The researchers simulated the lung damage and immune response induced by the new coronavirus infection

Jan. 13 (Xinhua) -- The
Dalian Institute of Chemical Physics Qin Jianhua Researcher Team and Zheng Yongtang Researcher Team worked together to establish an in-body lung organ microphysiological system using organ chip technology to simulate lung tissue damage and immune response caused by new coronavirus infection, providing new strategies and new technologies for the study and rapid drug evaluation of the disease-causing mechanism of the new coronavirus, the official website of China
Kunming Animal Research Institute announced on the 13th.
new coronavirus (SARS-CoV-2) infection has led to a global pandemic. The lungs are the main target organs for SARS-CoV-2 infections. At present, the clinical treatment of new crown pneumonia is mainly comprehensive treatment, but there is still a lack of special drugs. Although early cell and animal models have been used in the study of new coronavirus, there are still many limitations to some extent. At present, there is still a lack of a research model that can reflect the human body's response to new coronavirus infection at the level of tissue organs, which is also one of the bottlenecks that seriously restrict the current research and development process of new coronavirus drugs.
organ chip is a new frontier cross-technology, which integrates physics, chemistry, engineering and biology and other multidisciplinary methods, can be bionic on a few square centimeters of flow control chip bionics to build a variety of human tissue organs micro-model, used to reflect the key structure of human organs and biological functions. In particular, it has the potential to reproduce the human body's response to a variety of external factors in an unprecedented way, and has wide application potential in life science research, disease research and new drug research and development.
the study, the researchers first used organ chip technology bionics to build a functional unit of the human alba bubble, and further experiments on new coronavirus infections. Based on the complex structure and functional characteristics of human lung tissue, the researchers simulated the micro-environment of human altrual tissue in perfusionable microchips with multi-layer cavity design, and in experiments, through human altruums in micro-cavities on both sides of the chip porous membrane (alfurum side/vascular side). The dynamic co-culture of endoblast cells, pulmonary microvascular endoblast cells and exovascular immune cells establishes functional alcupile-capillaries barrier containing complex factors such as human-sourced cells, mechanical fluids and tissue interfaces, and then conducts experiments on new coronavirus infection on the chip.
results show that when the albavirus side skin cells on the chip are exposed to the new coronavirus, a large number of virus replications can be seen in the endoculocytes, and the integrity of the lung tissue barrier is damaged. The transcription group analysis found that SARS-CoV-2 infection triggered different response mechanisms in two cells, activating the type I interferon pathline in the endoskin cells and the JAK-STAT pathline in the endostrote cells, respectively. According to the viral load calculation, human anticulmonary endocrine cells show a stronger susceptible to the virus, is the main place of virus replication, and the human pulmonary microvascular enditer cells have a lower viral load, suggesting that the virus may indirectly affect endothorte cells by infecting pulmonary endothelectrine cells.
In addition, the study found that viral infections can also lead to increased adhesion of chip vascular exoglobular blood immune cells to endoblast cells in blood vessels and release a large number of inflammatory factors (e.g. IL-1 beta, IL-6, IL-8, TNF-α), suggesting that neo-coronavirus infection of pulmonary tissue may release a large number of inflammatory factors by activating human immune cells, inducing pulmonary microvascular endothial damage. Using this model, the researchers also conducted preliminary tests and evaluations against the ability of viral compounds.
The study uses organ chip technology to establish a model of human neocycell pneumonia disease based on tissue level, and simulates a series of key pathophysiological processes such as lung barrier dysfunction, immune cell adhesion, inflammatory factor release and endodertic cell damage caused by neo-coronavirus infection, reflecting the pathogen-host interaction in which multicellular complex factors in new coronavirus infection are involved. This model system has the characteristics of short modeling cycle, low cost, human origin and easy monitoring, which can obtain dynamic biological information which is difficult to obtain by traditional methods, and can be extended to the study of the mechanism of new coronary pneumonia, which is multi-organ-tired.
related research results were published recently in Advanced Science.