Viral respiratory infection increases alveolar macrophage cytoplasmic motility in rats: role of NO

1995 ◽  
Vol 268 (3) ◽  
pp. L399-L406 ◽  
Author(s):  
T. Fukushima ◽  
K. Sekizawa ◽  
M. Yamaya ◽  
S. Okinaga ◽  
M. Satoh ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Viral Infection ◽  
Respiratory Infection ◽  
Sendai Virus ◽  
The Body ◽  
Particle Rotation ◽  
Nitrite Production ◽  
Viral Respiratory Infection ◽  
Viral Respiratory

Ingested ferrimagnetic (Fe3O4) particles were used to estimate noninvasively the motion of organelles in alveolar macrophages (AM) in intact rats during viral respiratory infection by parainfluenza type 1 (Sendai) virus. Four days after instillation of Fe3O4 particles (3 mg/kg) into the lung, remnant field strength (RFS) was measured at the body surface immediately after magnetization of Fe3O4 particles by an externally applied magnetic field. RFS decreases with time, due to particle rotation (relaxation) which is related to cytoplasmic motility of AM. Viral infection increased the relaxation rate (lambda o per min), and increases in lambda o reached a maximum 3 days after nasal inoculation (day 3). Viral infection (day 3)-induced increases in lambda o were dose dependently inhibited by either the L-arginine analogue N-nitro-L-arginine or by methylene blue, an inhibitor of guanylate cyclase activity. Bronchoalveolar lavage fluid obtained from infected rats contained significantly higher levels of nitrite than that from control rats (P < 0.01). In in vitro experiments, AM from infected rats showed significantly higher lambda o, nitrite production, and intracellular guanosine 3',5'-cyclic monophosphate levels than those from control rats (P < 0.01). Sodium nitroprusside, known to release nitric oxide concentration dependently, increased lambda o of AM from noninfected rats in vitro. These results suggest that nitric oxide plays an important role in AM cytoplasmic motility during viral respiratory infection.

scholarly journals The Cellular Immunity Agent Based Model (CIABM): Replicating the cellular immune response to viral respiratory infection

2019 ◽  
Author(s):  
Andrew Becker ◽  
Gary An ◽  
Chase Cockrell
Keyword(s):  
Immune Response ◽  
Viral Infection ◽  
Respiratory Infection ◽  
Viral Infections ◽  
Immune Memory ◽  
Agent Based Model ◽  
Agent Based ◽  
Viral Respiratory Infection ◽  
Cellular Immune ◽  
Viral Respiratory

AbstractViral respiratory infections, such as influenza, result in over 1 million deaths worldwide each year. To date, there are few therapeutic interventions able to affect the course of the disease once acquired, a deficit with stark consequences that were readily evident in the current COVID-19 pandemic. We present the Cellular Immune Agent Based Model (CIABM) as a flexible framework for modeling acute viral infection and cellular immune memory development. The mechanism/rule-based nature of the CIABM allows for interrogation of the complex dynamics of the human immune system during various types of viral infections. The CIABM is an extension of a prior agent-based model of the innate immune response, incorporating additional cellular types and mediators involved in the response to viral infection. The CIABM simulates the dynamics of viral respiratory infection in terms of epithelial invasion, immune cellular population changes and cytokine measurements. Validation of the CIABM involved effectively replicating in vivo measurements of circulating mediator levels from a clinical cohort of influenza patients. The general purpose nature of the CIABM allows for both the representation of various types of known viral infections and facilitates the exploration of hypothetical, novel viral pathogens.

Viral respiratory infection increases susceptibility of young rats to hypoxia-induced pulmonary edema

1998 ◽  
Vol 84 (3) ◽  
pp. 1048-1054 ◽  
Author(s):  
Todd C. Carpenter ◽  
John T. Reeves ◽  
Anthony G. Durmowicz
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Respiratory Infection ◽  
Sendai Virus ◽  
Lung Water ◽  
Young Rats ◽  
Cell Counts ◽  
High Altitude Pulmonary Edema ◽  
Viral Respiratory Infection ◽  
Viral Respiratory

Recent clinical observations of a high incidence of preexisting respiratory infections in pediatric cases of high-altitude pulmonary edema prompted us to ask whether such infections would increase the susceptibility to hypoxia-induced pulmonary edema in young rats. We infected weanling rats with Sendai virus, thus causing a mild respiratory infection. Within 7 days of infection, Sendai virus was essentially undetectable by using viral culture and immunohistochemical techniques. Animals at day 7 of Sendai virus infection were then exposed to normobaric hypoxia (fraction of inspired O2= 0.1) for 24 h and examined for increases in gravimetric lung water and in vascular permeability, as well as for histological evidence of increased lung water. Bronchoalveolar lavage was performed on a separate series of animals. Compared with control groups, infected hypoxic animals showed significant increases in perivascular cuffing, gravimetric lung water, and lung protein leak. In addition, infected hypoxic animals had increases in lavage fluid cell counts and protein content compared with controls. We conclude that young rats, exposed to moderate hypoxia while recovering from a mild viral respiratory infection, may demonstrate evidence of early pulmonary edema formation, a finding of potential relevance to human high-altitude pulmonary edema.

Virus induces airway hyperresponsiveness to tachykinins: role of neutral endopeptidase

1989 ◽  
Vol 67 (4) ◽  
pp. 1504-1511 ◽  
Author(s):  
D. J. Dusser ◽  
D. B. Jacoby ◽  
T. D. Djokic ◽  
I. Rubinstein ◽  
D. B. Borson ◽  
...  
Keyword(s):  
Substance P ◽  
Respiratory Infection ◽  
Sendai Virus ◽  
Electrical Field Stimulation ◽  
Neutral Endopeptidase ◽  
Airway Responsiveness ◽  
Endopeptidase Activity ◽  
Viral Respiratory Infection ◽  
Tracheal Epithelial

We examined the effects of viral respiratory infection by Sendai virus on airway responsiveness to tachykinins in guinea pigs. We measured the change in total pulmonary resistance induced by substance P or capsaicin in the presence or absence of the neutral endopeptidase inhibitor, phosphoramidon, in infected and in noninfected animals. In the absence of phosphoramidon, the bronchoconstrictor responses to substance P and to capsaicin were greater in infected than in noninfected animals. Phosphoramidon did not further potentiate the responses to substance P and to capsaicin in the infected animals, whereas it did so in noninfected animals. Studies performed in vitro showed that nonadrenergic noncholinergic bronchial smooth muscle responses to electrical field stimulation were also increased in tissues from infected animals and that phosphoramidon increased the response of tissues from noninfected animals greatly but increased the responses of tissues from infected animals only slightly. Responses to acetylcholine were unaffected by viral infection. Neutral endopeptidase activity was decreased by 40% in the tracheal epithelial layer of the infected animals. We suggest that respiratory infection by Sendai virus causes enhanced airway responsiveness to tachykinins by decreasing neutral endopeptidase-like activity in the airway epithelium.

scholarly journals Acute Otitis Media and Other Complications of Viral Respiratory Infection

PEDIATRICS ◽  
2016 ◽  
Vol 137 (4) ◽  
pp. e20153555-e20153555 ◽  
Author(s):  
T. Chonmaitree ◽  
R. Trujillo ◽  
K. Jennings ◽  
P. Alvarez-Fernandez ◽  
J. A. Patel ◽  
...  
Keyword(s):  
Otitis Media ◽  
Respiratory Infection ◽  
Acute Otitis Media ◽  
Viral Respiratory Infection ◽  
Viral Respiratory

Nitric oxide and interval hypoxic training in COVID-19 rehabilitation— new research direction

2021 ◽  
pp. 30-41
Author(s):  
Tatyana Nikolaevna Tsyganova ◽  
Egor Egorov ◽  
Tamara Nikolaevna Voronina
Keyword(s):  
Nitric Oxide ◽  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Viral Infection ◽  
Distress Syndrome ◽  
The Body ◽  
Lung Damage ◽  
Specific Method ◽  
Hypoxic Training

COVID-19, a disease caused by the novel coronavirus SARS-CoV-2, primarily affects lung tissue and disrupts gas exchange, leading to acute respiratory distress syndrome, systemic hypoxia, and lung damage. The search for methods of prevention and rehabilitation, especially after suffering from pneumonia caused by COVID-19, is on the agenda. This article discusses the possibilities of the interval hypoxic training (IHT) method for preventing infections by initiating nitric oxide production in the body. One of the main effects of IHT is the balanced stimulation of nitric oxide (NO) secretion. Over the past two decades, there has been an increasing interest in the function of nitric oxide (NO) in the human body. Nitric oxide plays a key role in maintaining normal vascular function and regulating inflammatory processes, including those leading to lung damage and the development of acute respiratory distress syndrome (ARDS). Our immune system destroys bacteria and viruses by oxidative burst, i.e. when oxygen accumulates inside the cell. This process also involves nitric oxide, a signaling molecule that has an antibacterial and antiviral effect, as well as regulates vascular tone and affects the permeability of the cell wall. Interval hypoxytherapy enhances endogenous oxidative protection and increases the amount of nitric oxide, thus allowing the body’s cells to resist infection more effectively. Mitochondrial NOS induction and mitochondrial NO synthesis increase under the action of pathogenic factors on the cell. By modulating the activity of mtNOS and the synthesis of mitochondrial NO, it is possible to increase the resistance to hypoxic effects. Interval hypo-hyperoxic training as an effective non-specific method of increasing the body’s defenses is indispensable not only in the prevention of viral infection, but also in rehabilitation after viral pneumonia, as well as as a method that reduces the severity of viral infection in the event of infection.

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