Dominguez-Flores Adriana, Rodríguez López Gloria M, Soria-Castro Rodolfo, López-Santiago Rubén, Rodríguez-Cortés Octavio, Pérez-Tapia Sonia M, Chávez-Blanco Alma D, Estrada-Parra Sergio, Flores-Mejía Raúl, Chacón-Salinas Rommel
Departamento de Inmunología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, ENCB-IPN, Mexico City, Mexico.
Departamento de Microbiología e Inmunología, Facultad de Medicina Veterinaria y Zootecnia, Universidad Nacional Autónoma de México, Mexico.
Microb Pathog. 2023 Mar;176:106005. doi: 10.1016/j.micpath.2023.106005. Epub 2023 Jan 28.
The Gram-negative bacteria Brucella abortus is a major cause of brucellosis in animals and humans. The host innate immune response to B. abortus is mainly associated with phagocytic cells such as dendritic cells, neutrophils, and macrophages. However, as mast cells naturally reside in the main bacterial entry sites they may be involved in bacterial recognition. At present, little is known about the role of mast cells during B. abortus infection. The role of the innate immune receptors TLR2 and TLR4 in activation of mast cells by B. abortus (strain RB51) infection was analyzed in this study. The results showed that B. abortus did not induce mast cell degranulation, but did induce the synthesis of the cytokines IL-1β, IL-6, TNF-α, CCL3, CCL4, and CCL5. Furthermore, B. abortus stimulated key cell signaling molecules involved in mast cell activation such as p38 and NF-κB. Blockade of the receptors TLR2 and TLR4 decreased TNF-α and IL-6 release by mast cells in response to B. abortus. Taken together, our results demonstrate that mast cells are activated by B. abortus and may play a role in inducing an inflammatory response during the initial phase of the infection.
革兰氏阴性菌流产布鲁氏菌是动物和人类布鲁氏菌病的主要病因。宿主对流产布鲁氏菌的固有免疫反应主要与吞噬细胞有关，如树突状细胞、中性粒细胞和巨噬细胞。然而，由于肥大细胞自然存在于主要的细菌入侵部位，它们可能参与细菌识别。目前，关于肥大细胞在流产布鲁氏菌感染过程中的作用知之甚少。本研究分析了固有免疫受体TLR2和TLR4在流产布鲁氏菌（RB51菌株）感染激活肥大细胞中的作用。结果表明，流产布鲁氏菌不会诱导肥大细胞脱颗粒，但会诱导细胞因子IL-1β、IL-6、TNF-α、CCL3、CCL4和CCL5的合成。此外，流产布鲁氏菌刺激参与肥大细胞激活的关键细胞信号分子，如p38和NF-κB。阻断受体TLR2和TLR4可降低肥大细胞对流产布鲁氏菌反应时TNF-α和IL-6的释放。综上所述，我们的结果表明肥大细胞被流产布鲁氏菌激活，可能在感染初期诱导炎症反应中发挥作用。
