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HDAC6 Promotes Host Defense Against Chlamydial Lung Infections by Regulating M2-Th2 Responses.

Jinxi Yu1, Shuaini Yang1, Xiaoyu Zha1

  • 1Key Laboratory of Immune Microenvironment and Disease of the Ministry of Education, Tianjin Institute of Immunology, Department of Immunology, Tianjin Medical University, Tianjin 300070, China.

International Journal of Molecular Sciences
|April 14, 2026
PubMed
Summary

Histone deacetylase 6 (HDAC6) deficiency worsens Chlamydia muridarum respiratory infections by promoting harmful Th2 immune responses and M2 macrophage polarization. HDAC6 is crucial for controlling these immune responses during infection.

Keywords:
Chlamydia muridarumHDAC6T cell differentiationTh2-M2 responsesmacrophage polarizationrespiratory infection

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Area of Science:

  • Immunology
  • Molecular Biology
  • Microbiology

Background:

  • Histone deacetylase 6 (HDAC6) is involved in immune responses, but its role in Chlamydia muridarum infection is unclear.
  • Chlamydia muridarum causes respiratory infections with significant health implications.

Purpose of the Study:

  • To investigate the function and mechanism of HDAC6 during C. muridarum respiratory infection.
  • To determine the impact of HDAC6 deficiency on host immune responses and disease progression.

Main Methods:

  • Comparative analysis of wild-type and HDAC6-deficient mice infected with C. muridarum.
  • Assessment of pulmonary inflammation, bacterial clearance, and immune cell populations (Th2, M1, M2 macrophages).
  • In vitro studies using bone marrow-derived macrophages (BMDMs) and co-culture experiments.

Main Results:

  • HDAC6 deficiency exacerbated C. muridarum respiratory infection, leading to increased weight loss, inflammation, and reduced bacterial clearance.
  • HDAC6-deficient mice showed elevated Th2 responses (Stat6, Gata3, IL-4) and enhanced M2 macrophage polarization (CD206, Arg-1).
  • In vitro, HDAC6-deficient BMDMs promoted M2 polarization and supported Th2 differentiation.

Conclusions:

  • HDAC6 plays a critical role in regulating Th2-M2 immune responses against C. muridarum respiratory infection.
  • Targeting HDAC6 may offer a novel therapeutic strategy for treating chlamydial respiratory infections.