Upon infection by Trypanosoma cruzi, adipocytes adopt a clearly defined inflammatory phenotype with concomitant down-regulation of adiponectin expression, which influences the pathogenesis of Chagas heart disease. Herein, we examined how T. cruzi interferes with transcriptional regulation of adiponectin production in mouse adipocytes. The invading pathogen activates the Ca²⁺/calcineurin/NFATc4 signaling pathway in 3T3-L1 cells. Parasite-induced early activation of NFATc4 is involved in repressing adiponectin expression through recognition of the specific response element located at (−363 to −344) of the gene promoter. Nuclear import of dephosphorylated NFATc4 and decreased adiponectin levels were further demonstrated in white adipose tissue from acutely infected mice. Our current findings point to better clarify the complex role of adipose tissue in the modulation of inflammatory mechanisms operative during T. cruzi infection.

被克氏锥虫感染后，脂肪细胞采用明确定义的炎症表型，伴随着脂联素表达的下调，这影响了恰加斯心脏病的发病机制。在此，我们研究了T. cruzi如何干扰小鼠脂肪细胞中脂联素产生的转录调控。入侵病原体激活 Ca ²⁺3T3-L1 细胞中的 /calcineurin/NFATc4 信号通路。寄生虫诱导的 NFATc4 早期激活参与通过识别位于基因启动子 (-363 至 -344) 的特定反应元件来抑制脂联素表达。在急性感染小鼠的白色脂肪组织中进一步证明了去磷酸化 NFATc4 的核输入和脂联素水平的降低。我们目前的研究结果表明，脂肪组织在调节T. cruzi感染期间起作用的炎症机制中的复杂作用。