Instituto do Coração (InCor), Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo (HCFMUSP), São Paulo, Brazil.
Department of Pathology, Experimental Air Pollution Laboratory, Laboratório de Investigação Médica 05 (LIM 05) - School of Medicine, University of São Paulo, São Paulo, Brazil.
Front Cell Infect Microbiol. 2022 Jul 19;12:830761. doi: 10.3389/fcimb.2022.830761. eCollection 2022.
Chagas disease is characterized by intense myocardial fibrosis stimulated by the exacerbated production of inflammatory cytokines, oxidative stress, and apoptosis. Air pollution is a serious public health problem and also follows this same path. Therefore, air pollution might amplify the inflammatory response of Chagas disease and increase myocardial fibrosis.
We studied groups of Trypanosoma cruzi infected Sirius hamsters (Chagas=CH and Chagas exposed to pollution=CH+P) and 2 control groups (control healthy animals=CT and control exposed to pollution=CT+P). We evaluated acute phase (60 days post infection) and chronic phase (10 months). Echocardiograms were performed to assess left ventricular systolic and diastolic diameter, in addition to ejection fraction. Interstitial collagen was measured by morphometry in picrosirius red staining tissue. The evaluation of inflammation was performed by gene and protein expression of cytokines IL10, IFN-γ, and TNF; oxidative stress was quantified by gene expression of NOX1, MnSOD, and iNOS and by analysis of reactive oxygen species; and apoptosis was performed by gene expression of BCL2 and Capsase3, in addition to TUNEL analysis.
Chagas groups had increased collagen deposition mainly in the acute phase, but air pollution did not increase this deposition. Also, Chagas groups had lower ejection fraction in the acute phase (p = 0.002) and again air pollution did not worsen ventricular function or dilation. The analysis of the inflammation and oxidative stress pathways were also not amplified by air pollution. Apoptosis analysis showed increased expression of BCL2 and Caspase3 genes in chagasic groups in the acute phase, with a marginal p of 0.054 in BCL2 expression among infected groups, and TUNEL technique showed amplified of apoptotic cells by pollution among infected groups.
A possible modulation of the apoptotic pathway was observed, inferring interference from air pollution in this pathway. However, it was not enough to promote a greater collagen deposition, or worsening ventricular function or dilation caused by air pollution in this model of Chagas cardiomyopathy.
恰加斯病的特征是炎症细胞因子、氧化应激和细胞凋亡加剧导致的强烈心肌纤维化。空气污染是一个严重的公共卫生问题，也遵循同样的途径。因此，空气污染可能放大恰加斯病的炎症反应，增加心肌纤维化。
我们研究了感染克氏锥虫的西里乌斯仓鼠（恰加斯病=CH 和暴露于污染的恰加斯病=CH+P）的两组和两组对照（健康对照动物=CT 和暴露于污染的对照=CT+P）。我们评估了急性期（感染后 60 天）和慢性期（10 个月）。进行超声心动图检查以评估左心室收缩和舒张直径，以及射血分数。通过 picrosirius 红染色组织的形态计量学测量间质胶原。通过细胞因子 IL10、IFN-γ 和 TNF 的基因和蛋白表达评估炎症；通过 NOX1、MnSOD 和 iNOS 的基因表达和活性氧分析评估氧化应激；通过 BCL2 和 Capsase3 的基因表达以及 TUNEL 分析评估细胞凋亡。
恰加斯病组在急性期胶原沉积增加，但空气污染并未增加这种沉积。此外，恰加斯病组在急性期射血分数降低（p=0.002），空气污染也没有进一步恶化心室功能或扩张。炎症和氧化应激途径的分析也没有因空气污染而放大。凋亡分析显示，在急性期，感染组的 BCL2 和 Caspase3 基因表达增加，感染组中 BCL2 表达的 p 值为 0.054，TUNEL 技术显示感染组中凋亡细胞增加。
观察到凋亡途径的可能调节，推断空气污染对该途径的干扰。然而，在这种恰加斯心肌病模型中，空气污染不足以促进更多的胶原沉积，或加重空气污染引起的心室功能或扩张。
