Abstract:Our results in infants in rural Japan support the hypothesis that a compositional difference in intestinal Bifidobacterium species may be associated with the development of allergy in early infancy, although the responsible species might vary among countries or races.
“…Annunziato et al [47] demonstrated that Th17 cells play critical roles in the pathogenesis of Crohn’s disease. The oral administration of LAB has been reported to improve the clinical symptoms of Crohn’s disease [48], suggesting that the suppression of CCL20 by LAB found in this study may reflect the mechanisms underlying this clinical observation, at least in part.…”
Background: Recently, some strains of lactic acid bacteria (LAB) have been reported to prevent the development of atopic dermatitis and to improve allergic symptoms, especially in young children. However, the mechanisms involved in these effects are not fully understood. Intestinal microbiota play critical roles in the development of host immune development and are recognized and regulated by the host through intestinal epithelial cells (IECs). We thus hypothesized that LAB influence the host immune system through the activation of IECs. To begin testing this hypothesis, chemokine expression in IECs exposed to intestinal bacteria was investigated. Methods: Caco-2 cell monolayers were stimulated with different concentrations of various live or heat-killed intestinal bacteria or bacterial components for up to 3 h. Changes in the gene expressions of various chemokines were measured using quantitative real-time PCR. Results: The expressions of CCL20, CXCL8, CXCL10 and CX3CL1 were strongly induced by nonpathogenic Escherichia coli in a dose-dependent manner and were partially induced by some commensal LAB. In contrast, Lactobacillus rhamnosus GG (LGG) and Lactobacillus casei did not induce these chemokine expressions. In addition, LGG significantly suppressed the expressions of CCL20 and CXCL10 induced by E. coli, peptidoglycan or flagellin when cultured simultaneously. Conclusions:LGG and L. casei markedly suppressed E. coli-induced chemokine expression, presumably through the suppression of the Toll-like receptor-mediated signal transduction pathway, at least in part. The clinical importance of this suppressive effect and the mechanisms involved require further investigation; however, such effects can be used as a marker to identify clinically useful LAB.
“…Annunziato et al [47] demonstrated that Th17 cells play critical roles in the pathogenesis of Crohn’s disease. The oral administration of LAB has been reported to improve the clinical symptoms of Crohn’s disease [48], suggesting that the suppression of CCL20 by LAB found in this study may reflect the mechanisms underlying this clinical observation, at least in part.…”
Background: Recently, some strains of lactic acid bacteria (LAB) have been reported to prevent the development of atopic dermatitis and to improve allergic symptoms, especially in young children. However, the mechanisms involved in these effects are not fully understood. Intestinal microbiota play critical roles in the development of host immune development and are recognized and regulated by the host through intestinal epithelial cells (IECs). We thus hypothesized that LAB influence the host immune system through the activation of IECs. To begin testing this hypothesis, chemokine expression in IECs exposed to intestinal bacteria was investigated. Methods: Caco-2 cell monolayers were stimulated with different concentrations of various live or heat-killed intestinal bacteria or bacterial components for up to 3 h. Changes in the gene expressions of various chemokines were measured using quantitative real-time PCR. Results: The expressions of CCL20, CXCL8, CXCL10 and CX3CL1 were strongly induced by nonpathogenic Escherichia coli in a dose-dependent manner and were partially induced by some commensal LAB. In contrast, Lactobacillus rhamnosus GG (LGG) and Lactobacillus casei did not induce these chemokine expressions. In addition, LGG significantly suppressed the expressions of CCL20 and CXCL10 induced by E. coli, peptidoglycan or flagellin when cultured simultaneously. Conclusions:LGG and L. casei markedly suppressed E. coli-induced chemokine expression, presumably through the suppression of the Toll-like receptor-mediated signal transduction pathway, at least in part. The clinical importance of this suppressive effect and the mechanisms involved require further investigation; however, such effects can be used as a marker to identify clinically useful LAB.
“…It is well documented that early bacterial colonization patterns are associated with antibody production in the gut (Suzuki et al, 2007), and that the variation of microbiota modestly influences the host gene expression (Rawls et al, 2006). However, there is little information regarding interaction between the host gene expression and the structure of gut microbiota.…”
The transition from a sterile gut environment to the development of microbiota in the newborns is not fully understood. The objective of this study was to investigate the impact of exposure to bacterial communities on the development of gut microbiota in the newly hatched chicken. A total of 90 as-hatched chicks were divided into three groups. Groups A and B were treated with inocula of the cecal origin, whereas group C was fed with sterile water. The major bacteria in Inoculum-I to treat group A included Bacteroides (20.7%), Lachnospiraceae (17.2%) and unclassified Ruminococcaceae (16.1%), whereas group B was introduced with Inoculum-II composed of Prevotella (37.9%), Acidaminococcus (16.1%) and Dorea (12.6%). Analyses of the ileal and cecal contents over a period of 15 days showed that Inoculum-I resulted in a higher rate of colonization than Inoculum-II, but the colonization was predominantly in the cecum. The influence of Inoculum-II on group B was similar to that of water on group C, showing only a marginal effect on colonization. Microarray analysis showed that each group presented a distinct pattern of gene expression in the ileum. In group A, the most obvious changes were noted in genes controlling the function of ion transport, cell cycle and chromosome maintenance, suggesting that the inocula influenced gene expression. Our findings indicate that initial exposure to different bacterial communities could lead to the development of distinct microbiota and gene expression in the gut. It is possible to manipulate the gut microbiota by feeding to a proper bacterial composition at an early age.
“…Evidence shows that probiotics induce several beneficial host responses by blocking pathogenic effects of invasive bacteria and inhibiting excessive responses in innate immunity, thus supporting intestinal epithelial cell homeostasis [2]. Cross-sectional/prospective cohort studies indicated that allergic children were less often colonized with Bifidobacterium than non-allergic children [3,4,5,6,7,8,9,10]. Recent clinical trials have suggested that probiotic bacteria decrease and prevent allergic symptoms, especially in atopic dermatitis [11,12].…”
Background: Recent studies suggest that probiotics alleviate pathophysiological processes of allergic diseases and inflammatory bowel diseases, whereas ‘non-probiotic’ microflora has negative effects. However, the underlying mechanisms are not well known, especially in relation to eosinophils, the major effector cells of these inflammatory diseases. Objective: To investigate the effects of probiotic Bifidobacterium bifidum (BB) on human eosinophil functions compared with pathogenic Clostridium difficile (CD). Methods: Peripheral human eosinophils were cultured with heat-killed BB or CD. FISH-labeled CD and BB were incubated with eosinophils visualized by confocal laser scanning microscopy. Superoxide generation and degranulation of eosinophils were measured with the cytochrome c reduction method and the eosinophil-derived neurotoxin (EDN) release assay, respectively. Results: Confocal microscopy revealed that Cy3-labeled CD and BB were apparently ingested by eosinophils. Both bacteria induced minimal superoxide generation. However, CD elicited significantly higher EDN release than BB. GM-CSF significantly enhanced EDN release by CD but not by BB. Bacterial-induced EDN release was calcium dependent. Conclusion: The beneficial effect of probiotic BB might be explained, at least in part, by its ability to decrease EDN release from eosinophils compared with ‘pathogenic’ CD.
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