支气管腔闭塞症（BO）是一种可在吸入某些化学物质后发展的毁灭性肺病。当在职业水平吸入时，二乙酰（DA）是与BO发展常见相关的化学物质之一。以往对大鼠的研究表明，重复的DA蒸汽暴露会增加肺部CD4+CD25+ T细胞和支气管肺泡（BAL）白细胞介素-17A（IL-17A）浓度，并伴随着气道重塑的发展。我们假设IL-17A的中和会减轻重复DA蒸汽暴露后气道重塑的严重程度。我们将斯普拉格-道利大鼠接触200ppm DA蒸汽或过滤空气（RA）6小时/天x 5天，并在接触后的两周进行监测。接触后立即开始IL-17A中和（αIL-17A）或IgG（对照）处理，并每周进行两次直到研究结束。取肺组织行组织学、流式细胞术和BAL分析。存活率、氧饱和度和体重百分比发生较DA暴露组相比显著下降，但DA+αIL-17A组与DA+IgG组相比没有显著差异。同样，在DA+αIL-17A组与DA+IgG组之间，气道病变的数量和严重性也没有显著差异，即使肺调节性T细胞百分比增加，BAL中IL-17A浓度减少。对远端肺实质进行Ashcroft评分表明，在DA+αIL-17A组中，与DA+IgG组相比，实质重塑更为严重，并有肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）和核因子-κB（NF-ĸB）的表达增加。总体而言，DA暴露大鼠中对IL-17A的中和未能减轻气道重塑，且导致促炎细胞因子TNF-α、IL-1β和NF-ĸB的表达增加。

Bronchiolitis obliterans (BO) is a devastating lung disease that can develop following inhalation exposure to certain chemicals. Diacetyl (DA) is one chemical commonly associated with BO development when inhaled at occupational levels. Previous studies in rats have shown repetitive DA vapor exposures increased lung CD4+CD25+ T cells and bronchoalveolar (BAL) interleukin-17A (IL-17A) concentrations concurrent with the development of airway remodeling. We hypothesized that IL-17A neutralization would attenuate the severity of airway remodeling after repetitive DA vapor exposures. Sprague-Dawley rats were exposed to 200 parts-per-million DA vapor or filtered air (RA) for 6hrs/day x 5 days and monitored for 2 weeks post-exposure. Treatment with IL-17A neutralization (αIL-17A) or IgG (control) began immediately following exposures and continued twice weekly until study's end. Lungs were harvested for histology, flow cytometry, and BAL analyses. Survival, oxygen saturations and percent weight change decreased significantly in DA-exposed vs RA-exposed rats, but did not differ significantly between DA+αIL-17A vs. DA+IgG. Similarly, the number nor severity of airway lesions did not differ significantly between DA+αIL-17A vs DA+IgG rats despite the percent of lung regulatory T cells increasing with decreased BAL IL-17A concentrations. Ashcroft scoring of the distal lung parenchyma suggested worse parenchymal remodeling in DA+αIL-17A vs. DA+IgG rats with increased expression of tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and nuclear factor-kappa B (NF-ĸB). Collectively, IL-17A neutralization in DA-exposed rats failed to attenuate airway remodeling with increased expression of pro-inflammatory cytokines TNF-α, IL-1β and NF-ĸB.