厦门大学:食源性肥胖如何影响皮肤的抗菌防御
创作:szx 审核:szx 01月28日
  • DIO减少皮肤前脂肪细胞,抑制反应性脂肪生成及抗菌肽表达,增加小鼠皮肤对金黄色葡萄球菌感染的易感性;
  • DIO抑制小鼠皮肤成纤维细胞(dFB)分化为脂肪细胞及表达抗菌肽的能力;
  • 成熟脂肪细胞失去了产生抗菌肽的能力,且可通过TGF-β-TGFBR-SMAD2/3通路抑制dFB的分化及抗菌肽表达;
  • 在体外培养的脂肪细胞祖细胞中及小鼠体内,TGF-β受体抑制剂或PPAR-γ激动剂可逆转上述抑制作用,并恢复小鼠对金黄色葡萄球菌皮肤感染的抗性。
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感染是肥胖的主要并发症之一,但肥胖导致抗菌防御损伤的机制尚未明确。厦门大学的张凌娟团队与国外研究团队合作在Science Translational Medicine上发表的一项最新研究,在食源性肥胖(DIO)小鼠中发现,DIO可促进成熟脂肪细胞的扩增,后者在失去产生抗菌肽能力的同时,可分泌TGF-β以抑制皮肤成纤维细胞向脂肪细胞的分化及抗菌肽的产生,从而损伤小鼠皮肤对致病菌感染的抗性。
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Diet-induced obesity promotes infection by impairment of the innate antimicrobial defense function of dermal adipocyte progenitors

饮食诱导的肥胖通过损伤皮肤脂肪细胞祖细胞的先天性抗菌防御功能以促进感染

10.1126/scitranslmed.abb5280

01-20, Article

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Infections are a major complication of obesity, but the mechanisms responsible for impaired defense against microbes are not well understood. Here, we found that adipocyte progenitors were lost from the dermis during diet-induced obesity (DIO) in humans and mice. The loss of adipogenic fibroblasts from mice resulted in less antimicrobial peptide production and greatly increased susceptibility to Staphylococcus aureus infection. The decrease in adipocyte progenitors in DIO mice was explained by expression of transforming growth factor–β (TGFβ) by mature adipocytes that then inhibited adipocyte progenitors and the production of cathelicidin in vitro. Administration of a TGFβ receptor inhibitor or a peroxisome proliferator–activated receptor–γ agonist reversed this inhibition in both cultured adipocyte progenitors and in mice and subsequently restored the capacity of obese mice to defend against S. aureus skin infection. Together, these results explain how obesity promotes dysfunction of the antimicrobial function of reactive dermal adipogenesis and identifies potential therapeutic targets to manage skin infection associated with obesity.

First Authors:
Lingjuan Zhang

Correspondence Authors:
Lingjuan Zhang,Richard L Gallo

All Authors:
Lingjuan Zhang,Christian F Guerrero-Juarez,Stella X Chen,Xiaowei Zhang,Meimei Yin,Fengwu Li,Shuai Wu,Joyce Chen,Min Li,Yingzi Liu,Shang I B Jiang,Tissa Hata,Maksim V Plikus,Richard L Gallo

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