Animal Science Department, Federal University of Lavras, Lavras, Minas Gerais, Brazil.
Large Animal Clinical Sciences, Western College of Veterinary Medicine, University of Saskatchewan, 52 Campus Drive, Saskatoon, SK, S7N 5B4, Canada.
Vet Res Commun. 2024 Apr;48(2):991-1001. doi: 10.1007/s11259-023-10257-0. Epub 2023 Dec 4.
Swine dysentery, spirochetal colitis, and salmonellosis are production-limiting enteric diseases of global importance to the swine industry. Despite decades of efforts, mitigation of these diseases still relies on antibiotic therapy. A common knowledge gap among the 3 agents is the early B-cell response to infection in pigs. Thus, this study aimed to characterize the porcine B-cell response to Brachyspira hyodysenteriae, Brachyspira hampsonii (virulent and avirulent strains), Brachyspira pilosicoli, and Salmonella Typhimurium, the agents of the syndromes mentioned above. Immortalized porcine B-cell line derived from a crossbred pig with lymphoma were co-incubated for 8 h with each pathogen, as well as E. coli lipopolysaccharide (LPS) and a sham-inoculum (n = 3/treatment). B-cell viability following treatments was evaluated using trypan blue, and the expression levels of B-cell activation-related genes was profiled using reverse transcription quantitative PCR. Only S. Typhimurium and LPS led to increased B-cell mortality. B. pilosicoli downregulated B-lymphocyte antigen (CD19), spleen associated tyrosine Kinase (syk), tyrosine-protein kinase (lyn), and Tumour Necrosis Factor alpha (TNF-α), and elicited no change in immunoglobulin-associated beta (CD79b) and swine leukocyte antigen class II (SLA-DRA) expression levels, when compared to the sham-inoculated group. In contrast, all other treatments significantly upregulated CD79b and stimulated responses in other B-cell downstream genes. These findings suggest that B. pilosicoli does not elicit an immediate T-independent B-cell response, nor does it trigger antigen-presenting mechanisms. All other agents activated at least one trigger within the T-independent pathways, as well as peptide antigen presenting mechanisms. Future research is warranted to verify these findings in vivo.
猪痢疾、螺旋体性结肠炎和沙门氏菌病是对全球养猪业具有重要影响的限制生产的肠道疾病。尽管已经努力了几十年，但这些疾病的缓解仍然依赖于抗生素治疗。这三种病原体的一个常见知识空白是猪对感染的早期 B 细胞反应。因此，本研究旨在描述猪对博氏疏螺旋体、猪痢疾密螺旋体（毒力和非毒力株）、短螺旋体和肠炎沙门氏菌的 B 细胞反应，这些病原体是上述综合征的病原体。从杂交猪的淋巴瘤中衍生的永生化猪 B 细胞系与每种病原体、大肠杆菌脂多糖（LPS）和假接种物（n = 3/处理）共同孵育 8 小时。使用台盼蓝评估处理后 B 细胞的存活率，并使用逆转录定量 PCR 分析 B 细胞激活相关基因的表达水平。只有肠炎沙门氏菌和 LPS 导致 B 细胞死亡率增加。与假接种组相比，短螺旋体下调了 B 淋巴细胞抗原（CD19）、脾脏相关酪氨酸激酶（syk）、酪氨酸蛋白激酶（lyn）和肿瘤坏死因子-α（TNF-α），而免疫球蛋白相关β（CD79b）和猪白细胞抗原 II 类（SLA-DRA）的表达水平没有变化。相比之下，其他所有治疗方法都显著上调了 CD79b，并刺激了其他 B 细胞下游基因的反应。这些发现表明，短螺旋体不会引起立即的 T 细胞非依赖性 B 细胞反应，也不会触发抗原呈递机制。所有其他试剂至少激活了 T 细胞非依赖性途径以及肽抗原呈递机制中的一个触发因素。需要进一步的研究来验证这些发现是否在体内存在。
