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Complement expression in common carp (Cyprinus carpio L.) during infection with Ichthyophthirius multifiliis
Santiago F Gonzalez1, Kurt Buchmann, Michael E Nielsen
1Department of Veterinary Pathobiology, Laboratory of Fish Diseases, The Royal Veterinary and Agricultural University, Stigbøjlen 7, DK-1870 Frederiksberg C, Denmark. xanti@usc.es
This study developed a real-time PCR assay to measure carp's complement response to Ichthyophthirius multifiliis infection. The assay revealed significant changes in complement gene expression, particularly Bf/C2-A, highlighting its role in carp immunity.
Area of Science:
- Immunology
- Aquatic Animal Health
- Molecular Biology
Background:
- Ichthyophthirius multifiliis (white spot disease) is a major ectoparasite affecting carp health.
- The complement system plays a crucial role in innate immunity against parasitic infections.
- Understanding the complement response in carp is vital for disease management.
Purpose of the Study:
- To develop a real-time PCR assay for analyzing the complement response in carp infected with I. multifiliis.
- To investigate the expression patterns of key complement genes across different tissues and time points post-infection.
Main Methods:
- Designed specific primers for carp complement genes (C1r/s, C3, C4, C5, factor I, Bf/C2-A, MBL, MASP).
- Analyzed gene expression using real-time PCR on RNA from carp skin, liver, and blood.
- Samples were collected at 3, 12, 24, 36, and 48 hours post-infection (pi).
Main Results:
- Significant up-regulation of factor B/C2-A (Bf/C2-A) in skin, blood, and liver at later time points (24-48 h pi).
- Intermediate down-regulation of MBL-associated serine protease (MASP) in skin and liver.
- Complement factor C3 showed significant up-regulation in the liver at 24 h pi.
Conclusions:
- Carp complement gene expression is significantly stimulated by I. multifiliis infection.
- Early and dramatic up-regulation of Bf/C2-A suggests its role as an acute-phase reactant in carp skin.
- Fish skin is an important extra-hepatic site for complement molecule expression and regulation; leukocytes also contribute.
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