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Inflammatory Cell Differentiation and Chemotaxis and Extracellular Tissue Repair Markers Are Correlated with Pulmonary Dysfunction in HIV Infected Individuals Presenting with Community-Acquired Pneumonia.
Journal of Interferon & Cytokine Research ( IF 1.9 ) Pub Date : 2019-10-22 , DOI: 10.1089/jir.2019.0090
Ruochen Mao 1 , Adriana Trajtman 1 , Breanne Head 1 , Iván Arturo Rodríguez Sabogal 2 , Ruth Cabrera 3 , Diana Marín 3 , Lucelly López 3 , Jenniffer Rodiño 3 , Yudy Aguilar 2 , Mariana Herrera Díaz 2 , Lázaro Agustín Vélez 2, 4 , Zulma Vanessa Rueda 3 , Yoav Keynan 1
Affiliation  

Prior studies have shown that HIV patients develop permanent pulmonary dysfunction following an episode of community-acquired pneumonia (CAP). However, the mechanism causing pulmonary dysfunction remains an enigma. HIV patients experience chronic inflammation. We hypothesized that CAP exacerbates inflammation in HIV patients resulting in an accelerated decline in lung function. A prospective cohort pilot study enrolled HIV patients hospitalized in Medellin, Colombia, with a diagnosis of CAP. Sixteen patients were eligible for the study; they were split into 2 groups: HIV and HIV+CAP. Plasma, sputum, and pulmonary function test (PFT) measurements were retrieved within 48 h of hospital admission and at 1 month follow-up. The concentrations of 13 molecules and PFT values were compared between the 2 cohorts. The HIV+CAP group had lower lung function compared to the HIV group; forced vital capacity (FVC)% predicted and forced expiratory volume in 1 s (FEV1)% predicted decreased, while FEV1/FVC remained constant. APRIL, BAFF, CCL3, and TIMP-1 correlated negatively with FVC% predicted and FEV1% predicted; the relationships however were moderate in strength. Furthermore, the concentrations of BAFF, CCL3, and TIMP-1 were statistically significant between the 2 groups (P ≤ 0.05). Our results indicate that HIV patients with CAP have a different inflammatory pattern and lower lung function compared to HIV patients without CAP. BAFF, CCL3, and TIMP-1 were abnormally elevated in HIV patients with CAP. Future studies with larger cohorts are required to verify these results. In addition, further investigation is required to determine if BAFF, CCL3, and TIMP-1 play a role in the process causing pulmonary dysfunction.

中文翻译:

炎症细胞分化和趋化性以及细胞外组织修复标志物与出现社区获得性肺炎的 HIV 感染者的肺功能障碍相关。

先前的研究表明,HIV 患者在社区获得性肺炎 (CAP) 发作后会出现永久性肺功能障碍。然而,导致肺功能障碍的机制仍然是个谜。HIV 患者会经历慢性炎症。我们假设 CAP 会加剧 HIV 患者的炎症,导致肺功能加速下降。一项前瞻性队列试点研究招募了在哥伦比亚麦德林住院并诊断为 CAP 的 HIV 患者。16 名患者符合研究条件;他们被分成两组:HIV 和 HIV+CAP。在入院 48 小时内和 1 个月的随访中检索血浆、痰和肺功能测试 (PFT) 测量值。在 2 个队列之间比较了 13 个分子的浓度和 PFT 值。HIV+CAP组的肺功能低于HIV组;用力肺活量 (FVC)% 预测值和 1 秒用力呼气量 (FEV1)% 预测值降低,而 FEV1/FVC 保持不变。APRIL、BAFF、CCL3 和 TIMP-1 与 FVC% 预测值和 FEV1% 预测值呈负相关;然而,这种关系的强度适中。此外,BAFF、CCL3和TIMP-1的浓度在2组之间具有统计学意义(P≤0.05)。我们的结果表明,与没有 CAP 的 HIV 患者相比,有 CAP 的 HIV 患者具有不同的炎症模式和较低的肺功能。患有 CAP 的 HIV 患者的 BAFF、CCL3 和 TIMP-1 异常升高。未来需要更大的队列研究来验证这些结果。此外,还需要进一步调查以确定 BAFF、CCL3、
更新日期:2019-11-01
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