Biglino A, Forno B, Pollono A M, Ghio P, Albera C
Istituto di Malattie Infettive, University of Torino, Italy.
Chest. 1993 Feb;103(2):439-43. doi: 10.1378/chest.103.2.439.
In order to elucidate the role played by alveolar cytokines in the pathogenesis of HIV-related lung damage, levels of interleukin (IL) 1 beta, IL-2, IL-6, tumor necrosis factor (TNF)-alpha, and interferon (Ifn) were assessed on supernatant of bronchoalveolar lavage fluid from 30 consecutive HIV-1 seropositive (HIVAb+) patients with clinical and radiologic evidence of pneumonia, from 20 HIV- seronegative (HIVAb-) patients with pulmonary sarcoidosis, and from 10 HIVAb- healthy control subjects. Cytokine levels were expressed as picogram (IL-1, TNF), nanogram (IL-6), and international unit (IL-2, Ifn) per milligram of albumin per deciliter. Total and differential cell counts, cytofluorimetric enumeration of CD3+, CD3+/DR+, CD4+, CD8+, and CD8+/CD16+ cells, as well as microbiologic investigations for opportunistic agents were performed on lavage pellets. HIV-related pneumonia was characterized by higher mean alveolar level of IL-2 (12 +/- 5 IU), and by more elevated mean counts of T cells (109 +/- 16), activated T cells (60 +/- 12), and CD8+ cells (90 +/- 13)/microliters if compared with both active sarcoidosis and control subjects, where respective values of 0.2 +/- 0.1 and 0.3 +/- 0.2 IU IL-2/mgAlb/dl, of 52 +/- 11 and 7 +/- 2 T cells, of 20 +/- 5 and 1.2 +/- 0.3 activated T cells, and of 11 +/- 2 and 3 +/- 0.6 CD8+ cells per microliter were found. HIV-infected patients with opportunistic lung infections (OIs) showed the highest mean IL-2 level (21 +/- 4 IU), and higher counts of both CD8+ (117 +/- 20) and CD8+/CD16+ (36 +/- 7) cells per microliter if compared with patients without evidence of OIs (respectively, 62 +/- 13 CD8+ and 18 +/- 3 CD8+/CD16+ cells per microliter). By contrast, extremely high IL-1 levels (1,463 +/- 760 pg), and IL-2 levels similar to control subjects (3.4 +/- 1.2 IU), were found in the absence of OIs. Different mechanisms depending respectively on IL-2-mediated cytotoxic cell recruitment and activation, or IL-1-mediated tissue injury may account for HIV-related lung damage, depending on the presence or absence of opportunistic agents.
为阐明肺泡细胞因子在HIV相关肺损伤发病机制中所起的作用，对30例连续的有肺炎临床及影像学证据的HIV-1血清阳性（HIVAb+）患者、20例患有肺结节病的HIV血清阴性（HIVAb-）患者以及10例HIVAb-健康对照者的支气管肺泡灌洗 fluid上清液中的白细胞介素（IL）-1β、IL-2、IL-6、肿瘤坏死因子（TNF）-α和干扰素（Ifn）水平进行了评估。细胞因子水平以每分升每毫克白蛋白中的皮克数（IL-1、TNF）、纳克数（IL-6）和国际单位数（IL-2、Ifn）表示。对灌洗沉淀物进行了总细胞计数和分类计数、CD3+、CD3+/DR+、CD4+、CD8+以及CD8+/CD16+细胞的细胞荧光计数，以及机会性病原体的微生物学检测。与活动性结节病患者和对照者相比，HIV相关肺炎的特征在于IL-2的平均肺泡水平较高（12±5 IU），T细胞（109±16）、活化T细胞（60±12）以及CD8+细胞（90±13）/微升的平均计数更高，而活动性结节病患者和对照者的相应值分别为0.2±0.1和0.3±0.2 IU IL-2/mgAlb/dl、52±11和7±2个T细胞、20±5和1.2±0.3个活化T细胞，以及11±2和3±0.6个CD8+细胞/微升。与无机会性肺部感染（OIs）证据的患者相比，患有机会性肺部感染的HIV感染患者的平均IL-2水平最高（21±4 IU），CD8+（117±20）和CD8+/CD16+（36±7）细胞/微升的计数也更高（无OIs证据的患者分别为62±13个CD8+细胞和18±3个CD8+/CD16+细胞/微升）。相比之下，在无OIs的情况下发现IL-1水平极高（1463±760 pg），IL-2水平与对照者相似（3.4±1.2 IU）。取决于机会性病原体的存在与否，分别依赖于IL-2介导的细胞毒性细胞募集和活化或IL-1介导的组织损伤的不同机制可能导致HIV相关的肺损伤。
