Nascimento Carolina Martins, Casaro Mateus Campos, Perez Evelyn Roxana, Ribeiro Willian Rodrigues, Mayer Marcia Pinto Alves, Ishikawa Karin Hitomi, Lino-Dos-Santos-Franco Adriana, Pereira Joice Naiara Bertaglia, Ferreira Caroline Marcantonio
Institute of Environmental, Chemistry and Pharmaceutical Sciences, Department of Pharmaceutics Sciences, Universidade Federal de São Paulo, Diadema, SP, Brazil.
Department of Microbiology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, SP, Brazil.
Heliyon. 2023 Jun 3;9(6):e16429. doi: 10.1016/j.heliyon.2023.e16429. eCollection 2023 Jun.
/Aims: Epidemiological data show that there is an important relationship between respiratory and intestinal diseases. To improve our understanding on the interconnectedness between the lung and intestinal mucosa and the overlap between respiratory and intestinal diseases, our aim was to investigate the influence of ovalbumin (OVA)-induced allergic airway inflammation on gut homeostasis.
A/J mice were sensitized and challenged with OVA. The animals were euthanized 24 h after the last challenge, lung inflammation was determined by evaluating cells in Bronchoalveolar lavage fluid, serum anti-OVA IgG titers and colon morphology, inflammation and integrity of the intestinal mucosa were investigated. IL-4 and IL-13 levels and myeloperoxidase activity were determined in the colon samples. The expression of genes involved in inflammation and mucin production at the gut mucosa was also evaluated.
OVA challenge resulted not only in lung inflammation but also in macroscopic alterations in the gut such as colon shortening, increased myeloperoxidase activity and loss of integrity in the colonic mucosal. Neutral mucin intensity was lower in the OVA group, which was followed by down-regulation of transcription of and up-regulation of and . In addition, the OVA group had higher levels of IL-13 and IL-4 in the colon. Ova-specific IgG1 and OVA-specific IgG2a titers were higher in the serum of the OVA group than in controls.
Our data using the OVA experimental model suggested that challenges in the respiratory system may result not only in allergic airway inflammation but also in the loss of gut homeostasis.
/目的：流行病学数据表明，呼吸道疾病和肠道疾病之间存在重要关联。为了增进我们对肺与肠道黏膜之间的相互联系以及呼吸道疾病和肠道疾病重叠情况的理解，我们的目的是研究卵清蛋白（OVA）诱导的过敏性气道炎症对肠道稳态的影响。
用OVA对A/J小鼠进行致敏和激发。在最后一次激发后24小时对动物实施安乐死，通过评估支气管肺泡灌洗液中的细胞、血清抗OVA IgG滴度以及结肠形态来确定肺部炎症，研究肠道黏膜的炎症和完整性。测定结肠样本中的IL-4和IL-13水平以及髓过氧化物酶活性。还评估了肠道黏膜中参与炎症和黏蛋白产生的基因的表达。
OVA激发不仅导致肺部炎症，还导致肠道出现宏观改变，如结肠缩短、髓过氧化物酶活性增加以及结肠黏膜完整性丧失。OVA组中性黏蛋白强度较低，随后 、 和 的转录下调以及 上调。此外，OVA组结肠中IL-13和IL-4水平较高。OVA组血清中卵清蛋白特异性IgG1和卵清蛋白特异性IgG2a滴度高于对照组。
我们使用OVA实验模型的数据表明，呼吸系统的激发可能不仅导致过敏性气道炎症，还导致肠道稳态丧失。
