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Inflammation

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Exogenous Hydrogen Sulfide Regulates Mycoplasma pneumoniae Lipid-Associated Membrane Proteins to Induce Expression of Heme Oxygenase-1 and Proinflammatory Cytokines

  • Xinnian Hu
  • Wuwei Zeng
  • Xiaoxing You
  • Weiyan Ding
  • Peng Liu
  • Liesong Chen
  • Yanhua Zeng
  • Cuiming ZhuEmail author
Original Article
  • 39 Downloads

Abstract

This study was designed to investigate the effect of exogenous hydrogen sulfide (H2S) on the secretion of Heme oxygenase (HO-1) and proinflammatory cytokines in human mononuclear cell line THP-1 stimulated by lipid-associated membrane proteins (LAMPs) prepared from Mycoplasma pneumoniae (M. pneumoniae) and explore its regulatory mechanism. Cultured cells were stimulated with M. pneumoniae LAMPs after pretreatment with H2S to analyze the production of proinflammatory cytokines and HO-1 by enzyme-linked immunosorbent assay (ELISA) and Western blot. The results showed that THP-1 cells, which were stimulated by LAMPs after pretreatment with H2S, had decreased production of interleukin-6 (IL-6) and interleukin-8 (IL-8) by inhibiting the mitogen-activated protein kinases (MAPKs)/nuclear factor-kappa B (NF-κB) signaling pathway and increased expression of HO-1 by activating the nuclear factor E2–related factor 2 (Nrf2) signaling pathway. Our results indicate that H2S may play an important role in attenuating inflammation induced by M. pneumoniae LAMPs due to its ability to decrease the production of IL-6 and IL-8 and increase the expression of the HO-1. These findings support further studies for possible clinical applications.

KEY WORDS

mycoplasma pneumoniae hydrogen sulfide (H2S) lipid-associated membrane proteins (LAMPs) proinflammatory cytokines Heme oxygenase-1(HO-1) 

Abbreviations

H2S

Hydrogen sulfide

HO-1

Heme oxygenase-1

HP-1

Human monocytic cell line

LAMPs

Lipid associated membrane proteins

MAPKs

Mitogen-activated protein kinase

NF-κB

Nuclear factor-kappa B

CABP

Community-acquired bacterial pneumonias

TLRs

Toll-like receptors

IL-1R

Interleukin-1R

MyD88

Myeloid differentiation factor 88

IRAK

Interleukin-1 receptor–associated kinase

TRAF6

Tumor necrosis factor receptor–associated factor 6

AP-1

Activating protein 1

IL-1β

Interleukin-1β

IL-6

Interleukin-6

IL-8

Interleukin-8

TNF-α

Tumor necrosis factor

ROS

Reactive oxygen species

Nrf2

Nuclear factor E2–related factor 2

COX-2

Cyclooxygenase-2

iNOS

Inducible nitric oxide synthase

NO

Nitric oxide

PGE2

Prostaglandin E2

CO

Carbon monoxide

RPMI

Roswell Park Memorial Institute

FBS

Fetal bovine serum

TBS

Tris-buffered saline

PBS

Phosphate-buffered saline

PVDF

Polyvinylidene difluoride

TBST

Tris-buffered saline with Tween

Notes

Acknowledgments

We thank Xiaoxing You for providing the exogenous hydrogen sulfide. We also thank Peng Liu for modifying the manuscript.

Authors’ Contributions

All authors have approved this manuscript

Funding Information

This work was supported by the National Natural Science Foundation of China (No. 81441065, No. 31970177); Natural Science Foundation of Hunan Province, China (Grant No. 2019JJ40253); Key Fund Project of Hunan Provincial Department of Education (Grant No. 18A234); and Scientific Research Foundation for the Returned Overseas Chinese Scholars, University of South China (Grant No. 2017XQD25).

Compliance with Ethical Standards

Competing Interests

The authors declare that they have no competing interests.

Ethics Approval

Study procedures were approved by the University of South China.

Supplementary material

10753_2019_1170_MOESM1_ESM.docx (39 kb)
ESM 1 (DOCX 39 kb)

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Copyright information

© Springer Science+Business Media, LLC, part of Springer Nature 2020

Authors and Affiliations

  1. 1.Institute of Pathogenic Biology, Hengyang Medical College, Hunan Provincial Key Laboratory for Special Pathogens Prevention and Control, Hunan Province Cooperative Innovation Center for Molecular Target New Drug StudyUniversity of South ChinaHengyangChina
  2. 2.Qingyuan Maternal and Child Health HospitalQingyuanChina

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