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Evaluation of the Interplay Between the Complement Protein C1q and Hyaluronic Acid in Promoting Cell Adhesion
Published on: June 15, 2019
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Complement component C1q plays a critical role in VLRA/VLRC-mediated immune response
Jun Li1, Qinghua Ma2, Huaixiu Liu2
1College of Life Science, Liaoning Normal University, Dalian, 116029, China; Lamprey Research Center, Liaoning Normal University, Dalian, 116029, China; Collaborative Innovation Center of Seafood Deep Processing, Dalian Polytechnic University, Dalian, 116034, China; Liaoning Key Laboratory of Aquatic Animal Infectious Diseases Control and Prevention, Liaoning Institute of Freshwater Fisheries Sciences, Liaoyang, 111000, China.
Developmental and Comparative Immunology
|May 25, 2020
Summary
Lamprey complement component C1q (LC1q) is crucial for immune defense, particularly in the VLRA/VLRC pathway. Knockdown of LC1q significantly reduces survival rates against bacterial infections, highlighting its essential role in lamprey immunity.
Area of Science:
- Immunology
- Marine Biology
- Evolutionary Biology
Background:
- Lamprey complement component C1q (LC1q) functions as a lectin, activating complement component C3 (LC3) via the lectin pathway.
- LC1q may also interact with variable lymphocyte receptor B (VLRB) and antigens to activate LC3, leading to cytolysis.
Purpose of the Study:
- To investigate the role of LC1q in the lamprey immune response, specifically in VLRA/VLRC-mediated immunity.
- To determine the impact of LC1q on lamprey survival following bacterial infection.
Main Methods:
- Isolation and identification of bacterial pathogens from infected Lampetra morii using 16s rRNA sequencing.
- Immune stimulation experiments using Aeromonas hydrophila and analysis of LC1q expression via Q-PCR and immunofluorescence.
- Morpholino-mediated knockdown of LC1q in lamprey larvae (LC1q MO) to assess its role in embryonic development and immune response.
- Comparative analysis of gene expression profiles and immunohistochemical examination of LC1q-deficient and control lamprey larvae.
Main Results:
- Aeromonas hydrophila was identified as a lethal pathogen in L. morii larvae.
- Exposure to A. hydrophila significantly upregulated LC1q RNA and protein expression.
- LC1q knockdown (LC1q MO) resulted in a drastically reduced median lethal time (LT50) after pathogen exposure (2 days vs. 5 days for controls).
- LC1q deficiency specifically affected genes and proteins associated with VLRA and VLRC, but not VLRB.
Conclusions:
- LC1q plays a critical role in the innate immune response of lamprey, particularly in the VLRA/VLRC-mediated pathway.
- LC1q is essential for lamprey survival against bacterial infections and plays a role in embryonic development.
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