment group (LT: Control: 62327 ± 9108; OA-PE: 97315 ± 10083; OA-PS: 45127 ± 10034, P < 0.05; BALF: Control: 7771 ± 1768; OA-PE: 8097 ± 1799; OA-PE: 3651 ± 1027, P < 0.05). Furthermore, DSPC secretory rate (SR) in the lungs was significantly lower in the PS treatment group at 4 h after injection (Control: 0.014 ± 0.003; OA-PE: 0.011 ± 0.004; OA-PS: 0.023 ± 0.006, P < 0.05). Therefore, we hypothesize that exogenous PS treatments may adversely affect endogenous de novo synthetic and secretory phospholipid pathways via feedback inhibition. This novel finding reveals the specific involvement of exogenous PS in endogenous synthetic and secretory phospholipid pathways during the treatment of ARDS. This information improves our understanding of how PS treatment is beneficial against ARDS and opens new opportunities for expanding its use.

show abstract

Secretion of Thioredoxin Peroxidase Protein of Cat Liver Fluke Opisthorchis felineus during Modeling of Experimental Opisthorchiasis

et al. 2017

View full text Add to dashboard Cite

Mechanisms of thioredoxin peroxidase secretion by Opisthorchis felineus were studied in vivo and in vitro. Specific antibodies were obtained and used for western blotting and immunohistochemical detection in Syrian hamster model of opisthorchiasis. Secreted thioredoxin peroxidase protein was accumulated in the worm incubation medium under conditions of oxidative stress and in bile duct cells of hamsters with chronic opisthorchiasis.

show abstract

Morphofunctional Characteristics of Pulmonary Surfactant System and Its Effect on Immune Cells in Influenza A (H1N1) Pathogenesis

Cited by 3 publications

References 24 publications

Death Mechanisms of Pulmonary Alveolocytes in Mice Infected with Influenza Viruses A/H1N1/California/04/2009 and A/H5N1/Goose/Krasnoozerskoye/627/05

Death Mechanisms of Pulmonary Alveolocytes in Mice Infected with Influenza Viruses A/H1N1/California/04/2009 and A/H5N1/Goose/Krasnoozerskoye/627/05

Synthesis of phosphatidylcholine in rats with oleic acid-induced pulmonary edema and effect of exogenous pulmonary surfactant on its De Novo synthesis

Secretion of Thioredoxin Peroxidase Protein of Cat Liver Fluke Opisthorchis felineus during Modeling of Experimental Opisthorchiasis

Contact Info

Product

Resources

About