Laboratório de Biologia do Reconhecer, Centro de Biociências e Biotecnologia, Universidade Estadual do Norte Fluminense Darcy Ribeiro, Campos dos Goytacazes, Rio de Janeiro, Brazil.
Faculdade de Medicina de Campos, Campos dos Goytacazes, Rio de Janeiro, Brazil.
PLoS One. 2024 Jun 12;19(6):e0300704. doi: 10.1371/journal.pone.0300704. eCollection 2024.
Leprosy is a chronic infectious disease caused by the bacillus Mycobacterium leprae. The disease may evolve for inflammatory reactions, reversal reaction (RR) and erythema nodosum leprosum (ENL), the major cause of irreversible neuropathy in leprosy, which occur in 1 in 3 people with leprosy, even with effective treatment of M. leprae. Leprosy remains persistently endemic in our region where it predominantly affects lowest socioeconomic conditions people, as Toxoplasma gondii infection in the municipality studied. Previously, we have shown T. gondii coinfection as a risk marker for leprosy, mainly in its severe form. This present study assessed whether T. gondii infection is also a risk factor for leprosy reactions and the predictive value of immunoglobulin production prior to development of leprosy reactions. Patients with leprosy (n = 180), co-infected or not with T. gondii, had their serum investigated for levels of IgA, IgE, IgG1, IgG2, IgG3 and IgG4 anti-PGL-1 by ELISA prior to development of leprosy reactions. The serologic prevalence for T. gondii infection was 87.7% in leprosy reaction patients reaching 90.9% in those with ENL. The leprosy reaction risk increased in T. gondii seropositive individuals was two-fold ([OR] = 2.366; 95% confidence interval [CI 95%]: 1.024-5.469) higher than those seronegative, and considering the risk of ENL, this increase was even more evident (OR = 6.753; 95% CI: 1.050-72.85) in coinfected individuals. When evaluated the prediction of anti-PGL-1 immunoglobulin levels for development of leprosy reactions in patients coinfected or not with T. gondii, only the increase IgE levels were associated to occurrence of reactional episodes of leprosy, specifically ENL type, in patients coinfected with T. gondii, compared to those not coinfected or no reaction. Thus, the immunomodulation in co-parasitism T. gondii-M. leprae suggest increased levels of IgE as a biomarker for early detection of these acute inflammatory episodes and thereby help prevent permanent neuropathy and disability in leprosy patients.
麻风病是一种由麻风分枝杆菌引起的慢性传染病。该疾病可能会发生炎症反应、逆转反应（RR）和结节性红斑麻风（ENL），这是麻风病不可逆性神经病的主要原因，在每 3 个麻风病患者中就有 1 人会出现这种情况，即使采用有效的麻风分枝杆菌治疗也是如此。麻风病在我们地区持续流行，主要影响社会经济条件最低的人群，就像在所研究的城市中弓形虫感染一样。此前，我们已经表明，弓形虫合并感染是麻风病的一个风险标志物，主要与严重形式的麻风病有关。本研究评估了弓形虫感染是否也是麻风病反应的一个危险因素，以及在发生麻风病反应之前免疫球蛋白产生的预测价值。我们对 180 例麻风病患者（无论是否合并感染弓形虫）的血清进行了调查，检测了抗 PGL-1 的 IgA、IgE、IgG1、IgG2、IgG3 和 IgG4 水平，这些患者在发生麻风病反应之前进行了 ELISA 检测。在发生麻风病反应的患者中，弓形虫感染的血清流行率为 87.7%，在发生 ENL 的患者中达到 90.9%。在弓形虫血清阳性个体中，麻风病反应的风险增加了两倍（OR = 2.366；95%置信区间 [95%CI]：1.024-5.469），高于血清阴性个体，而考虑到 ENL 的风险，在合并感染个体中，这种增加更为明显（OR = 6.753；95%CI：1.050-72.85）。在评估合并或未合并感染弓形虫的患者中，抗 PGL-1 免疫球蛋白水平对麻风病反应发生的预测时，只有 IgE 水平的增加与合并感染弓形虫的患者发生麻风病反应性发作（特别是 ENL 类型）相关，而与未合并感染或无反应的患者无关。因此，弓形虫-麻风分枝杆菌共寄生的免疫调节提示 IgE 水平升高可作为早期检测这些急性炎症发作的生物标志物，从而有助于预防麻风病患者发生永久性神经病和残疾。
