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SP-A Can Protect Lung Epidermis From HBD3

SP-A can protect the lung epidermis from hBD3. In the innate immune system, defensins are important molecules that can remove foreign microorganisms. But at high concentrations, they can be toxic to their own cells. For a long time, the mechanism by which the human body protects its cells from the hazards of defensins is not very clear. Yoshio Kuroki, et al. Of Sapporo Medical University, Japan, found that hBD3 (human β The toxicity of defensin 3) to pulmonary epidermal cells will be attenuated by SP-A (pulmonary surfactant related protein A), so SP-A is likely to become a therapeutic drug to protect tissues during inflammation.
Since it was found that epithelial cells pre cultured in SP-A were not subject to the cytotoxicity of hBD3, the direct interaction between SP-A and hBD3 may make SP-A an important factor to reduce the toxicity of hBD3. Consistent with the in vitro analysis, compared with the effect on WT mice, after intratracheal administration of hBD3 to SP-A -/- mice, more severe tissue damage will occur to the lung epidermis. These data indicate that SP-A protects the lung epithelium from tissue damage caused by hBD3.
In addition, the study found that the functional region of SP-A lies in Tyr161-Lys201. At present, this area has been artificially synthesized and is temporarily called SP-A Y161-G200. Subsequent experiments showed that it could also inhibit the cytotoxicity of hBD3. Therefore, SP-A Y161-G200 is likely to become a therapeutic drug to protect tissues during inflammation.
At present, Wuxi Donglin Science and Technology Development Co., Ltd. has developed a variety of Elisa products related to surfactant associated protein A. If you want to know about SP-A Elisa reagent, you can directly visit the website:

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