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Decreased phagocytic capacity accompanied by autophagy activation in blood monocytes of tuberculosis patients
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  • Xianyan Zhang,
  • Xuexuan Zhang,
  • Jialong Xu,
  • Xiaoxin Huang,
  • Ying Wu,
  • Tianming Liu,
  • Ying E Wu
Xianyan Zhang
The First Affiliated Hospital of Shantou University Medical College

Corresponding Author:[email protected]

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Xuexuan Zhang
The First Affiliated Hospital of Shantou University Medical College
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Jialong Xu
The First Affiliated Hospital of Shantou University Medical College
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Xiaoxin Huang
The First Affiliated Hospital of Shantou University Medical College
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Ying Wu
The First Affiliated Hospital of Shantou University Medical College
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Tianming Liu
The First Affiliated Hospital of Shantou University Medical College
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Ying E Wu
The First Affiliated Hospital of Shantou University Medical College
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Abstract

Developing host-directed therapies against resistant tuberculosis requires a better understanding of the changes in the innate immune response of the peripheral blood monocytes. Here, we investigated the phagocytic capacity of blood phagocytes, the changing of the mammalian target of rapamycin (mTOR) pathway and autophagy process of circulating monocytes in untreated tuberculosis patients. Phagocytic capacity of blood phagocytes and the expression of key regulators of the mTOR pathway were analysed using flow cytometry. We detected the mRNA and protein expression of autophagy proteins using RT-PCR and capillary western blotting. Compared with healthy controls, the increase of monocytes phagocytizing E.coli was lower in tuberculosis patients after 37°C activation (15.46% vs. 23.31%); The percentages of Rheb+ and mTOR+ Raptor+ circulating monocytes were higher, while that of AMPK+ monocytes were lower. Although ATG5 and ATG12 mRNA expression increased, the protein complex expression was decreased in the monocytes of tuberculosis patients. Beclin-1 and ULK1 Ser 757 levels were increased at both transcriptional and protein levels; LC3 II protein level also was higher. Our current study suggests a decrease in the phagocytic capacity of circulating monocytes, accompanied by autophagy activation in active tuberculosis patients.