4.6 Article

A Shrimp C-type Lectin Inhibits Proliferation of the Hemolymph Microbiota by Maintaining the Expression of Antimicrobial Peptides

期刊

JOURNAL OF BIOLOGICAL CHEMISTRY
卷 289, 期 17, 页码 11779-11790

出版社

AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M114.552307

关键词

Antimicrobial Peptides; Invertebrates; Lectin; Pattern Recognition Receptor; RNA Interference (RNAi); C-type Lectin; Hemolymph Microbiota; Shrimp

资金

  1. National Natural Science Foundation of China [31130056, 31302217]
  2. Provincial Natural Science Foundation of Shandong, China [ZR2011CM014]
  3. Ph.D. Program Foundation of the Ministry of Education of China [20110131130003]
  4. China Postdoctoral Science Foundation [2013M540553]
  5. National Science Foundation [IOS-1050518, IOB-0618409, IOS-0822257]
  6. National Institutes of Health [5R01GM070589-06]

向作者/读者索取更多资源

Background: The hemolymph of healthy shrimp contains low albeit stable numbers of bacteria. Results: Knockdown of C-type lectin MjHeCL led to suppressed expression of antimicrobial peptides, bacterial proliferation, and shrimp death. Conclusion: MjHeCL protects shrimp by inhibiting the proliferation of hemolymph microbiota. Significance: This study demonstrated a novel role for soluble C-type lectins in antibacterial response. Some aquatic invertebrates such as shrimp contain low albeit stable numbers of bacteria in the circulating hemolymph. The proliferation of this hemolymph microbiota in such a nutrient-rich environment is tightly controlled in healthy animals, but the mechanisms responsible had remained elusive. In the present study, we report a C-type lectin (MjHeCL) from the kuruma shrimp (Marsupenaeus japonicus) that participates in restraining the hemolymph microbiota. Although the expression of MjHeCL did not seem to be modulated by bacterial challenge, the down-regulation of its expression by RNA interference led to proliferation of the hemolymph microbiota, ultimately resulting in shrimp death. This phenotype was rescued by the injection of recombinant MjHeCL, which restored the healthy status of the knockdown shrimp. A mechanistic analysis revealed that MjHeCL inhibited bacterial proliferation by modulating the expression of antimicrobial peptides. The key function of MjHeCL in the shrimp immune homeostasis might be related to its broader recognition spectrum of the hemolymph microbiota components than other lectins. Our study demonstrates the role of MjHeCL in maintaining the healthy status of shrimp and provides new insight into the biological significance of C-type lectins, a diversified and abundant lectin family in invertebrate species.

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