Antimicrobial antiphlogistic antagonism polypeptide simulating MD2

Abstract

The invention provides an antagonistic peptide which can simulate the key sequence for bonding MD2 and LPS and competitively antagonize the specific bonding which is generated by LPS and MD2, thus achieving the mitigation of the excessive activation of the immune inflammatory cells of LPS and further easing the caused excessive septic damages to the body. The amino acid sequence of the antagonist peptide includes: a sequence 1 of Lys Thr Val Pro Asp Asn His; and the sequence 2 of Ile Gly Lys Phe Leu Tyr Arg. The peptide can effectively mitigate the septic inflammation damage which is induced by the intracellular toxin LPS, thus significantly improving the survival rate of mouses which are infected by the intracellular toxin and maintaining the body immune defense function at the same time of specifically inhibiting the excessive stimulation of the LPS on the inflammatory cells. The antagonistic peptide can be used for preparing the treatment drugs of the inflammatory diseases which are caused by gram-negative bacteria and are related to a toll-like receptor protein.

Description

technical field [0001] The invention belongs to the field of biomedicine, and in particular relates to an antibacterial and anti-inflammatory antagonistic polypeptide simulating MD2, and the preparation of the antagonistic polypeptide is used for the treatment of Gram-negative bacterial infection and related excessive inflammatory damage-like diseases. in the application. Background technique: [0002] Sepsis caused by bacterial infection, especially Gram-negative bacterial infection, has become the main cause of death in clinical patients, especially surgical ICU patients. Data show that the proportion of sepsis in inpatients is 1 / 3, in ICU patients > 50%, and in surgical ICU is more than 80%. Unfortunately, despite the emergence of high-efficiency and broad-spectrum antibiotics, sepsis is still an important cause of death in clinical ICU patients. The main reason is a series of inflammatory damage caused by excessive stimulation of bacterial toxins on the body. Althou...

AI Technical Summary

Problems solved by technology

Data confirm that the affinity between CD14 and TLR4 / MD2 is weak, while the affinity between TLR4 / MD2 is strong, and the binding of MD2 (myeloid differential protein 2, myeloid differentiation protein 2) to TLR4 (toll like receptor 4, Toll-like receptor 4) Occurs before binding to LPS, and MD2 that has lost its LPS-binding function cannot confer TLR4's responsiveness to LPS even if it binds to the extracellular domain of TLR4

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