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表面活性蛋白D通过促进肠道定植影响腹部脓毒症期间的死亡率。

Surfactant Protein D Influences Mortality During Abdominal Sepsis by Facilitating Colonization in the Gut.

作者信息

Varon Jack, Arciniegas Rubio Antonio, Amador-Munoz Diana, Corcoran Alexis, DeCorte Joseph A, Isabelle Colleen, Pinilla Vera Miguel, Walker Katherine, Brown Luke, Cernadas Manuela, Bry Lynn, Yang Haopu, Kitsios Georgios D, McVerry Bryan J, Morris Alison, Lee Hyunwook, Howrylak Judie, Englert Joshua A, Baron Rebecca M

机构信息

Division of Pulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, MA.

Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA.

出版信息

Crit Care Explor. 2022 May 18;4(5):e0699. doi: 10.1097/CCE.0000000000000699. eCollection 2022 May.

Abstract

UNLABELLED

Determine the role of surfactant protein D (SPD) in sepsis.

DESIGN

Murine in vivo study.

SETTING

Research laboratory at an academic medical center.

PATIENTS

SPD knockout (SPD) and wild-type (SPD) mice.

INTERVENTIONS

SPD and SPD mice were subjected to cecal ligation and puncture (CLP). After CLP, bacteremia was assessed in both groups. Cecal contents from both groups were cultured to assess for colonization by . To control for parental effects on the microbiome, SPD and SPD mice were bred from heterozygous parents, and levels of in their ceca were measured. Gut segments were harvested from mice, and SPD protein expression was measured by Western blot. SPD mice were gavaged with green fluorescent protein, expressing and recombinant SPD (rSPD).

MEASUREMENTS AND MAIN RESULTS

SPD mice had decreased mortality and decreased bacteremia compared with SPD mice following CLP. At baseline, SPD mice had decreased in their cecal flora. When SPD and SPD mice were bred from heterozygous parents and then separated after weaning, less was cultured from the ceca of SPD mice. gut colonization was increased by gavage of rSPD in SPD mice. The source of enteric SPD in SPD mice was the gallbladder.

CONCLUSIONS

Enteral SPD exacerbates mortality after CLP by facilitating colonization of the mouse gut with .

摘要

未标记

确定表面活性蛋白D(SPD)在脓毒症中的作用。

设计

小鼠体内研究。

地点

一所学术医疗中心的研究实验室。

患者

SPD基因敲除(SPD)小鼠和野生型(SPD)小鼠。

干预措施

对SPD和SPD小鼠进行盲肠结扎和穿刺(CLP)。CLP后,评估两组的菌血症情况。对两组的盲肠内容物进行培养,以评估[具体细菌名称未给出]的定植情况。为控制亲代对微生物群的影响,将SPD和SPD小鼠由杂合子亲代繁殖而来,并测量它们盲肠中的[具体细菌名称未给出]水平。从小鼠身上采集肠道片段,通过蛋白质免疫印迹法测量SPD蛋白表达。给SPD小鼠灌喂表达绿色荧光蛋白的[具体细菌名称未给出]和重组SPD(rSPD)。

测量指标和主要结果

与CLP后的SPD小鼠相比,SPD小鼠死亡率降低,菌血症减少。在基线时,SPD小鼠盲肠菌群中的[具体细菌名称未给出]减少。当SPD和SPD小鼠由杂合子亲代繁殖,然后在断奶后分开饲养时,从SPD小鼠盲肠中培养出的[具体细菌名称未给出]较少。给SPD小鼠灌喂rSPD可增加肠道[具体细菌名称未给出]的定植。SPD小鼠肠道SPD的来源是胆囊。

结论

肠内SPD通过促进[具体细菌名称未给出]在小鼠肠道的定植,加重CLP后的死亡率。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3796/9119639/6018077cd82c/cc9-4-e0699-g001.jpg

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