期刊
JCI INSIGHT
卷 7, 期 3, 页码 -出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/jci.insight.149870
关键词
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资金
- German Research Foundation [CO 2096/1-1, BA1606/3-1, BA1606/4-1, ZA428/14-1, KFO342, DR1013/1-1, KFO309, SFB/TR-84]
- International Anesthesia Research Society Mentored Research Awards
- Interdisciplinary Center for Clinical Research grants [IZKF Za2/001/18, SEED12/18]
- Hessisches Ministerium fur Wissenschaft und Kunst (LOEWE Diffusible Signals)
- German Federal Ministry of Education and Research (ERACoSysMed2 - SysMed-COPD) [FKZ 031L0140]
- German Federal Ministry of Education and Research (e:Med CAPSys) [FKZ 01ZX1604E]
- von-Behring-Roentgen-Stiftung [66-LV07]
- National Science Foundation [CHE-1904865]
- Robert A. Welch Foundation Research Grant [C-1680]
- US NIH [R01 HL133900, R01 HL130324, AI125445, AI160167]
Acute respiratory distress syndrome (ARDS) is a disease that causes severe lung failure and there is a pressing need for better early detection and treatment. Neutrophil influx, which is associated with tissue destruction, is a defining characteristic of ARDS. Inhibiting ADAM8 may help regulate neutrophil responses and improve therapeutic outcomes in acute inflammatory lung diseases like pneumonia and ARDS.
Acute respiratory distress syndrome (ARDS) results in catastrophic lung failure and has an urgent, unmet need for improved early recognition and therapeutic development. Neutrophil influx is a hallmark of ARDS and is associated with the release of tissue-destructive immune effectors, such neutrophil transmigration. In mouse pneumonia models, both genetic deletion and pharmacologic containment. Unexpectedly, the alterations of neutrophil function were not attributable to impaired disease severity. We propose that in acute inflammatory lung diseases such as pneumonia and ARDS, ADAM8 inhibition might allow fine-tuning of neutrophil responses for therapeutic gain.
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