HDAC5 promotes Mycoplasma pneumoniae-induced inflammation in macrophages through NF-κB activation

Excessive inflammation is fundamental in the pathophysiology of Mycoplasma pneumoniae (MP)-induced respiratory infection in children. Histone deacetylase 5 (HDAC5) is involved in the regulation of inflammation, however, whether it associates with immunity against MP infection is not determined. We r...

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Bibliographic Details
Published in:Life sciences (1973) 2019-03, Vol.221, p.13-19
Main Authors: Zhao, Yuehua, Ma, Guorui, Yang, Xingge
Format: Article
Language:English
Subjects:
Cell activation
Children
Cytokines
Depletion
HDAC5
Histone deacetylase
Immunity
Infections
Inflammation
Inflammatory response
Leukocytes (mononuclear)
Macrophage
Macrophages
Mycoplasma pneumoniae
NF-κB
NF-κB protein
Peripheral blood mononuclear cells
Peritoneum
Pharmacology
Pneumonia
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Summary:Excessive inflammation is fundamental in the pathophysiology of Mycoplasma pneumoniae (MP)-induced respiratory infection in children. Histone deacetylase 5 (HDAC5) is involved in the regulation of inflammation, however, whether it associates with immunity against MP infection is not determined. We report here that HDAC5 expression is decreased in peripheral blood mononuclear cells (PBMCs) from Mycoplasma pneumoniae pneumonia (MPP) children as well as in MP-infected peritoneal and THP-1 macrophages. Functionally, HDAC5 overexpression promotes and its depletion inhibits MP-induced proinflammatory cytokine production in THP-1 macrophages. Mechanistically, HDAC5 modulates NF-κB activation in MP-infected THP-1 macrophages, and moreover, inhibition of NF-κB activity via pharmacological inhibitor Bay 11-7082 attenuates the promotive effect of HDAC5 on MP-induced proinflammatory cytokine production in THP-1 macrophages, hence suggesting that HDAC5 promotes MP-induced inflammatory response in macrophages through NF-κB activation. Together, this study reveals a novel function of HDAC5 in promoting MP-induced inflammation and implies the possible clinical significance in controlling inflammation that underlies MMP pathophysiology.
ISSN:0024-3205
1879-0631
DOI:10.1016/j.lfs.2019.02.004