Effects of Insulin and Glucose Stimulation on the Anti-Viral Response in Bronchial Epithelial Cells
(2020) MOBY01 20192Degree Projects in Molecular Biology
- Abstract
- Asthma exacerbation is among the leading causes of mortality and morbidity. Bronchial epithelial cells (BECs) are of interest because they represent not only a physical barrier against infections, but also a biological barrier between the inhaled agents, such as allergens, and the immune system. As known, systemic inflammation of the lungs, or dietary factors could have effects on lung disease worsening. Metabolic syndrome is another crucial medical condition that exhibits high levels of glucose (hyperglycaemia), systemic inflammation, obesity, as well as insulin resistance which is a risk factor for asthma development. Insulin resistance also links asthma with metabolic syndrome and obesity. Deficient production of anti-viral interferons... (More)
- Asthma exacerbation is among the leading causes of mortality and morbidity. Bronchial epithelial cells (BECs) are of interest because they represent not only a physical barrier against infections, but also a biological barrier between the inhaled agents, such as allergens, and the immune system. As known, systemic inflammation of the lungs, or dietary factors could have effects on lung disease worsening. Metabolic syndrome is another crucial medical condition that exhibits high levels of glucose (hyperglycaemia), systemic inflammation, obesity, as well as insulin resistance which is a risk factor for asthma development. Insulin resistance also links asthma with metabolic syndrome and obesity. Deficient production of anti-viral interferons (IFNs) may be involved in causing viral-induced asthma exacerbations. Allergens also a risk factor for viral-induced asthma exacerbation. Hence, drugs inducing lung IFN production would be warranted. In the current project, the effects of elevated levels of glucose and insulin on viral-induced IFNβ in BECs and in-vitro asthma exacerbation model have been investigated. Although our results are preliminary, we have showed that glucose and insulin might increase viral-induced IFNβ production in BECs and restored house dust mite (HDM)-impaired IFNβ expression in an in-vitro asthma exacerbation model. We assume that insulin effects are abrogated in the presence of insulin resistance conditions, which could be a risk factor for asthma exacerbation development in obese and diabetes asthmatics. We have shown that PRRs, including TLR-3, RIG-I, and MDA5, are not involved in the process of the enhancement of IFNβ by insulin and glucose actions. (Less)
- Popular Abstract
- Asthma Exacerbation, when Every Breath Matters
Asthma is one of the most common pulmonary diseases in the world. This disease is mainly induced by allergens and cause shortness of breath, airway inflammation, chest pain and wheezing. It is a chronic disease, however its symptoms can be highly increased during a short period of time, the so-called asthma exacerbations. These periods of worsening of symptoms can be triggered by allergens such as House Dust Mite (HDM) and viruses, especially the rhinovirus (RV). Some researchers have demonstrated that the production of some anti-viral immune mediators are decreased in patients with asthma compared to healthy people. This deficiency in the immune response is believed to be the reason why... (More) - Asthma Exacerbation, when Every Breath Matters
Asthma is one of the most common pulmonary diseases in the world. This disease is mainly induced by allergens and cause shortness of breath, airway inflammation, chest pain and wheezing. It is a chronic disease, however its symptoms can be highly increased during a short period of time, the so-called asthma exacerbations. These periods of worsening of symptoms can be triggered by allergens such as House Dust Mite (HDM) and viruses, especially the rhinovirus (RV). Some researchers have demonstrated that the production of some anti-viral immune mediators are decreased in patients with asthma compared to healthy people. This deficiency in the immune response is believed to be the reason why asthmatics suffer from severe pulmonary symptoms when the rest of us only get a common cold.
The metabolic syndrome is another crucial medical condition characterized by the presence of high levels of glucose, systemic inflammation, obesity, as well as insulin resistance. Insulin resistance is when the cells of the body do not respond well to insulin, and they cannot use glucose from the blood. Therefore, the glucose increases in the bloodstream resulting in a well-known disease called diabetes. Sometimes, the response of the body to the increase of glucose in the bloodstream is further increasing the levels of insulin. Some investigations have shown that insulin resistance per se is a risk factor for developing asthma. Interestingly, insulin has been shown to have multiple functions that directly contribute to our immune response. In the same way, obesity is another disease that is commonly associated with diabetes and people with obesity are also more susceptible to suffer from asthma.
In the current study, we have investigated the effects of high levels of glucose and insulin on the cells that cover the airways, the bronchial epithelium, because they constitute the first defence line against invading organisms. For these experiments, we cultured the bronchial cells in the laboratory, and we have treated them with high levels of glucose and insulin. Afterwards, we infected the cells with the virus, and we checked the changes in particular inflammatory mediators and anti-viral molecules. Interestingly, both the presence of insulin and glucose in the airway epithelium show ability to exhibit a protective effect against the viral infection. We assume that the effects of insulin are abrogated in the presence of insulin resistance, and therefore, this could be an explanation of the higher risk to suffer from asthma exacerbations in subjects that are obese or diabetic and at the same time asthmatics.
Master’s Degree Project in Molecular Biology, 30 credits, 2020
Department of Biology, Lund University
Professor: Lena Uller
Department of Respiratory Immunopharmacology, Biomedical Centre (BMC), Lund University (Less)
Please use this url to cite or link to this publication:
http://lup.lub.lu.se/student-papers/record/9029891
- author
- Naqchi, Omeyme
- supervisor
-
- Lena Uller LU
- organization
- course
- MOBY01 20192
- year
- 2020
- type
- H2 - Master's Degree (Two Years)
- subject
- language
- English
- id
- 9029891
- date added to LUP
- 2020-09-24 10:43:45
- date last changed
- 2020-09-24 10:43:45
@misc{9029891,
abstract = {{Asthma exacerbation is among the leading causes of mortality and morbidity. Bronchial epithelial cells (BECs) are of interest because they represent not only a physical barrier against infections, but also a biological barrier between the inhaled agents, such as allergens, and the immune system. As known, systemic inflammation of the lungs, or dietary factors could have effects on lung disease worsening. Metabolic syndrome is another crucial medical condition that exhibits high levels of glucose (hyperglycaemia), systemic inflammation, obesity, as well as insulin resistance which is a risk factor for asthma development. Insulin resistance also links asthma with metabolic syndrome and obesity. Deficient production of anti-viral interferons (IFNs) may be involved in causing viral-induced asthma exacerbations. Allergens also a risk factor for viral-induced asthma exacerbation. Hence, drugs inducing lung IFN production would be warranted. In the current project, the effects of elevated levels of glucose and insulin on viral-induced IFNβ in BECs and in-vitro asthma exacerbation model have been investigated. Although our results are preliminary, we have showed that glucose and insulin might increase viral-induced IFNβ production in BECs and restored house dust mite (HDM)-impaired IFNβ expression in an in-vitro asthma exacerbation model. We assume that insulin effects are abrogated in the presence of insulin resistance conditions, which could be a risk factor for asthma exacerbation development in obese and diabetes asthmatics. We have shown that PRRs, including TLR-3, RIG-I, and MDA5, are not involved in the process of the enhancement of IFNβ by insulin and glucose actions.}},
author = {{Naqchi, Omeyme}},
language = {{eng}},
note = {{Student Paper}},
title = {{Effects of Insulin and Glucose Stimulation on the Anti-Viral Response in Bronchial Epithelial Cells}},
year = {{2020}},
}