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Cytokine. 2015 Dec;76(2):328-333. doi: 10.1016/j.cyto.2015.09.003. Epub 2015 Sep 11.

The association between the Th-17 immune response and pulmonary complications in a trauma ICU population.

Author information

1
Department of Surgery, The University of Texas Health Science Center at San Antonio, TX 78229, United States.
2
US Army Institute of Surgical Research, Fort Sam Houston, TX 78234, United States.
3
Department of Surgery, The University of Texas Health Science Center at San Antonio, TX 78229, United States; US Army Institute of Surgical Research, Fort Sam Houston, TX 78234, United States. Electronic address: schwacha@uthscsa.edu.

Abstract

BACKGROUND:

The overall immunopathology of the T-helper cell (Th)-17 immune response has been implicated in various inflammatory diseases including pulmonary inflammation; however its potential role in acute respiratory distress syndrome (ARDS) is not defined. This study aimed to evaluate the Th-17 response in bronchoalveolar lavage fluid (BALF) and blood and from trauma patients with pulmonary complications.

METHODS:

A total of 21 severely injured intensive care unit (ICU) subjects, who were mechanically ventilated and undergoing bronchoscopy, were enrolled. BALF and blood were collected and analyzed for Th-1 (interferon [IFN]γ), Th-2 (interleukin [IL]-4, -10), Th-17 (IL-17A, -17F, -22, 23) and pro-inflammatory (IL-1β, IL-6, tumor necrosis factor [TNF]α) cytokine levels.

RESULTS:

Significant levels of the Th-17 cytokines IL-17A, -17F and -21 and IL-6 (which can be classified as a Th-17 cytokine) were observed in the BALF of all subjects. There were no significant differences in Th-17 cytokines between those subjects with ARDS and those without, with the exception of plasma and BALF IL-6, which was markedly greater in ARDS subjects, as compared with controls and non-ARDS subjects.

CONCLUSIONS:

Trauma patients with pulmonary complications exhibited a significant Th-17 response in the lung and blood, suggesting that this pro-inflammatory milieu may be a contributing factor to such complications.

KEYWORDS:

Acute lung injury; Acute respiratory distress syndrome; IL-17; Inflammation; Injury

PMID:
26364992
PMCID:
PMC4632975
DOI:
10.1016/j.cyto.2015.09.003
[Indexed for MEDLINE]
Free PMC Article

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