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Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits
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Serum amyloid A3 is required for normal weight and immunometabolic function in mice
Jennifer L Ather1, Matthew E Poynter1
1Vermont Lung Center, Division of Pulmonary Disease and Critical Care, Department of Medicine, University of Vermont, Burlington, VT, United States of America.
Plos One
|February 2, 2018
Summary
Serum amyloid A3 (SAA3) deficiency in mice leads to obesity and metabolic dysfunction. Lack of SAA3 also impairs innate immune development and alters immune cell responses, highlighting its role in homeostasis.
Area of Science:
- Immunology
- Metabolic disease research
- Molecular biology
Background:
- Serum amyloid A (SAA) is an acute-phase protein implicated in inflammation.
- Previous studies on SAA function in immunity yielded conflicting results.
- The specific role of endogenous SAA3 in immune-mediated diseases remains unclear.
Purpose of the Study:
- To investigate the contribution of SAA3 to immune-mediated disease using a knockout mouse model.
- To elucidate the role of endogenous SAA3 in metabolic and immune homeostasis.
Main Methods:
- Generation and analysis of SAA3 knockout (SAA3-/-) mice.
- Assessment of metabolic parameters including weight gain, adipose tissue deposition, and hepatic steatosis.
- Characterization of immune cell phenotype and cytokine production (IL-1β, IL-6, IL-23, TNFα) from bone marrow-derived dendritic cells (BMDCs).
- Evaluation of endotoxin tolerance and retinoic acid response in BMDCs.
Main Results:
- SAA3-/- mice exhibited adult-onset obesity, increased visceral fat, and hepatic steatosis compared to wild-type littermates.
- Leukocytes in adipose tissue of SAA3-/- mice displayed a pro-inflammatory phenotype.
- BMDCs from SAA3-/- mice secreted higher levels of pro-inflammatory cytokines (IL-1β, IL-6, IL-23, TNFα) upon LPS stimulation.
- BMDCs lacking SAA3 showed impaired endotoxin tolerance and reduced response to retinoic acid.
Conclusions:
- Endogenous SAA3 plays a crucial role in modulating metabolic homeostasis, preventing obesity and hepatic steatosis.
- SAA3 is essential for proper innate immune development and function, including regulating immune cell activation and cytokine production.
- Deficiency in SAA3 leads to dysregulated immune responses and impaired tolerance mechanisms, impacting overall immune homeostasis.
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