Po Ching Cheng

The immunomodulatory effects of lactic acid bacteria for improving immune functions and benefits

Probiotics have a number of beneficial health effects in humans and animals, such as reducing lactose intolerance symptoms and enhancing the bioavailability of nutrients. Probiotics help regulate intestinal microflora and immunomodulatory properties. Probiotics also decrease the prevalence of allergies in susceptible individuals, inhibit the inflammatory responses in the gut, and have antagonistic effects against intestinal and food-borne pathogens. Bacteria typically colonize the intestinal tract first and then reinforce the host defense systems by inducing generalized mucosal immune responses, including modulation of DC/NK interaction, a balanced T-helper cell response, self-limited inflammatory response, and the secretion of polymeric IgA. A lot of reports showed that lactic acid bacteria (LAB) as Lactobacillus and Bifidobacterium and their fermented products are effective at enhancing innate and adaptive immunity, prevent gastric mucosal lesion development, alleviate allergies, and put up defense against intestinal pathogen infection. In this review paper, we compared the influence of immunomodulatory effects on the function and efficacy of lactobacillus products with different strains. We also discuss the beneficial effects of several LAB strain and its derivative products for human immunity and related diseases.

Anti-obesity effects of gut microbiota are associated with lactic acid bacteria

The prevalence of obesity is rapidly becoming endemic in industrialized countries and continues to increase in developing countries worldwide. Obesity predisposes people to an increased risk of developing metabolic syndrome. Recent studies have described an association between obesity and certain gut microbiota, suggesting that gut microbiota might play a critical role in the development of obesity. Although probiotics have many beneficial health effects in humans and animals, attention has only recently been drawn to manipulating the gut microbiota, such as lactic acid bacteria (LAB), to influence the development of obesity. In this review, we first describe the causes of obesity, including the genetic and environmental factors. We then describe the relationship between the gut microbiota and obesity, and the mechanisms by which the gut microbiota influence energy metabolism and inflammation in obesity. Lastly, we focus on the potential role of LAB in mediating the effects of the gut microbiota in the development of obesity.

Time-dependent persistence of enhanced immune response by a potential probiotic strain Lactobacillus paracasei subsp. paracasei NTU 101

The possible time-dependent role of lactic acid bacteria (LAB) in immunomodulation was investigated in BALB/c mice fed daily with Lactobacillus paracasei subsp. paracasei NTU 101 (10(8) colony forming units) for 3, 6, and 9 weeks, and following feeding with Lactobacillus-free food for a further 7 days. We observed up-regulation of the antigen-presenting ability of dendritic cells, and expression of natural killer group-2 D (NKG2D) molecules capable of trigger natural killer cell-mediated cytotoxicity. Lymphocyte proliferation and antibody production were also significantly increased in mice after treatment. Innate and adaptive immunity remained constant even at the most protracted feeding time, indicative of the time dependence of the bacterial-mediated enhanced immunity. To better correlate intestinal microflora with immunity, the intestinal contents of probiotics and harmful microorganisms were determined. Results showed an altered intestinal microflora, with increases in bifidobacteria and lactobacilli and a decreased content of Clostridium perfringens after feeding with L. paracasei subsp. paracasei NTU 101. It is possible that persistent activation of immunity might be induced by intestinal probiotics.

Immunomodulating activity of lactobacillus paracasei subsp. paracasei NTU 101 in enterohemorrhagic escherichia coli O157H7-infected mice

The present study investigated the immunomodulating activity of Lactobacillus paracasei subsp. paracasei NTU 101 in enterohemorrhagic Escherichia coli O157:H7-infected BALB/c mice. Mice were given L. paracasei subsp. paracasei NTU 101 (10(8) colony-forming units) for 7 days, before and after the challenge with E. coli O157:H7. Feeding Lactobacillus for 7 days resulted in an increased postchallenge weight gain and lower cumulative morbidity rates. We observed the upregulation of dendritic cells, helper T cell activation, and antibody production in post- and pretreated mice, compared with untreated mice in the E. coli O157:H7 infection group. Moreover, Lactobacillus can down-regulate the expression of toll-like receptors (TLRs) on macrophages and proinflammatory cytokines, and chemokines in the post- or prefeeding mice induce by E. coli O157:H7 infection. These results demonstrated the inhibition of inflammation among the mice in the pretreated group than in the post-treated group by modulating their immune response. These findings suggest that L. paracasei subsp. paracasei NTU 101 may be an effective candidate for use as a probiotic in the prevention of infection caused by E. coli O157:H7 in humans.

Effect of the administration of Lactobacillus paracasei subsp paracasei NTU 101 on Peyer's patch-mediated mucosal immunity

The role of lactic acid bacteria in gut mucosal immunity was investigated by comparing the enhanced effects in the Peyers patches and spleen of BALB/c mice fed daily with Lactobacillus paracasei subsp. paracasei NTU 101 for 3 to 9 weeks. After feeding with Lactobacillus, the percentage of CD4+ T cells in both Peyers patches and the spleen was significantly increased; however, expression of CD 154 molecules, which play a pivotal role in cell-to-cell communication, on CD4+ T cells and the percentage of B220+ B cells increased only in Peyers patches. Compared with systemic serum IgA, Peyers patch-derived immunomodulation induced higher levels of intestinal IgA+-producing cells in the lamina propria. Our data also showed that feeding with Lactobacillus induced stronger CD4+ T cell-dendritic cell interaction, enhanced CD4+ T cell and B cell proliferation, and increased IL-1beta, IL-10, IL-12, IFN-gamma, and TNF-alpha mRNA expression in Peyers patches, but not in the spleen. Here, we demonstrate that following Lactobacillus treatment, Peyers patches exhibited a more distinct capacity to induce CD4+ T cell-dendritic cell interactions, lymphocyte proliferation, and cytokine secretion than the spleen, and thereby promoted greater intestinal IgA production that could enhance immunosurveillance to prevent intestinal infections or other intestinal pathologies.

Evaluation of recombinant fructose-1,6-bisphosphate aldolase ELISA test for the diagnosis of Schistosoma japonicum in water buffaloes.

Fructose-1,6-bisphosphate aldolase (FBPA) is an ubiquitous enzyme essential for glycolysis, gluconeogenesis and the Calvin cycle. It has been demonstrated to induce immune responses and to be useful in the immunodiagnosis of malaria. In this study, FBPA was cloned from the adult worms of Schistosoma japonicum and tested as an antigen for the diagnosis of S. japonicum infection in water buffaloes. Enzyme-linked immunosorbent assay (ELISA) was performed on the sera from 32 infected water buffaloes and 20 negative controls using the recombinant FBPA protein or soluble worm antigen preparation (SWAP) as an antigen. The OD cut-off values were determined to be 0.57 with 100% specificity and 100% sensitivity for the FBPA ELISA and 1.13 with 93.8% specificity and 95.0% sensitivity for the SWAP ELISA. These findings indicate that the recombinant FBPA of S. japonicum should be an useful diagnostic tool for the detection of antibodies against S. japonicum.

Triggering receptor expressed on myeloid cells (TREM)-1 participates in Schistosoma mansoni inflammatory responses

Inflammatory responses to microbial products are amplified by a pathway mediated by triggering a receptor expressed on the myeloid cells (TREM)‐1. Relatively a few studies have been performed to investigate the role of TREM‐1 in macrophage activation in response to parasitic infection. In this study, we delineate the role of the innate immunoreceptor TREM‐1 in the parasite Schistosoma mansoni infection model from early to late (chronic) phases of infection. Flow cytometry analysis revealed gradual increase in the production of TREM‐1 protein on CD11b+ myeloid cells, with maximum production at 5 weeks p.i. Similar results in the pattern of TREM‐1 mRNA expressions in splenic CD11b+ cells from infected mice were obtained by real‐time PCR. However, unlike in spleen, the TREM‐1 mRNA expression in liver tissue showed no significant increase throughout the infection, including periods of maximum production of parasite eggs. Administration of schistosoma egg homogenate antigen to stimulate J774A.1 cells inhibited TREM‐1 expression on the surface, indicating that some substances of the Schistosma eggs may inhibit the expression of TREM‐1 on macrophages, lowering the macrophage‐mediated inflammatory response of infected hosts.

Evaluating the potential of a new isotope-labelled glyco-ligand for estimating the remnant liver function of schistosoma-infected mice

A new glyco‐derivative compound (OCTAM) was developed and labelled with isotope to form 188Re‐OCTAM as a candidate nuclear medicine imaging agent for testing the liver function. We evaluated the potential of isotope‐labelled OCTAM for estimating the remnant liver function in vitro and in vivo schistosoma‐infected mice. The affinity of OCTAM to liver asialoglycoprotein receptors (ASGPR) was assessed by competitive inhibition assay in vitro. In vivo assessments were performed to score the remnant liver function in mice at different schistosomal infection stages. OCTAM binds specifically to ASGPR and showed competitive inhibition of anti‐ASGPR antibody binding to hepatocytes, and was higher than that of other galactosyl ligands. Micro‐SPECT/CT images of uninfected mice revealed strong liver uptake. Quantified serial images of mice infected for 9, 12 and 18 weeks showed delayed liver uptake, and the retention of uptake was inversely correlated with stage and grade of schistosoma infection. Pathological and biochemical analysis demonstrated that gradually accumulating liver injury caused by infection significantly influenced uptake of 188Re‐OCTAM. Hepatic ASGPR expression diminished only in the chronic infection stage. This study demonstrated that the isotope‐labelled OCTAM could accumulate in the liver, might have potential as an imaging agent for in vivo hepatic function evaluation of schistosomiasis.