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Published on: September 9, 2015
SIGIRR deficiency aggravates Mycobacterium marinum induced mortality and hepatic apoptosis in zebrafish
Ting Yu1, Haoxiang Chen1, Peipei Yu1
1Engineering Research Center of Ecology and Agricultural Use of Wetland, Ministry of Education, Yangtze University, Jingzhou, 434024, China.
Abstract:
SIGIRR is a cell membrane protein in the TIR superfamily, widely expressed in tissues and organs. It has a unique structure and acts as a negative regulator of downstream inflammatory signaling pathways. Danio rerio (zebrafish) were experimentally infected with Mycobacterium marinum to investigate the role of SIGIRR in modulating host immune responses to bacterial infection. Following intraperitoneal injection of M. marinum, SIGIRR gene-deficient zebrafish exhibited an earlier onset of mortality compared to wild type, with the first death occurring sooner and all individuals dying by the fifth week. Wild-type zebrafish began dying in week two and all died by week seven, while SIGIRR-/- mutants died significantly faster. A zebrafish liver cell model was established, and apoptosis was measured by flow cytometry 24 h post-infection. Apoptosis was 16 % in wild-type cells and 25 % in SIGIRR-/- mutant cells. The addition of SIGIRR polyclonal antibody to wild-type liver cells increased apoptosis to 18 % after M. marinum challenge. Significant differences were observed among the three groups. These results show that SIGIRR critically suppresses the inflammatory response during bacterial infection.
Insights
SIGIRR (Single Ig IL-1-related receptor) deficiency accelerates mortality in zebrafish infected with Mycobacterium marinum. This suggests SIGIRR plays a crucial role in suppressing inflammatory responses during bacterial infections.
Area of Science:
- Immunology
- Genetics
- Cell Biology
Background:
- Single Ig IL-1-related receptor (SIGIRR) is a cell membrane protein regulating inflammatory signaling.
- SIGIRR is widely expressed and functions as a negative regulator of inflammatory pathways.
Purpose of the Study:
- To investigate the role of SIGIRR in modulating host immune responses to bacterial infection using a Mycobacterium marinum zebrafish model.
- To determine the impact of SIGIRR deficiency on host survival and apoptosis during infection.
Main Methods:
- Zebrafish (Danio rerio) were infected with Mycobacterium marinum.
- SIGIRR gene-deficient and wild-type zebrafish were compared for mortality rates.
- Apoptosis was measured in liver cell models using flow cytometry.
Main Results:
- SIGIRR-deficient zebrafish exhibited earlier mortality compared to wild-type controls.
- Apoptosis rates were significantly higher in SIGIRR-deficient liver cells post-infection.
- Blocking SIGIRR function in wild-type cells increased apoptosis, indicating SIGIRR's suppressive role.
Conclusions:
- SIGIRR critically suppresses inflammatory responses during bacterial infection.
- SIGIRR deficiency leads to increased susceptibility and mortality in zebrafish infected with M. marinum.
- SIGIRR is a key negative regulator of the host immune response to bacterial pathogens.
