Obesity is a risk factor for severe influenza. Studies on mice confirm that obese mice experience more extensive lung damage and higher mortality from influenza compared to non-obese counterparts. Research on influenza patients hospitalized due to the virus reveals that obese individuals exhibit a compromised immune response.
The primary protective response against respiratory viral infections is the production of interferons I and III (IFN). Essential cells generating IFN in the lungs include epithelial cells, plasmacytoid dendritic cells, and macrophages.
Scientists from Imperial College London conducted a study on the protective response to influenza in lower respiratory tract cells of obese patients. These cells were obtained during bariatric surgery under general anesthesia.
Research Findings
Obesity disrupts the antiviral response of interferons I and III types to influenza. Individuals with obesity experience impaired fatty acid metabolism, suppressing the immune function of macrophages and interferon responses. This occurs because the concentration of leptin, a hormone produced by fat cells stimulating fatty acid oxidation, is elevated in the respiratory pathways of obese individuals. Leptin receptors are present on the surface of immune cells, and leptin can increase oxidative stress in macrophages. Elevated leptin concentrations in the respiratory pathways suppress the interferon I type response.
Experiments on mice demonstrated that administering leptin reduces the protective interferon I type response to influenza in the respiratory pathways. Another experiment on obese mice showed increased leptin levels contribute to virus spread, inflammation, and mortality. Administering leptin antibodies reduces inflammation and improves survival.
In individuals with obesity, the antiviral response of macrophages to influenza is weakened. Interferon responses of interferon I and III types are disrupted in macrophages. However, bronchial epithelial cells and plasmacytoid dendritic cells maintain average interferon production.
Alveolar macrophages are crucial for protecting against respiratory failure and are necessary for the immune response to influenza. Mouse studies revealed that macrophage removal leads to severe influenza progression and mortality.
Disruption of the antiviral response in macrophages may increase virus replication before symptom onset. Increased replication by the 5th to 6th day post-infection may lead to heightened antiviral and pro-inflammatory respiratory responses and intensified influenza symptoms.
Treating obesity is likely the most effective method for reducing the risk of severe viral infections. Studies confirm that sustained weight loss can enhance the immune response:
- The risk of hospitalization due to influenza decreases after bariatric surgery.
- Impaired interferon II type response in peripheral blood mononuclear cells in obese individuals can be improved through weight loss.
For some patients, weight loss is unattainable. In such cases, pharmaceutical interventions targeting leptin levels or interferon administration may protect against severe infections.
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Reference
Obesity dysregulates the pulmonary antiviral immune response
