4.6 Article

Ddb1-Cullin4-Associated-Factor 1 in Macrophages Restricts the Staphylococcus aureus-Induced Osteomyelitis

期刊

JOURNAL OF INFLAMMATION RESEARCH
卷 14, 期 -, 页码 1667-1676

出版社

DOVE MEDICAL PRESS LTD
DOI: 10.2147/JIR.S307316

关键词

DCAF1; macrophages; Staphylococcus aureus; osteomyelitis; inflammation

资金

  1. Municipal Human Resources Development Program for Outstanding Leaders in Medical Disciplines in Shanghai [2018BR38]
  2. National Natural Science Foundation of China [81873993]

向作者/读者索取更多资源

Deficiency of DCAF1 in macrophages may exacerbate symptoms of osteomyelitis, including reduced bacterial load and bone loss.
Introduction: Ddb1-cullin4-associated-factor 1 (DCAF1) is known to regulate protein ubiquitination, while the roles of DCAF1 in osteomyelitis remain unknown. This study aims to investigate the effects of DCAF1 deficiency in macrophages on osteomyelitis and elucidate the molecular mechanism. Methods: Staphylococcus aureus-induced mouse model of osteomyelitis was established on the DCAF1(fl/fl)Lyz2(cre/+) and DCAF1(fl/fl)Lyz2(+/+) (control) mice. Flow cytometry was conducted to analyze the populations of adaptive and innate immune cells. Lipopolysaccharides (LPS)-induced bone marrow-derived macrophages (BMDMs) were established. qRT-PCR and immunoblot analysis were used to determine the levels of inflammation-related biomarkers. ELISA was used to determine the release of inflammatory cytokines including IL-1 beta, IL-6, and TNF. Results: The populations of immune cells in the bone marrow and spleen were not affected due to DCAF1 deficiency in macrophages. DCAF1 suppressed inflammatory cytokines in LPS-induced BMDMs. Additionally, DCAF1 deficiency in macrophages induced severe symptoms including less bacterial load in the femur, cortical bone loss, and reactive bone formation. Mechanistic study revealed that DCAF1 deficiency induced p38 hyperactivation. Discussion: DCAF1 in macrophages suppressed the Staphylococcus aureus-induced mouse model of osteomyelitis.

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