Carmen-Orozco Rogger P, Dávila-Villacorta Danitza G, Delgado-Kamiche Ana D, Celiz Rensson H, Trompeter Grace, Sutherland Graham, Gavídia Cesar, Garcia Hector H, Gilman Robert H, Verástegui Manuela R
Infectious Diseases Laboratory Research-LID, Faculty of Science and Philosophy, Alberto Cazorla Talleri, Universidad Peruana Cayetano Heredia, Lima, Perú.
Cellular and Molecular Medicine Program, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.
PLoS Negl Trop Dis. 2021 Apr 27;15(4):e0009295. doi: 10.1371/journal.pntd.0009295. eCollection 2021 Apr.
The parasite Taenia solium causes neurocysticercosis (NCC) in humans and is a common cause of adult-onset epilepsy in the developing world. Hippocampal atrophy, which occurs far from the cyst, is an emerging new complication of NCC. Evaluation of molecular pathways in brain regions close to and distant from the cyst could offer insight into this pathology.
Rats were inoculated intracranially with T. solium oncospheres. After 4 months, RNA was extracted from brain tissue samples in rats with NCC and uninfected controls, and cDNA was generated. Expression of 38 genes related to different molecular pathways involved in the inflammatory response and healing was assessed by RT-PCR array.
Inflammatory cytokines IFN-γ, TNF-α, and IL-1, together with TGF-β and ARG-1, were overexpressed in tissue close to the parasite compared to non-infected tissue. Genes for IL-1A, CSF-1, FN-1, COL-3A1, and MMP-2 were overexpressed in contralateral tissue compared to non-infected tissue.
The viable cysticerci in the rat model for NCC is characterized by increased expression of genes associated with a proinflammatory response and fibrosis-related proteins, which may mediate the chronic state of infection. These pathways appear to influence regions far from the cyst, which may explain the emerging association between NCC and hippocampal atrophy.
猪带绦虫可导致人类患神经囊尾蚴病（NCC），是发展中国家成人癫痫发作的常见病因。远离囊肿发生的海马萎缩是NCC一种新出现的并发症。评估囊肿附近和远离囊肿的脑区分子途径可能有助于深入了解这种病理情况。
将猪带绦虫六钩蚴颅内接种到大鼠体内。4个月后，从患有NCC的大鼠和未感染对照的脑组织样本中提取RNA，并生成cDNA。通过逆转录聚合酶链反应（RT-PCR）阵列评估与炎症反应和愈合相关的不同分子途径的38个基因的表达。
与未感染组织相比，寄生虫附近组织中炎性细胞因子IFN-γ、TNF-α和IL-1以及TGF-β和ARG-1过表达。与未感染组织相比，对侧组织中IL-1A、CSF-1、FN-1、COL-3A1和MMP-2的基因过表达。
NCC大鼠模型中活囊尾蚴的特征是与促炎反应和纤维化相关蛋白相关的基因表达增加，这可能介导感染的慢性状态。这些途径似乎影响远离囊肿的区域，这可能解释了NCC与海马萎缩之间新出现的关联。
