Pulmonary innate immune response in Sars-cov-2 infection
Introduction: The emerging infection caused by the new SARS-CoV-2 coronavirus has become a real challenge for the scientific community. Currently, there is little knowledge about the pathogenesis of COVID-19 and in recent times the participation of the host's own immune response in the progress...
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| Autores principales: | , |
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| Formato: | Artículo revista |
| Lenguaje: | Español |
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Universidad Nacional Córdoba. Facultad de Ciencias Médicas. Secretaria de Ciencia y Tecnología
2022
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| Acceso en línea: | https://revistas.unc.edu.ar/index.php/med/article/view/30642 |
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| Sumario: | Introduction: The emerging infection caused by the new SARS-CoV-2 coronavirus has become a real challenge for the scientific community. Currently, there is little knowledge about the pathogenesis of COVID-19 and in recent times the participation of the host's own immune response in the progression of the disease has been proposed. Innate pulmonary immunity is the first barrier against different toxins, which can cause tissue damage, with the consequent alteration of respiratory function. However, a loss in the regulation of these inflammatory mechanisms can cause a disruption in the homeostasis of the affected tissue. Objective: To evaluate the role of the pulmonary innate immune response in the pathogenesis of COVID-19. Materials and methods: A systematic review of studies published in scientific search engines was carried out: PubMed, Google Scholar, Science Direct. The following keywords were used: “COVID-19”; "Acute Respiratory Distress Syndrome"; "SARS-CoV-2"; "Innate pulmonary immunity"; "Innate immune response". Results: A global alteration of the pulmonary innate immune response was found in SARS-CoV-2 infection, which would have relevance in the pathogenesis of COVID-19. Conclusion: The global involvement of the innate immune response and consequently of lung tissue homeostasis, in SARS-CoV-2 infection, requires the design of new therapeutic strategies aimed at modulating the altered pro-inflammatory mechanisms in COVID-19. |
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