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LL-37

Cathelicidin, hCAP-18, FALL-39, CAP-18

Quick Stats
Studies 2230
Trials 95
Score 2
2018 pubmed 26 citations

Astragalus polysaccharides exerts anti-infective activity by inducing human cathelicidin antimicrobial peptide LL-37 in respiratory epithelial cells.

Zhao. Lin L; Tan. Shuai S; Zhang. Hai H; Liu. Peng P; Tan. Yu-Zhu YZ; Li. Jia-Chuan JC; Jia. Da D; Shen. Xiao-Fei XF

Key Findings

  • APS raises LL‑37 mRNA and protein levels in respiratory epithelial cells
  • APS‑treated cells show antibacterial activity that is reduced when LL‑37 is blocked
  • The increase in LL‑37 depends on p38 MAPK, JNK and NF‑κB signaling pathways

Practical Outcomes

  • APS may help enhance airway immunity by increasing LL‑37, so Astragalus extracts could be explored as a natural immune‑support supplement. However, human dosing, safety, and real‑world effectiveness are not established yet, so use cautiously and look for clinical studies before adopting as a protocol.

Summary

Astragalus polysaccharides (APS) can boost the body's own antimicrobial peptide LL‑37 in airway cells, leading to stronger antibacterial effects in lab dishes, but this is only shown in cell cultures, not in people.

Abstract

Astragalus polysaccharides (APS), one of the major active components in Astragalus membranaceus, is an effective immunomodulator used in the treatment of immunological diseases in China. However, the anti-infective action and mechanism of APS is not fully known. In the present study, we found that APS induced the expression of human cathelicidin antimicrobial peptide LL-37, a key host anti-infective molecule, in both mRNA and protein levels in respiratory epithelial cells HBE16 and A549. Furthermore, the lysate and supernatant from APS-treated HBE16 cells both exhibited an obvious antibacterial action, which was partially neutralizated by LL-37 monoclonal antibody. In addition, APS also significantly elevated the phosphorylation of p38 MAPK and JNK and caused the degradation of IκBα. Specific inhibitors of p38 MAPK, JNK, or NF-κB obviously abolished APS-induced LL-37 synthesis and antibacterial activity, respectively. Taken together, our results confirmed the enhancement of APS on LL-37 induction and antibacterial action in respiratory epithelial cells, which may be attributed to activation of p38 MAPK/JNK and NF-κB pathways. Furthermore, these results also supported the clinical application of APS in the treatment of infectious diseases.

Study Information

Provider

pubmed

Year

2018

Date

2018-04-19T00:00:00.000Z

DOI

10.1002/ptr.6080

Citations

26

References

48