| Babesia microti is a blood protozoan that parasitizes in the red blood cells of mouse,humans or other mammals,and can cause zoonotic diseases.Host infected with B.microti develops a series of clinical symptoms such as fever,anemia,and hemoglobinuria,causing damage to the liver and kidneys.If the person with low immunity suffers from B.microti,it can induce many complications and even cause death.The B.microti are widely distributed,mainly in the Americas,Europe,Asia and Africa.China is also one of the major countries in which the disease occurs,posing a serious threat to the development of animal husbandry and human health,and is of great significance for its research.This study found that mouse were infected with B.microti,and the liver tissue was severely damaged,with obvious swelling,lipid droplets deposited in the cytoplasm,and morphological changes in cell appearance and organelles such as mitochondria.In order to further explore the molecular mechanism of liver damage caused by B.microti,we used DIA quantitative proteomics to study the changes of protein expression and phosphorylation in liver tissues from infection stage to recovery stage after infection by B.microti,and to explore the regularity and function of protein changes in liver during injury and repair.This will lay a foundation for studying the damage caused by B.microti to the host and the mechanism of body repair,and provide new ideas and methods for the more effective diagnosis and treatment of this disease.The results of mass spectrometry identification of global proteins in the liver tissues of the infected B.microti showed that a total of 2559 proteins were identified at 0 d,5 d,8 d,11 d and 19 d,among which 1138 proteins were identified in all five periods,and 618 proteins showed changes in expression.Further bioinformatics analysis of these proteins revealed that the expression levels of some key proteins in the peroxisome and PPAR signaling pathway changed at different infection stages,among which acyl-CoA-binding protein,peroxisomal carnitine transferase,peroxisomal bifunctional enzyme,3-ketoacyl-CoA thiolase A,peroxisomal acyl-coenzyme A oxidase and malonyl-CoA decarboxylase play important roles in regulating lipid metabolism.Changes in the expression of these proteins can lead to abnormal lipid metabolism and lipid deposition in the liver.On the other hand,the expression of proteins such as fatty acid synthase,acetyl-CoA carboxylase and acyl-CoA thioesterase,which are related to fatty acid synthesis,were down-regulated at 11 d and 19 d,and synthesis of less fatty acids can improve the lipid deposition.We also found increased expression of various immune-related proteins,such as proteasome subunit ?-10,proteasome subunit ?-9,interferon-inducible GTPase 1,and cathepsin C,which play an important role in the immune response of the liver against infection.The infestation of B.microti also changed the phosphorylation of various proteins in liver.A total of 10890 phosphorylated peptides were identified on the 0 d,5 d,8 d,11 d and 19 d of infection,1138 peptides were identified in all five periods,among which 3767 peptides had changes in the degree of phosphorylation,corresponding to 1484 phosphorylated proteins.A series of bioinformatics analysis revealed changes in the degree of phosphorylation of some proteins in the insulin signaling pathway,AMPK signaling pathway,and mTOR signaling pathway,such as the degree of phosphorylation of AMP-activated protein kinases,hormone-sensitive lipases,acetyl-CoA carboxylase 1 and acetyl-CoA carboxylase 2 changes,affecting lipid metabolism in the liver.Receptor-type tyrosine-protein phosphatase C increases phosphorylation and can improves the body's immunity.Changes in the phosphorylation of insulin receptor substrate 1,mitogen-activated protein kinase 2 and serine/threonine-protein kinase mTOR,affect the growth and development of the body and cause damage to liver tissues. |
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