Role of the ceramide-CD300f interaction in gram-negative bacterial skin infections.
Role of the ceramide-CD300f interaction in gram-negative bacterial skin infections.
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神经酰胺-CD300f 相互作用在革兰氏阴性细菌皮肤感染中的作用。
DOI：
10.1016/j.jid.2017.11.025
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发表时间：
2018
期刊：
影响因子：
--
通讯作者：
Kitaura J.
中科院分区：
文献类型：
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作者：
Maehara A;Kaitani A;Izawa K;Shiba E;Nagamine M;Takamori A;Isobe M;Uchida S;Uchida K;Ando T;Keiko M;Nakano N;Voehringer D;Roers A;Shimizu T;Ogawa H;Okumura K;Kitamura T;Kitaura J.
急性细菌性皮肤和皮肤结构感染（ABSSSIs），包括蜂窝织炎和丹毒，伤口感染和脓肿，是医疗保健中最常见的感染。革兰氏阳性微生物在引起ABSSSI的多种病原体中占主导地位，但革兰氏阴性细菌感染也是免疫功能低下患者的主要临床问题。尽管抗生素是标准治疗的标准，但耐药性细菌的流行促使我们开发针对ABSSSI的不同疗法（科隆纳，2003，Itani和Shorr，2014，Modlin，2012，Rittirsch等人，CD 300 f，也称为白细胞单免疫球蛋白样受体3（LMIR 3）或CMRF-35样分子-1（CLM-1），是一种抑制性受体，主要在骨髓细胞中表达，包括肥大细胞和嗜中性粒细胞（Chung et al.，2003，Izawa等人，2007年）。小鼠CD 300 f识别组织肥大细胞周围的细胞外神经酰胺，从而抑制IgE介导的过敏反应或三磷酸腺苷介导的结肠炎症（Izawa等人，2012年，Matsukawa等人，2016年）。此外，神经酰胺-CD 300 f结合抑制小鼠中脂多糖（LPS）诱导的皮肤水肿和中性粒细胞积聚（Shiba等人，2017年）。相反，破坏神经酰胺-CD 300 f相互作用通过促进嗜中性粒细胞向感染部位的募集来防止盲肠结扎和穿孔诱导的脓毒性腹膜炎，所述感染部位有效地吞噬和杀死大肠杆菌（Izawa等人，2017年）。然而，CD 300 f是否调节人肥大细胞和中性粒细胞对E.大肠杆菌或LPS和革兰氏阴性细菌皮肤感染的小鼠和人类仍然难以捉摸。
Acute bacterial skin and skin structure infections (ABSSSIs), including cellulitis and erysipelas, wound infections, and abscesses, are the most common infections in health care. Gram-positive organisms predominate among a variety of pathogens that cause ABSSSI, but Gram-negative bacterial infections are also a major clinical problem for immunocompromised patients. Although antibiotics are the criterion standard therapy, the prevalence of antibiotic-resistant bacteria prompts us to develop different therapies for ABSSSI (Colonna, 2003, Itani and Shorr, 2014, Modlin, 2012, Rittirsch et al., 2008).CD300f, also called leukocyte mono-immunoglobulin–like receptor 3 (LMIR3) or CMRF-35–like molecule-1 (CLM-1), is an inhibitory receptor that is mainly expressed in myeloid cells, including mast cells and neutrophils (Chung et al., 2003, Izawa et al., 2007). Mouse CD300f recognizes extracellular ceramide in the surroundings of tissue mast cells, thereby suppressing IgE-mediated allergic responses or adenosine triphosphate-mediated colonic inflammation (Izawa et al., 2012, Matsukawa et al., 2016). In addition, the ceramide-CD300f binding inhibits lipopolysaccharide (LPS)-induced skin edema and neutrophil accumulation in mice (Shiba et al., 2017). Conversely, disrupting the ceramide-CD300f interaction prevents cecal ligation and puncture-induced septic peritonitis by promoting the recruitment of neutrophils to sites of infection that efficiently engulf and kill Escherichia coli (Izawa et al., 2017). However, whether CD300f regulates human mast cell and neutrophil activation in response to E. coli or LPS and Gram-negative bacterial skin infections in mice and humans remains elusive.