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Metabolic reprogramming induced by CRP deficiency or human CRP transgenic in influenza-infected mice
Junhao Luo1, Zhuohan Zhang1, Song Zhao1
1NHC Key Laboratory of Biosafety, NHC Key Laboratory of Medical Virology and Viral Diseases, Chinese National Influenza Center, National Institute for Viral Disease Control and Prevention, Chinese Center for Disease Control and Prevention, Beijing, China.
Introduction:
C-reactive protein (CRP) plays dual roles in influenza infection, contributing to immune protection but potentially exacerbating severe outcomes.
Methods:
Here, we investigated CRP-driven metabolic reprogramming in influenza A (H1N1)-infected mice. Metabolomic profiling was performed on lung tissues from wild-type (WT), CRP-deficient (KO), and human CRP transgenic (KI) mice. Correlations were analyzed between metabolites and immune checkpoint LAIR-1, viral load, and serum IL-17/IFN-γ levels.
Results:
In WT mice, H1N1 infection triggered metabolic resource redistribution, dynamic inflammatory regulation, antioxidant responses, and immune cell activation. Conversely, KI mice exhibited impaired PUFA/PLA2-mediated inflammatory control. KO mice showed hypoimmunity with premature tryptophan-kynurenine shift, glutathione and proline synthesis defects, etc. Oxidized glutathione and kynurenine correlated significantly with immune checkpoint LAIR-1, or viral TCID50.
Discussion:
These findings demonstrate that CRP deficiency or human CRP transgenic induces distinct metabolic reprogramming post-infection. Metabolic alterations, particularly in energy redistribution, antioxidant defense, and immune-related pathways, may serve as biomarkers for disease progression in severe influenza. The results highlighted CRP's role in balancing metabolic and immune homeostasis during viral infection.
