动物实验,肺部炎症 z-bo 2020-09-18 267

　　Chronic obstructive pulmonary disease (COPD) is a very serious type of lung disease. When the condition of COPD patients deteriorates rapidly, it will be accompanied by viral or bacterial infections, and will produce a severe over-immune response. Many studies have found that smoking can cause inflammation in the body, so smoking is considered to be one of the main causes of COPD. However, the mechanism by which smoking affects the body's immune response and ultimately causes chronic immune disorders is still unclear. Some studies have pointed out that IL-33, a type of cytokine, is secreted in large quantities near the lesions of COPD patients. However, it is not clear whether IL-33 is actually involved in this process.

　　Recently, Dr. Alison A. Humbles of MedImmune LLC and his research team published a study in "Immunity". They used a mouse model of COPD and stimulated smoking to prove that smoking induces an excessive immune response through IL-33. The production.

　　First, the author stimulated mice of different strains (wild type, IL-33-/-, IL-1R-/-) in a smoke chamber, and then artificially received influenza virus infection. The results showed that after the wild-type mice received delayed stimulation, the influenza virus infection ability increased, which was reflected in the significant weight loss of the mice. The two mutant mice did not have this change. In addition, the author analyzed the activation of immune cells and the expression of cytokines in mice in different treatment groups, and found that influenza virus infection caused obvious inflammation in wild-type mice after being stimulated by smoke. However, in mutant mice There is no such reaction. The above experiments indicate that IL-33 may be involved in the stimulation of inflammatory response by smoke.

　　After

　　, the author placed wild-type mice in a smoky environment to stimulate for 4 weeks, 8 weeks, and 16 weeks. After the last stimulation, the lung tissue of the mouse was removed and stained for observation. The staining results show that smoke stimulation can induce the expression of IL-33 in lung tissues, and subsequent influenza stimulation promotes the secretion of IL-33 to the outside of the cell.

　　"In order to further verify the function of IL-33, the author artificially injected IL-33 to stimulate mice after flu stimulation. The results showed that IL-33 stimulation can aggravate the inflammatory response caused by influenza virus infection.

　　"IL-33 can further stimulate the production of downstream inflammatory factors. For example, IL-33 can promote type II innate immune cells (ILC) to produce Th2 cytokines IL-5 and IL-13. The author compared the difference between smoke stimulation or not on the perception of IL-33 in lung tissue. The results show that smoke stimulation can inhibit the production of IL-5 and IL-13. In addition, the authors also found that IL-33 can promote the activation of macrophages and NK cells.

　　Finally, the author verified through in vivo experiments that the amount of IL-33 secretion near the lesions of COPD patients at different periods will increase accordingly. In summary, the author has proved through a series of experiments that smoking promotes the molecular mechanism of lung inflammation.