Perdigón G, Vintiñi E, Alvarez S, Medina M, Medici M
Centro de Referencias para Lactobacilos (CERELA), Tucumán, Argentina.
J Dairy Sci. 1999 Jun;82(6):1108-14. doi: 10.3168/jds.S0022-0302(99)75333-6.
The induction of a mucosal immune response is not easy due to the development of oral tolerance, but under some conditions, bacteria can activate this immune system. Antigens administered orally can interact with M cells of Peyer's patches or bind to the epithelial cells. We have demonstrated that certain lactic acid bacteria are able to induce specific secretory immunity, and others will enhance the gut inflammatory immune response. The aim of this work was to establish the reason for these different behaviors and to define possible mechanisms involved in the interaction of lactic acid bacteria at the intestinal level. We studied IgA+ and IgM+ B cells comparatively in bronchus and intestine and CD4+ T cells and IgA anti-lactic acid bacteria antibodies in the intestinal fluid, induced by oral administration of Lactobacillus casei, Lb. delbrueckii ssp. bulgaricus, Lb. acidophilus, Lb. plantarum, Lb. rhamnosus, Lactococcus lactis, and Streptococcus salivarius ssp. thermophilus. The increase in the IgA+ B cells in the bronchus means that these lactic acid bacteria were able to induce the IgA cycle by interaction with M cells from Peyer's patches or intestinal epithelial cells. The IgM+ cells increased when the stimulus did not induce the switch from IgM+ to IgA+. The increase in the CD4+ cells suggests interaction of Peyer's patches and enhancement of the B- and T-cell migration. The anti-lactic acid bacteria antibody is related to the processing and presentation of the microorganisms to the immune cells. We demonstrated that Lb. casei and Lb. plantarum were able to interact with Peyer's patch cells and showed an increase in IgA-, CD4+ cells, and antibodies specific for the stimulating strain. Lactobacillus acidophilus induced gut mucosal activation by interaction with the epithelial cells without increase in the immune cells associated with the bronchus. Although Lb. rhamnosus and Strep. salivarius ssp. thermophilus interact with epithelial cells, they also induced an immune response against their epitopes. Lactococcus lactis and Lb. delbrueckii ssp. bulgaricus induced an increase of IgA+ cells entering the IgA cycle but not CD4+ cells; thus, these bacteria would have been bound to epithelial cells that activated B lymphocytes without processing and presenting of their epitopes. We did not determine specific antibodies against Lc. lactis or Lb. bulgaricus.
由于口服耐受的形成，诱导黏膜免疫反应并不容易，但在某些条件下，细菌可以激活这种免疫系统。口服给予的抗原可与派尔集合淋巴结的M细胞相互作用或与上皮细胞结合。我们已经证明，某些乳酸菌能够诱导特异性分泌免疫，而其他乳酸菌则会增强肠道炎症免疫反应。这项工作的目的是确定这些不同行为的原因，并确定乳酸菌在肠道水平相互作用中可能涉及的机制。我们比较研究了口服干酪乳杆菌、德氏保加利亚乳杆菌、嗜酸乳杆菌、植物乳杆菌、鼠李糖乳杆菌、乳酸乳球菌和嗜热链球菌后，支气管和肠道中的IgA+和IgM+ B细胞，以及肠道液中的CD4+ T细胞和抗乳酸菌抗体。支气管中IgA+ B细胞的增加意味着这些乳酸菌能够通过与派尔集合淋巴结的M细胞或肠道上皮细胞相互作用来诱导IgA循环。当刺激未诱导从IgM+向IgA+的转换时，IgM+细胞增加。CD4+细胞的增加表明派尔集合淋巴结的相互作用以及B细胞和T细胞迁移的增强。抗乳酸菌抗体与微生物向免疫细胞的加工和呈递有关。我们证明，干酪乳杆菌和植物乳杆菌能够与派尔集合淋巴结细胞相互作用，并显示出IgA-、CD4+细胞以及针对刺激菌株的特异性抗体增加。嗜酸乳杆菌通过与上皮细胞相互作用诱导肠道黏膜激活，而支气管相关免疫细胞没有增加。尽管鼠李糖乳杆菌和嗜热链球菌与上皮细胞相互作用，但它们也诱导了针对其表位的免疫反应。乳酸乳球菌和德氏保加利亚乳杆菌诱导进入IgA循环的IgA+细胞增加，但CD4+细胞未增加；因此，这些细菌可能已与激活B淋巴细胞但未加工和呈递其表位的上皮细胞结合。我们未测定针对乳酸乳球菌或保加利亚乳杆菌的特异性抗体。
