scholarly journals Surfactant protein-A enhances respiratory syncytial virus clearance in vivo

1999 ◽  
Vol 103 (7) ◽  
pp. 1015-1021 ◽  
Author(s):  
Ann Marie LeVine ◽  
Jodie Gwozdz ◽  
James Stark ◽  
Michael Bruno ◽  
Jeffrey Whitsett ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Protein A ◽  
Surfactant Protein ◽  
Surfactant Protein A ◽  
Virus Clearance ◽  
Syncytial Virus

scholarly journals Surfactant Protein A Binds to the Fusion Glycoprotein of Respiratory Syncytial Virus and Neutralizes Virion Infectivity

1999 ◽  
Vol 180 (6) ◽  
pp. 2009-2013 ◽  
Author(s):  
Reena Ghildyal ◽  
Carol Hartley ◽  
Annalisa Varrasso ◽  
Jayesh Meanger ◽  
Dennis R. Voelker ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Protein A ◽  
Surfactant Protein ◽  
Surfactant Protein A ◽  
Fusion Glycoprotein ◽  
Syncytial Virus

Lung Surfactant Protein A Provides a Route of Entry for Respiratory Syncytial Virus into Host Cells

2000 ◽  
Vol 13 (1) ◽  
pp. 125-135 ◽  
Author(s):  
TIMOTHY P. HICKLING ◽  
RAJNEESH MALHOTRA ◽  
HELEN BRIGHT ◽  
WILLIAM MCDOWELL ◽  
EDWARD D. BLAIR ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Lung Surfactant ◽  
Protein A ◽  
Surfactant Protein ◽  
Host Cells ◽  
Surfactant Protein A ◽  
Syncytial Virus ◽  
Lung Surfactant Protein

SURFACTANT PROTEIN A GENETIC VARIANTS IN CHILDREN HOSPITALIZED WITH RESPIRATORY SYNCYTIAL VIRUS DISEASE

2004 ◽  
Vol 32 (Supplement) ◽  
pp. A115
Author(s):  
Neal J Thomas ◽  
Susan L DiAngelo ◽  
Joanna Floros ◽  
Douglas F Willson ◽  
Wenlei Liu ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Genetic Variants ◽  
Virus Disease ◽  
Protein A ◽  
Surfactant Protein ◽  
Surfactant Protein A ◽  
Respiratory Syncytial Virus Disease ◽  
Syncytial Virus

Exposure of surfactant protein A to ozone in vitro and in vivo impairs its interactions with alveolar cells

1992 ◽  
Vol 262 (1) ◽  
pp. L63-L68 ◽  
Author(s):  
R. S. Oosting ◽  
J. F. Van Iwaarden ◽  
L. Van Bree ◽  
J. Verhoef ◽  
L. M. Van Golde ◽  
...  
Keyword(s):  
Superoxide Anion ◽  
Protein A ◽  
Surfactant Protein ◽  
Surfactant Protein A ◽  
Alveolar Type ◽  
Type Ii ◽  
Superoxide Anion Production ◽  
Anion Production

This study focused on the question of whether exposure of surfactant protein A (SP-A) to ozone affected properties of this protein that may be involved in regulating alveolar type II cell and alveolar macrophage functions. In vitro exposure of human or canine SP-A to ozone reduced the ability of this protein to inhibit phorbol-ester induced secretion of [3H]phosphatidylcholine by alveolar type II cells in culture. Ozone-exposed human SP-A showed a decreased ability to enhance phagocytosis of herpes simplex virus and to stimulate superoxide anion production by alveolar macrophages. Experiments with elastase showed that ozone-exposed canine SP-A was more susceptible to proteolysis. A conformational change of the protein could underlie this phenomenon. Surfactant isolated from ozone-exposed rats (0.4 ppm ozone for 12 h) was also less able to stimulate superoxide anion production by alveolar macrophages than surfactant from control rats, which suggested that SP-A in vivo was also susceptible to ozone. The results of this study suggest that SP-A-alveolar cell interactions can be inhibited by ozone exposure, which may contribute to the toxicity of ozone in the lungs.

scholarly journals Eosinophils contribute to innate antiviral immunity and promote clearance of respiratory syncytial virus

Blood ◽  
2007 ◽  
Vol 110 (5) ◽  
pp. 1578-1586 ◽  
Author(s):  
Simon Phipps ◽  
Chuan En Lam ◽  
Suresh Mahalingam ◽  
Matthew Newhouse ◽  
Ruben Ramirez ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Host Defense ◽  
No Production ◽  
Wild Type ◽  
Interleukin 5 ◽  
Virus Clearance ◽  
Lung Dysfunction ◽  
Rsv Infection ◽  
Syncytial Virus

AbstractEosinophils are recruited to the lungs in response to respiratory syncytial virus (RSV) infection; however, their role in promoting antiviral host defense remains unclear. Here, we demonstrate that eosinophils express TLRs that recognize viral nucleic acids, are activated and degranulate after single-stranded RNA (ssRNA) stimulation of the TLR-7–MyD88 pathway, and provide host defense against RSV that is MyD88 dependent. In contrast to wild-type mice, virus clearance from lung tissue was more rapid in hypereosinophilic (interleukin-5 transgenic) mice. Transfer of wild-type but not MyD88-deficient eosinophils to the lungs of RSV-infected wild-type mice accelerated virus clearance and inhibited the development of airways hyperreactivity. Similar responses were observed when infected recipient mice were MyD88 deficient. Eosinophils isolated from infected hypereosinophilic MyD88-sufficient but not MyD88-deficient mice expressed greater amounts of IFN regulatory factor (IRF)–7 and eosinophil-associated ribonucleases EAR-1 and EAR-2. Hypereosinophilia in the airways of infected mice also correlated with increased expression of IRF-7, IFN-β, and NOS-2, and inhibition of NO production with the NOS-2 inhibitor L-NMA partially reversed the accelerated virus clearance promoted by eosinophils. Collectively, our results demonstrate that eosinophils can protect against RSV in vivo, as they promote virus clearance and may thus limit virus-induced lung dysfunction.

Alterations in surfactant protein A after acute exposure to ozone

1996 ◽  
Vol 80 (5) ◽  
pp. 1560-1567 ◽  
Author(s):  
W. Y. Su ◽  
T. Gordon
Keyword(s):  
Neutralizing Antibodies ◽  
Time Course ◽  
Protein A ◽  
Surfactant Protein ◽  
Repeated Exposure ◽  
Ozone Exposure ◽  
Surfactant Protein A ◽  
Enzyme Linked Immunosorbent Assay

The surfactant layer covering the gas-exchange region of the lung serves as the initial site of interaction with inhaled oxidant gases. Among the endogenous compounds potentially vulnerable to oxidative injury are surfactant proteins. This study focused on the effect of ozone on surfactant protein A (SP-A) function, content, and gene expression. To determine the time course of response to ozone, guinea pigs were exposed to 0.2-0.8 parts/million (ppm) ozone for 6 h and were killed up to 120 h postexposure. To determine the effect of repeated exposure, animals were exposed to 0.8 ppm ozone for 6 h/day and were killed on days 3 and 5. A significant increase in surfactant's ability to modulate the respiratory burst induced by phorbol 12-myristate 13-acetate in naive macrophages was observed at 24 h after a single 0.8 ppm ozone exposure. Because neutralizing antibodies to SP-A blunted this stimulatory effect, we hypothesized that ozone enhanced the modulatory role of SP-A in macrophage function. This alteration in function was accompanied by an influx of inflammatory cells and only marginal changes in SP-A levels as determined by an enzyme-linked immunosorbent assay. No significant changes in steady-state levels of SP-A mRNA were observed after single or repeated exposure to ozone. Thus the inflammation that accompanies in vivo ozone exposure may result in a change in the structure and thus functional role of SP-A in modulating macrophage activity.

scholarly journals Staphylococcus aureus Lung Infection Results in Down-Regulation of Surfactant Protein-A Mainly Caused by Pro-Inflammatory Macrophages

2020 ◽  
Vol 8 (4) ◽  
pp. 577 ◽  
Author(s):  
Elisabeth Schicke ◽  
Zoltán Cseresnyés ◽  
Knut Rennert ◽  
Vanessa Vau ◽  
Karoline Frieda Haupt ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Influenza A ◽  
Protein A ◽  
Surfactant Protein ◽  
Immune Defense ◽  
Surfactant Protein A ◽  
Down Regulation ◽  
Complex Interactions ◽  
Inflammatory Macrophages

Pneumonia is the leading cause of hospitalization worldwide. Besides viruses, bacterial co-infections dramatically exacerbate infection. In general, surfactant protein-A (SP-A) represents a first line of immune defense. In this study, we analyzed whether influenza A virus (IAV) and/or Staphylococcus aureus (S. aureus) infections affect SP-A expression. To closely reflect the situation in the lung, we used a human alveolus-on-a-chip model and a murine pneumonia model. Our results show that S. aureus can reduce extracellular levels of SP-A, most likely attributed to bacterial proteases. Mono-epithelial cell culture experiments reveal that the expression of SP-A is not directly affected by IAV or S. aureus. Yet, the mRNA expression of SP-A is strongly down-regulated by TNF-α, which is highly produced by professional phagocytes in response to bacterial infection. By using the human alveolus-on-a-chip model, we show that the down-regulation of SP-A is strongly dependent on macrophages. In a murine model of pneumonia, we can confirm that S. aureus decreases SP-A levels in vivo. These findings indicate that (I) complex interactions of epithelial and immune cells induce down-regulation of SP-A expression and (II) bacterial mono- and super-infections reduce SP-A expression in the lung, which might contribute to a severe outcome of bacterial pneumonia.

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