scholarly journals Complement Inhibitors Vitronectin and Clusterin Are Recruited from Human Serum to the Surface of Coronavirus OC43-Infected Lung Cells through Antibody-Dependent Mechanisms

Viruses ◽  
2021 ◽  
Vol 14 (1) ◽  
pp. 29
Author(s):  
Candace R. Fox ◽  
Griffith D. Parks
Keyword(s):  
Human Serum ◽  
Membrane Attack Complex ◽  
Health Concern ◽  
Lung Cells ◽  
Complement Inhibitors ◽  
Human Lung Cells ◽  
Infected Cells ◽  
Human Coronaviruses ◽  
Necessary And Sufficient

Little is known about the role of complement (C’) in infections with highly prevalent circulating human coronaviruses such as OC43, a group of viruses of major public health concern. Treatment of OC43-infected human lung cells with human serum resulted in C3 deposition on their surfaces and generation of C5a, indicating robust C’ activation. Real-time cell viability assays showed that in vitro C’-mediated lysis of OC43 infected cells requires C3, C5 and C6 but not C7, and was substantially delayed as compared to rapid C’-mediated killing of parainfluenza virus type 5 (PIV5)-infected cells. In cells co-infected with OC43 and PIV5, C’-mediated lysis was delayed, similar to OC43 infected cells alone, suggesting that OC43 infection induced dominant inhibitory signals. When OC43-infected cells were treated with human serum, their cell surfaces contained both Vitronectin (VN) and Clusterin (CLU), two host cell C’ inhibitors that can alter membrane attack complex (MAC) formation and C’-mediated killing. VN and CLU were not bound to OC43-infected cells after treatment with antibody-depleted serum. Reconstitution experiments with purified IgG and VN showed that human antibodies are both necessary and sufficient for VN recruitment to OC43-infected lung cells–novel findings with implications for CoV pathogenesis.

scholarly journals Polyphosphate Reverses the Toxicity of the Quasi-Enzyme Bleomycin on Alveolar Endothelial Lung Cells In Vitro

Cancers ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 750
Author(s):  
Werner E. G. Müller ◽  
Meik Neufurth ◽  
Shunfeng Wang ◽  
Heinz C. Schröder ◽  
Xiaohong Wang
Keyword(s):  
Dna Damage ◽  
Human Lung ◽  
Dna Integrity ◽  
Lung Cells ◽  
Antitumor Antibiotic ◽  
Cell Toxicity ◽  
Inorganic Polyphosphate ◽  
Human Lung Cells ◽  
Anti Cancer

The anti-cancer antitumor antibiotic bleomycin(s) (BLM) induces athyminic sites in DNA after its activation, a process that results in strand splitting. Here, using A549 human lung cells or BEAS-2B cells lunc cells, we show that the cell toxicity of BLM can be suppressed by addition of inorganic polyphosphate (polyP), a physiological polymer that accumulates and is released from platelets. BLM at a concentration of 20 µg ml−1 causes a decrease in cell viability (by ~70%), accompanied by an increased DNA damage and chromatin expansion (by amazingly 6-fold). Importantly, the BLM-caused effects on cell growth and DNA integrity are substantially suppressed by polyP. In parallel, the enlargement of the nuclei/chromatin in BLM-treated cells (diameter, 20–25 µm) is normalized to ~12 µm after co-incubation of the cells with BLM and polyP. A sequential application of the drugs (BLM for 3 days, followed by an exposure to polyP) does not cause this normalization. During co-incubation of BLM with polyP the gene for the BLM hydrolase is upregulated. It is concluded that by upregulating this enzyme polyP prevents the toxic side effects of BLM. These data might also contribute to an application of BLM in COVID-19 patients, since polyP inhibits binding of SARS-CoV-2 to cellular ACE2.

Pathobiological Effects of Fibers and Tobacco-Related Chemicals in Human Lung Cells In Vitro

1989 ◽  
pp. 103-117
Author(s):  
C. C. Harris ◽  
J. C. Willey ◽  
N. Matsukura ◽  
J. F. Lechner ◽  
M. Miyashita ◽  
...  
Keyword(s):  
Human Lung ◽  
Lung Cells ◽  
Human Lung Cells

scholarly journals Measles Virus-Induced Immunosuppression In Vitro Is Independent of Complex Glycosylation of Viral Glycoproteins and of Hemifusion

2000 ◽  
Vol 74 (16) ◽  
pp. 7548-7553 ◽  
Author(s):  
Armin Weidmann ◽  
Christian Fischer ◽  
Shinji Ohgimoto ◽  
Claudia Rüth ◽  
Volker ter Meulen ◽  
...  
Keyword(s):  
Measles Virus ◽  
Human Lymphocytes ◽  
Lymphoid Cells ◽  
Oxygen Intermediates ◽  
Inhibitory Peptides ◽  
Viral Particles ◽  
Infected Cells ◽  
Necessary And Sufficient ◽  
Cellular Fusion

ABSTRACT Expression of the measles virus (MV) F/H complex on the surface of viral particles, infected cells, or cells transfected to express these proteins (presenter cells [PC]) is necessary and sufficient to induce proliferative arrest in both human and rodent lymphoid cells (responder cells [RC]). This inhibition was found to occur independent of apoptosis and soluble mediators excluded by a pore size filter of 200 nm released from either PC or RC. We now show that reactive oxygen intermediates which might be released by RC or PC also do not contribute to MV-induced immunosuppression in vitro. Using an inhibitor of Golgi-resident mannosidases (deoxymannojirimycin), we found that complex glycosylation of the F and H proteins is not required for the induction of proliferative arrest of RC. As revealed by our previous studies, proteolytic cleavage of the MV F protein precursor into its F1 and F2 subunits, but not of F/H-mediated cellular fusion, was found to be required, since fusion-inhibitory peptides such as Z-d-Phe-l-Phe-Gly (Z-fFG) did not interfere with the induction of proliferative inhibition. We now show that Z-fFG inhibits cellular fusion at the stage of hemifusion by preventing lipid mixing of the outer membrane layer. These results provide strong evidence for a receptor-mediated signal elicited by the MV F/H complex which can be uncoupled from its fusogenic activity is required for the induction of proliferative arrest of human lymphocytes.

Genomic responses of human lung cells exposure through a successful in vitro field deployment in Houston, Texas

2017 ◽  
Vol 280 ◽  
pp. S212
Author(s):  
Hang Nguyen ◽  
Kenneth Sexton ◽  
Lisa Smeester ◽  
Kjersti Marie Aagaard ◽  
Cynthia Do Shope ◽  
...  
Keyword(s):  
Human Lung ◽  
Lung Cells ◽  
Human Lung Cells ◽  
Field Deployment

Quantitation and characterization of leukotriene products released following immunologic stimulation of human lung cells in vitro

CHEST Journal ◽  
1983 ◽  
Vol 83 (5) ◽  
pp. 81S-82 ◽  
Author(s):  
A. G. Leitch ◽  
R. A. Lewis ◽  
E. J. Corey ◽  
K. F. Austen
Keyword(s):  
Human Lung ◽  
Lung Cells ◽  
Human Lung Cells ◽  
Stimulation Of

scholarly journals Application of an optimized system for the well-defined exposure of human lung cells to trichloramine and indoor pool air

2011 ◽  
Vol 9 (3) ◽  
pp. 586-596 ◽  
Author(s):  
C. Schmalz ◽  
H. G. Wunderlich ◽  
R. Heinze ◽  
F. H. Frimmel ◽  
C. Zwiener ◽  
...  
Keyword(s):  
Cell Viability ◽  
Lung Cells ◽  
Exposure Test ◽  
Alveolar Epithelial ◽  
Toxicological Effects ◽  
Human Lung Cells ◽  
Indoor Swimming Pool ◽  
Set Up ◽  
Epithelial Lung Cells

In this study an in vitro exposure test to investigate toxicological effects of the volatile disinfection by-product trichloramine and of real indoor pool air was established. For this purpose a set-up to generate a well-defined, clean gas stream of trichloramine was combined with biotests. Human alveolar epithelial lung cells of the cell line A-549 were exposed in a CULTEX® device with trichloramine concentrations between 0.1 and 40 mg/m3 for 1 h. As toxicological endpoints the cell viability and the inflammatory response by the cytokines IL-6 and IL-8 were investigated. A decreasing cell viability could be observed with increasing trichloramine concentration. An increase of IL-8 release could be determined at trichloramine concentrations higher than 10 mg/m3 and an increase of IL-6 release at concentrations of 20 mg/m3. Investigations of indoor swimming pool air showed similar inflammatory effects to the lung cells although the air concentrations of trichloramine of 0.17 and 0.19 mg/m3 were much lower compared with the laboratory experiments with trichloramine as the only contaminant. Therefore it is assumed that a mixture of trichloramine and other disinfection by-products in the air of indoor pool settings contribute to that effect.

scholarly journals Heme Oxygenase-1 Exerts Antiviral Activity against Hepatitis A Virus In Vitro

Pharmaceutics ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 1229
Author(s):  
Dong-Hwi Kim ◽  
Hee-Seop Ahn ◽  
Hyeon-Jeong Go ◽  
Da-Yoon Kim ◽  
Jae-Hyeong Kim ◽  
...  
Keyword(s):  
Antiviral Activity ◽  
Protein Expression ◽  
Heme Oxygenase ◽  
Hepatitis A ◽  
Hepatitis A Virus ◽  
Health Concern ◽  
Heme Oxygenase 1 ◽  
Infected Cells ◽  
In Cells

Hepatitis A virus (HAV), the causative pathogen of hepatitis A, induces severe acute liver injuries in humans and is a serious public health concern worldwide. However, appropriate therapeutics have not yet been developed. The enzyme heme oxygenase-1 (HO-1) exerts antiviral activities in cells infected with several viruses including hepatitis B and C viruses. In this study, we demonstrated for the first time the suppression of virus replication by HO-1 in cells infected with HAV. Hemin (HO-1 inducer) induced HO-1 mRNA and protein expression, as expected, and below 50 mM, dose-dependently reduced the viral RNA and proteins in the HAV-infected cells without cytotoxicity. Additionally, HO-1 protein overexpression using a protein expression vector suppressed HAV replication. Although ZnPP-9, an HO-1 inhibitor, did not affect HAV replication, it significantly inhibited hemin-induced antiviral activity in HAV-infected cells. Additionally, FeCl3, CORM-3, biliverdin, and the HO-1 inducers andrographolide and CoPP inhibited HAV replication in the HAV-infected cells; andrographolide and CoPP exhibited a dose-dependent effect. In conclusion, these results suggest that HO-1 effectively suppresses HAV infection in vitro, and its enzymatic products appear to exert antiviral activity. We expect that these results could contribute to the development of a new antiviral drug for HAV.

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