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1.
J Cell Mol Med ; 28(12): e18440, 2024 Jun.
Article in English | MEDLINE | ID: mdl-38890792

ABSTRACT

Hepatitis B virus (HBV) damages liver cells through abnormal immune responses. Mitochondrial metabolism is necessary for effector functions of white blood cells (WBCs). The aim was to investigate the altered counts and mitochondrial mass (MM) of WBCs by two novel indicators of mitochondrial mass, MM and percentage of low mitochondrial membrane potential, MMPlow%, due to chronic HBV infection. The counts of lymphocytes, neutrophils and monocytes in the HBV infection group were in decline, especially for lymphocyte (p = 0.034) and monocyte counts (p = 0.003). The degraded MM (p = 0.003) and MMPlow% (p = 0.002) of lymphocytes and MM (p = 0.005) of monocytes suggested mitochondrial dysfunction of WBCs. HBV DNA within WBCs showed an extensive effect on mitochondria metabolic potential of lymphocytes, neutrophils and monocytes indicated by MM; hepatitis B e antigen was associated with instant mitochondrial energy supply indicated by MMPlow% of neutrophils; hepatitis B surface antigen, antiviral therapy by nucleos(t)ide analogues and prolonged infection were also vital factors contributing to WBC alterations. Moreover, degraded neutrophils and monocytes could be used to monitor immune responses reflecting chronic liver fibrosis and inflammatory damage. In conclusion, MM combined with cell counts of WBCs could profoundly reflect WBC alterations for monitoring chronic HBV infection. Moreover, HBV DNA within WBCs may be a vital factor in injuring mitochondria metabolic potential.


Subject(s)
Hepatitis B virus , Hepatitis B, Chronic , Mitochondria , Humans , Hepatitis B, Chronic/virology , Hepatitis B, Chronic/pathology , Male , Female , Hepatitis B virus/pathogenicity , Adult , Mitochondria/metabolism , Middle Aged , Leukocyte Count , Leukocytes/metabolism , DNA, Viral/blood , Membrane Potential, Mitochondrial , Monocytes/metabolism , Monocytes/immunology , Monocytes/virology , Monocytes/pathology , Neutrophils/metabolism , Neutrophils/immunology
2.
Sci Rep ; 7(1): 16877, 2017 12 04.
Article in English | MEDLINE | ID: mdl-29203871

ABSTRACT

Corynebacterium pyruviciproducens (C. pyruviciproducens, CP), as a newly discovered immunomodulator, has been confirmed to have a stronger immunoregulation than Propionibacterium acnes (P. acnes) of the traditional immune adjuvant, by previous experiments with model antigen ovalbumin and sheep red blood cells. Here, it was designed to assess its ability to resist methicillin-resistant Staphylococcus aureus (MRSA), since MRSA as a vital gram positive pathogen is characterized by high morbidity and mortality. In this report, it was indicated that C. pyruviciproducens and its peptidoglycan (CP-PGN) could help to be against bloodstream infection of MRSA with raised survival rate, decreased bacteria load and alleviated systemic inflammation, and these effects of CP-PGN were more pronounced. However, the whole CP was inclined to prevent localized abdominal infection of MRSA from progressing to a systemic infection. And they showed the potential as a therapeutic drug alone or combined with vancomycin. The diversity of capacity of activating macrophages induced by CP and CP-PGN may result in distinct resistance to MRSA in different infection models. Furthermore, both CP and CP-PGN induced M1 macrophages. In conclusion, CP and its PGN could act as promising immune agents to treat and prevent MRSA infection.


Subject(s)
Corynebacterium/physiology , Macrophages/immunology , Peptidoglycan/therapeutic use , Staphylococcal Infections/drug therapy , Animals , Anti-Bacterial Agents/pharmacology , Anti-Bacterial Agents/therapeutic use , Cytokines/metabolism , Disease Models, Animal , Drug Therapy, Combination , Female , Kaplan-Meier Estimate , Macrophages/drug effects , Macrophages/metabolism , Methicillin-Resistant Staphylococcus aureus/drug effects , Mice , Mice, Inbred BALB C , Peptidoglycan/pharmacology , Phagocytosis , RAW 264.7 Cells , RNA Interference , RNA, Small Interfering/metabolism , Staphylococcal Infections/immunology , Staphylococcal Infections/microbiology , Staphylococcal Infections/mortality , Toll-Like Receptor 2/antagonists & inhibitors , Toll-Like Receptor 2/genetics , Toll-Like Receptor 2/metabolism , Vancomycin/pharmacology , Vancomycin/therapeutic use
3.
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi ; 27(11): 1217-9, 2011 Nov.
Article in Chinese | MEDLINE | ID: mdl-22078451

ABSTRACT

AIM: To detect the rabbit-derived polyclonal antibodies against extracellular protein segments of human glucocorticoid-inducible tumor necrosis factor receptors (anti-hGITR(aa27-165);PcAb) with regard to its capacity of linkage to natural GITR molecules and the function on CD4(+); T cells. METHODS: Human peripheral blood mononuclear cells (PBMCs) were isolated and cultured under stimulation; flow cytometry was applied to check the capacity of anti-hGITR(aa27-165);PcAb for linkage to natural GITR molecules on PBMCs; human CD4(+); T cells were isolated by immunological magnetic beads and (3);H-TdR incorporation tests were performed to observe improving-proliferation action of anti-hGITR(aa27-165);PcAb while CD4(+); T cells were cultured with or not with some cytokines. RESULTS: Anti-hGITR(aa27-165);PcAb was able to bind GITR molecules with natural conformation in a concentration-dependent way; furthermore, this PcAb could improve the reproduction of CD4(+); T cells. CONCLUSION: The rabbit-derived anti-hGITR(aa27-165);PcAb prepared in our laboratory is capable of linking to natural target molecules and possesses the activation function upon CD4(+); T cells, the further exploration should allow for its applications for diagnosis and treatment of relavent diseases.


Subject(s)
Antibodies/immunology , CD4-Positive T-Lymphocytes/metabolism , Glucocorticoid-Induced TNFR-Related Protein/immunology , Animals , Antibodies/administration & dosage , Antibodies/isolation & purification , CD4-Positive T-Lymphocytes/cytology , CD4-Positive T-Lymphocytes/drug effects , CD4-Positive T-Lymphocytes/immunology , Cell Proliferation/drug effects , Flow Cytometry , Glucocorticoid-Induced TNFR-Related Protein/isolation & purification , Glucocorticoid-Induced TNFR-Related Protein/metabolism , Humans , Rabbits
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