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Increased CD11b and Decreased CD62L in Blood and Airway Neutrophils from Long-Term Smokers with and without COPD.
Journal of Innate Immunity ( IF 5.3 ) Pub Date : 2020-08-21 , DOI: 10.1159/000509715
Marit Stockfelt 1, 2 , Karin Christenson 3 , Anders Andersson 4, 5 , Lena Björkman 6 , Médea Padra 7 , Bettina Brundin 8 , Koustav Ganguly 8, 9 , Helga Asgeirsdottir 10 , Sara Lindén 7 , Ingemar Qvarfordt 10 , Johan Bylund 3 , Anders Lindén 8, 11
Affiliation  

There is incomplete mechanistic understanding of the mobilization of neutrophils in the systemic and local compartment in smokers with chronic obstructive pulmonary disease (COPD). In this pilot study, we characterized how the adhesion molecules CD11b and CD62L, surface markers indicative of priming, are altered as neutrophils extravasate, and whether surface density of CD11b and CD62L differs between long-term tobacco smokers (LTS) with and without COPD compared with healthy never-smokers (HNS). Unstimulated blood neutrophils from LTS with (n = 5) and without (n = 9) COPD displayed lower surface density of CD62L compared with HNS (n = 8). In addition, surface density of CD11b was higher in bronchoalveolar lavage (BAL) neutrophils from LTS without COPD compared with those with COPD and HNS. Moreover, in BAL neutrophils from all study groups, CD62L was lower compared with matched blood neutrophils. In addition, BAL neutrophils responded with a further decrease in CD62L to ex vivo TNF stimulation. Thus, neutrophils in the airway lumen display a higher state of priming than systemic neutrophils and bear the potential to be further primed by local cytokines even with no smoking or the presence of COPD, findings that may represent a universal host defense mechanism against local bacteria. Moreover, systemic neutrophils are primed in LTS regardless of COPD. Further studies in larger materials are warranted to determine whether the priming of neutrophils is protective against COPD or merely preceding it.
J Innate Immun


中文翻译:

患有和不患有 COPD 的长期吸烟者血液和气道中性粒细胞中 CD11b 增加和 CD62L 减少。

对于慢性阻塞性肺疾病 (COPD) 吸烟者全身和局部区室中中性粒细胞的动员机制尚不完全清楚。在这项初步研究中,我们表征了粘附分子 CD11b 和 CD62L(指示启动的表面标志物)如何随着中性粒细胞外渗而改变,以及 CD11b 和 CD62L 的表面密度在长期吸烟者(LTS)之间是否存在差异健康的从不吸烟者 (HNS)。未刺激的嗜中性粒细胞的血液从与LTS(Ñ = 5)和不具有(Ñ = 9)COPD显示CD62L的下表面密度相比HNS(Ñ= 8)。此外,与患有 COPD 和 HNS 的患者相比,来自无 COPD 的 LTS 的支气管肺泡灌洗 (BAL) 中性粒细胞的 CD11b 表面密度更高。此外,在所有研究组的 BAL 中性粒细胞中,与匹配的血液中性粒细胞相比,CD62L 较低。此外,BAL 中性粒细胞对离体 TNF 刺激的反应是 CD62L 的进一步减少。因此,气道管腔中的中性粒细胞显示出比全身中性粒细胞更高的启动状态,并且即使在不吸烟或存在 COPD 的情况下也有可能被局部细胞因子进一步启动,这些发现可能代表了针对局部细菌的通用宿主防御机制。此外,无论慢性阻塞性肺病如何,全身性中性粒细胞都在 LTS 中被激发。
J先天免疫
更新日期:2020-08-21
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