Pulmonary surfactant itself must be a strong defender against SARS-CoV-2
Autor: | Hideyuki Takano |
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Rok vydání: | 2020 |
Předmět: |
0301 basic medicine
Phagocytosis viruses Ambroxol Alveolar epithelial type II cell Pneumonia Viral ACE2 medicine.disease_cause Crystallography X-Ray Article Microbiology 03 medical and health sciences Surface-Active Agents 0302 clinical medicine Viral envelope Pulmonary surfactant Pregnenediones medicine Humans Surface Tension Receptor Lung Coronavirus Clinical Trials as Topic Chemistry SARS-CoV-2 COVID-19 Pulmonary Surfactants General Medicine respiratory system Models Theoretical medicine.disease Lipids respiratory tract diseases COVID-19 Drug Treatment Pulmonary Alveoli Pneumonia Bromhexine 030104 developmental biology medicine.anatomical_structure Angiotensin-Converting Enzyme 2 030217 neurology & neurosurgery medicine.drug |
Zdroj: | Medical Hypotheses |
ISSN: | 1532-2777 |
Popis: | Pulmonary surfactant is considered to be one of the soaps. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the other enveloped viruses become very weak against surfactant. The SARS virus binds to angiotensin-converting enzyme (ACE2) receptor and causes pneumonia. In the lung, the ACE2 receptor sits on the top of lung cells known as alveolar epithelial type II (AE2) cells. These cells play an important role in producing surfactant. Pulmonary surfactant is believed to regulate the alveolar surface tension in mammalian lungs. To our knowledge, AE2 cells are believed to act as immunoregulatory cells; however, pulmonary surfactant itself has not been believed to act as a defender against the enveloped viruses. This study hypothesises that pulmonary surfactant may be a strong defender of enveloped viruses. Therefore, old coronaviruses merely cause pneumonia. On the contrary, new SARS-CoV-2 can suppress the production of surfactant that binds to the ACE2 of AE2 cells. The coronavirus can survive in the lung tissue because of the exhaustion of pulmonary surfactant. |
Databáze: | OpenAIRE |
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