Sristi Raj Rai, Amity University Kolkata
Biological models are experimental systems (in-vitro) used to recreate human cellular/tissue environments mimicking the body’s function. Aids in studying the biological phenomenon and how it is functioning, and in exploring diseases and their related effects on the system. Though modelling biological systems is not at all an easy job, as it requires interdisciplinary applications along with system biology, mathematical biology, and the use of model organisms. But with the growing field of stem cells and its researches, it is now easier to closely resemble these models to the living human system. With the sudden knock on the door by the unwelcoming zoonotic SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) our unsung heroes were put under the spotlight and Purkayastha et al decided to develop a model! To explore how cigarette smoking (CS) intensifies COVID-19 at the cellular and molecular level, as some of the demographic studies have indirectly suggested.
The inner lining of the upper respiratory system is the first line of defence for any airborne infections as they set up a mucous trap for pathogens/toxins. Thus the goal was to replicate the system exposed to air breathed in from the nose/mouth into the lungs passing through the cells responsible for mucus production. Moreover, most lung diseases, including cancer (oral/lung) and chronic obstructive pulmonary disease (COPD), along with many other illnesses (heart diseases), have one of its leading causes as cigarette smoking. The air-liquid interface (ALI) formed by tissue-cultured human airway stem cells closely mimics bodily conditions, was donated by five young, healthy nonsmoking individuals. These cultures were exposed for four days in a row for 3 min continuously as a control setup, whereas in the experimental setup the cells were also infected with live virus.
Observation suggests an almost three-fold increment in the mucociliary epithelial infection in the latter case, which also inhibited proliferation and repair response of the airway basal stem cells (ABSCs). Thus the smoke inhibits innate immunity making the body more susceptible to SARS-CoV-2 infection. The single-cell profiling showed the above was possible because of deterioration in Type I interferon (signalling molecule that alerts other cells about the invader) receptors and inhibition of gene expression of Type II interferon (via Stat1 phosphorylation). The team also reported a revival strategy for the infected cells i.e. treating the ALI with exogenous interferon β-1.
Also read:Wireless Chip can read neurological signals
SOURCE – Arunima Purkayastha et al, Direct exposure to SARS-CoV-2 and cigarette smoke increases infection severity and alters the stem cell-derived airway repair response, Cell Stem Cell (2020). DOI: 10.1016/j.stem.2020.11.010
One thought on “Cigarette smoking (CS) encourages SARS-CoV-2 infection!”