Department of Clinical Sciences, Faculty of Veterinary Medicine, Université de Montréal, Saint-Hyacinthe, Quebec, Canada.
Department of Veterinary Biomedical Sciences, Faculty of Veterinary Medicine, Université de Montréal, Saint-Hyacinthe, Quebec, Canada.
PLoS One. 2024 May 30;19(5):e0298361. doi: 10.1371/journal.pone.0298361. eCollection 2024.
The pathogenesis of anal sacculitis has not been extensively investigated, although atopic dogs seem to be predisposed to the disease. The aim of this study was therefore to characterize and compare the bacterial microbiota and pro-inflammatory cytokines in the anal sacs of dogs from three groups (healthy dogs, untreated atopic dogs and atopic dogs receiving antipruritic treatment or allergen-specific immunotherapy) in order to determine whether changes could be at the origin of anal sacculitis in atopic dogs. Bacterial populations of anal sac secretions from fifteen healthy dogs, fourteen untreated and six treated atopic dogs were characterized by sequencing the V4 region of the 16S rRNA gene using Illumina technology. Proinflammatory cytokines were analyzed with the Luminex multiplex test. Community membership and structure were significantly different between the anal sacs of healthy and untreated atopic dogs (P = 0.002 and P = 0.003, respectively) and between those of untreated and treated atopic dogs (P = 0.012 and P = 0.017, respectively). However, the community structure was similar in healthy and treated atopic dogs (P = 0.332). Among the proinflammatory cytokines assessed, there was no significant difference between groups, except for interleukin 8 which was higher in the anal sacs of untreated atopic dogs compared to treated atopic dogs (P = 0.02), and tumor necrosis factor-alpha which was lower in the anal sacs of healthy dogs compared to treated atopic dogs (P = 0.04). These results reveal a dysbiosis in the anal sacs of atopic dogs, which may partially explain the predisposition of atopic dogs to develop bacterial anal sacculitis. Treatments received by atopic dogs (oclacitinib, desloratadine and allergen-specific immunotherapy) shift the microbiota of the anal sacs towards that of healthy dogs. Further studies are required to identify significant cytokines contributing to anal sacculitis in atopic dogs.
肛门囊炎的发病机制尚未得到广泛研究,尽管特应性犬似乎容易患该病。因此,本研究的目的是对来自三组犬(健康犬、未治疗的特应性犬和接受止痒治疗或过敏原特异性免疫治疗的特应性犬)的肛门囊细菌菌群和促炎细胞因子进行特征描述和比较,以确定特应性犬的肛门囊炎是否起源于细菌菌群的变化。使用 Illumina 技术对 15 只健康犬、14 只未治疗的特应性犬和 6 只接受治疗的特应性犬的肛门囊分泌物的细菌种群进行了 V4 区 16S rRNA 基因测序。采用 Luminex 多重测试分析促炎细胞因子。健康犬和未治疗的特应性犬的肛门囊中(P = 0.002 和 P = 0.003)以及未治疗的和接受治疗的特应性犬的肛门囊中(P = 0.012 和 P = 0.017)的细菌群落组成和结构存在显著差异。然而,健康犬和接受治疗的特应性犬的细菌群落结构相似(P = 0.332)。在所评估的促炎细胞因子中,各组之间除白细胞介素 8 外无显著差异,白细胞介素 8 在未治疗的特应性犬的肛门囊中高于接受治疗的特应性犬(P = 0.02),肿瘤坏死因子-α在健康犬的肛门囊中低于接受治疗的特应性犬(P = 0.04)。这些结果揭示了特应性犬肛门囊中的菌群失调,这可能部分解释了特应性犬易患细菌性肛门囊炎的原因。特应性犬接受的治疗(奥卡替尼、地氯雷他定和过敏原特异性免疫治疗)使肛门囊的菌群向健康犬的菌群转移。需要进一步的研究来确定导致特应性犬肛门囊炎的显著细胞因子。