Saccharomyces Boulardii and the No-Knead Bread Recipe
Jacob Schor ND, FABNO
December 1, 2009
The French scientist Henri Boulard is credited with isolating Saccharomyces boulardii from lychee and mangosteen fruits in 1923. Boulard had observed people chewing lychee and mangosteen skins in order to control cholera symptoms.
This particular strain of yeast, obviously native to the tropics, is related to but is distinct from standard baker’s yeast, Saccharomyces cerevisiae. S. Boulardii has become popular as a nutritional supplement in recent years and though a yeast is still often called a probiotic; like acidophilus bacteria, it also maintains and restores normal flora to the small and large intestine and improves immune function. S. boulardii will quickly colonize the gut within three days of consumption but it doesn’t survive in the intestines very long; it will be completely gone in about five days. In the process though it appears to crowd out other unwanted bacteria and yeast. Probably because it is a tropical yeast, it only grows at a relatively high temperature of 37°C.
The National Library of Medicine’s search engine, PubMed, currently lists 302 papers on S. boulardii, far more than you want to read about here. Sorting through them, six main effects S. boulardii are described:
- Protection against gut pathogens
- Moderation of immune responses
- Decreased inflammation
- Inhibition of bacterial toxin action
- Enhanced function of gut enzymes and nutrient transport mechanisms.
- Increases gut immunoglobulin, secretory IgA.
Let’s just look at some studies published in the past year. A paper from Spring 2009, discussed the mechanisms by which S. Boulardii improves digestive function. Two papers published in early summer 2009 describe using S. boulardii to treat children with amebic dysentery in combination with the drug metronidazole. The first in the Turkish Journal of Pediatrics found it safe to use in children. The second reported that the combination of drug and yeast significantly shortened the time to recovery. The big uses up to this time had been to treat travelers diarrhea and antibiotic caused diarrhea and gastritis. The same team of Turks had published an article a few months earlier, in March, suggesting the use of S. boulardii in treating acute pancreatitis because it decreases bacterial translocation and lung injury. Another June article describes a well-known use for S. Boulardii, treating Clostridium difficile infections. Even the Merck Manual recommends S. boulardii for this use. Harvard researchers had a paper published in September describing the mechanisms by which S. Boulardii may prevent colon cancer. Another paper tells us this yeast decreases mucositis and other damage caused by the chemotherapy drug irinotecan; we probably should consider using it more often with cancer patients. A very recent paper, December 2009, describes how S. Boulardii inhibits the growth of Candida albicans and also decreases the virulence, that is the nastiness, of this often-problematic yeast. Another paper, this one from UCLA published in October 2009, describes S. Boulardii’s anti inflammatory effects as an explanation for why it is useful in treating inflammatory bowel disease.
One of the main fascinations with this yeast is that it appears to calm down hyperactive immune function. In an April paper German researchers explain how S. boulardii decreases the secretion of key pro-inflammatory cytokines such as tumor necrosis factor-alpha and interleukin (IL)-6 while increasing of anti-inflammatory IL-10. S. boulardii also inhibits the proliferation of naive T-cells and modulates dendritic cells.
I took Latin in high school and never learned French. This is my excuse for the many years that I misunderstood what this yeast was. I mistakenly thought the word boulardii had something to do with the French word, ‘Boulan,’ which means, ‘Bakery.’ Thus I mistakenly assumed that S. boulardii was a form of baker’s yeast.
Under this false impression, I conducted an interesting experiment last week. I used S. boulardii to bake bread.
Over the past three years there has been a quiet revolution in home baking over a ‘new’ recipe for ‘No Knead Bread.’ I came late to the party but over the past month have been catching up, churning out these ‘no-knead’ loaves regularly. Most of the breads have emerged tasting so good that I’m dumbfounded. Mark Bittman of the New York Times wrote about this recipe in November 2006: it was my first exposure to this business. It’s worth reading his article and then following the link to watch a demonstration on YouTube:
Anyways, under the delusion that S. boulardii was just overpriced baker’s yeast, I opened a few capsules and used it as my baking yeast last week. It certainly does need high temperatures to grow; at room temperature it did nothing, in fact I thought it was dead, but when the dough was left to rise on the hot radiator, it woke up and rose rapidly. It created an excellent loaf structurally. Admittedly though the flavors were not as well developed as those achieved using S. cervesiae, regular baker’s yeast. Still it worked surprisingly well all things considered.
Obviously by the time bread is fully baked and comes out of the oven, the yeast inside it is quite dead. Yet could my no-knead ‘Boulardii Boulan’ still have some health benefits?
There are studies on other strains of probiotic organisms suggesting they are of benefit whether the bugs are, ‘dead or alive.’ One example is VSL #3, a high dose strain of lactobacilli sold in pharmacies and used to treat ulcerative colitis. A study done by Italian researchers and published Summer 2009 examined the effects of VSL #3 on immune function especially focusing on immune-modulation and how T-helper cells were affected.
In this study, dead VSL #3 worked just as well as the live bugs did. There was a similar study several years ago but I can’t find it at the moment. Research interest on VSL #3 appears to be pretty hot. There are more than a dozen new papers in the last 12 months. I’ve used VSL #3 for making homemade yogurt. Another one of those home experiments I am prone to trying. It worked, but like my boulardii bread, it wasn’t the best tasting yogurt ever eaten. Still, it probably had health benefits above and beyond store bought yogurt.
Here’s the VSL #3 company’s website: http://www.vsl3.com/about.asp
The company does not appear to be updating their website with this newly published research. Amazingly even Wikipedia doesn’t have an entry for VSL #3. Whoever is in charge of marketing this product must be slacking off.
There is an interesting article in the October 2009 issue of In Focus a newsletter put out by a supplement company. Admittedly not peer reviewed but interesting nonetheless. You’ll notice that some of my information in this article was copied from their article on Saccharomyces boulardii on page 10. What’s more interesting though is the protocol suggested by Michael Ash on page 2 for treating Atypical Depression. He has a theory that many cases of depression are triggered by inflammatory cytokines triggered by atypical gut flora. He suggests S. boulardii as the first phase of treatment in restoring normal gut function and treating this variant of depression. I’ve just about finished eating my loaf of no-knead ‘boulardii bread.’ I don’t think I’m feeling any happier yet. Still this might be an interesting way to increase Secretory IgA and do all sorts of other nifty things to improve one's health. This could be some real Wonder Bread.
That In Focus newsletter is available at:
Here’s the recipe from the New York Times for No-Knead Bread:
Published: November 8, 2006
Adapted from Jim Lahey, Sullivan Street Bakery
Time: About 1½ hours plus 14 to 20 hours’ rising
3 cups all-purpose or bread flour, more for dusting
¼ teaspoon instant yeast
1¼ teaspoons salt
Cornmeal or wheat bran as needed.
1. In a large bowl combine flour, yeast and salt. Add 1 5/8 cups water, and stir until blended; dough will be shaggy and sticky. Cover bowl with plastic wrap. Let dough rest at least 12 hours, preferably about 18, at warm room temperature, about 70 degrees.
2. Dough is ready when its surface is dotted with bubbles. Lightly flour a work surface and place dough on it; sprinkle it with a little more flour and fold it over on itself once or twice. Cover loosely with plastic wrap and let rest about 15 minutes.
3. Using just enough flour to keep dough from sticking to work surface or to your fingers, gently and quickly shape dough into a ball. Generously coat a cotton towel (not terry cloth) with flour, wheat bran or cornmeal; put dough seam side down on towel and dust with more flour, bran or cornmeal. Cover with another cotton towel and let rise for about 2 hours. When it is ready, dough will be more than double in size and will not readily spring back when poked with a finger.
4. At least a half-hour before dough is ready, heat oven to 450 degrees. Put a 6- to 8-quart heavy covered pot (cast iron, enamel, Pyrex or ceramic) in oven as it heats. When dough is ready, carefully remove pot from oven. Slide your hand under towel and turn dough over into pot, seam side up; it may look like a mess, but that is O.K. Shake pan once or twice if dough is unevenly distributed; it will straighten out as it bakes. Cover with lid and bake 30 minutes, then remove lid and bake another 15 to 30 minutes, until loaf is beautifully browned.
Cool on a rack.
Yield: One 1½-pound loaf.
J Clin Microbiol. 2005 Mar;43(3):1133-7.
Typing of Saccharomyces cerevisiae clinical strains by using microsatellite sequence polymorphism.
Malgoire JY, Bertout S, Renaud F, Bastide JM, Mallié M.
Laboratoire de Parasitologie et Mycologie Médicale, MNERT EA 2413, Faculté de Pharmacie, Université de Montpellier I, 15 Av. Charles Flahault, B.P. 14 491, 34093 Montpellier cedex 5, France.
It seems that S. cerevisiae, which was thought for about 30 years to be a nonpathogenic yeast, should now be considered an opportunistic pathogen. In this study, we estimated the discrimination ability of the microsatellite sequence amplification technique within a sample of clinical and reference S. cerevisiae strains and S. boulardii reference strains.
Acta Gastroenterol Belg. 2009 Apr-Jun;72(2):274-6.
The probiotic Saccharomyces boulardii upgrades intestinal digestive functions by several mechanisms.
Turk J Pediatr. 2009 May-Jun;51(3):220-4.
Efficacy and safety of Saccharomyces boulardii in amebiasis-associated diarrhea in children.
Sava?-Erdeve S, Gökay S, Dallar Y.
Department of Pediatrics, Ankara Training and Research Hospital, Ankara, Turkey.
The efficacy and safety of adding Saccharomyces boulardii to antibiotic treatment for amebiasis-associated acute diarrhea in children were assessed in this study. Forty-five children in Group I received only metronidazole per oral for 10 days while 40 patients in Group II received S. boulardii in addition to the same medication. The major outcomes investigated were duration of acute and bloody diarrhea, frequency and consistency of stools, resolution time of the symptoms, and the tolerance and side effects of the treatment regimens. The median duration of acute diarrhea was 5 (1-10) days in Group I and 4.5 (1-10) days in Group II (p=0.965). The median number of stools on follow-up and duration of bloody diarrhea, fever, abdominal pain and vomiting were similar in the two groups. S. boulardii was well tolerated by the children and no side effects were recorded. Addition of S. boulardii to antibiotic treatment of amebiasis-associated acute diarrhea in children does not seem to be more effective than metronidazole treatment alone.
Am J Trop Med Hyg. 2009 Jun;80(6):953-5.
Clinical efficacy of Saccharomyces boulardii and metronidazole compared to metronidazole alone in children with acute bloody diarrhea caused by amebiasis: a prospective, randomized, open label study.
Dinleyici EC, Eren M, Yargic ZA, Dogan N, Vandenplas Y.
Eskisehir Osmangazi University Faculty of Medicine, Department of Pediatrics, Eskisehir, Turkey. email@example.com
The aim was to evaluate the efficacy of Saccharomyces boulardii (Sb) in addition to metronidazole in amebiasis. A prospective, randomized, open clinical trial was performed in 50 children presenting with acute bloody diarrhea caused by Entameba histolytica. Group A and B (each N = 25) was treated with metronidazole, but Sb (250 mg, twice daily) during the 7 days was added to Group B patients who were re-evaluated 2, 3, 5, 10, and 30 days after diagnosis. Duration of bloody diarrhea was significantly longer in Group A (72.0 +/- 28.5 versus 42.2 +/- 17.4 hours, P < 0.001). On day 5, amebic cysts had disappeared in all children in Group B, whereas in Group A, amebic cysts were still present in 6 children (P < 0.05). On day 10, all children were cured and cysts had disappeared in all. The addition of Sb to metronidazole in amebiasis significantly decreases duration of (bloody) diarrhea and enhances clearance of cysts.
Eur J Pediatr. 2009 Mar;168(3):253-65. Epub 2008 Dec 19.
Saccharomyces boulardii in childhood.
Vandenplas Y, Brunser O, Szajewska H.
Universitair Ziekenhuis Kinderen Brussel, Vrije Universiteit Brussel, Laarbeekl 101, 1090, Brussels, Belgium. Yvan.Vandenplas@uzbrussel.be
INTRODUCTION: Probiotics are live microorganisms which confer a health benefit on the host. Saccharomyces boulardii, a yeast, has been found to be an effective probiotic in double-blind placebo-controlled randomized clinical studies. MATERIALS AND METHODS: We reviewed the established mechanisms of actions and clinical efficacy in children of S. boulardii. CONCLUSIONS: The mechanisms of action of S. boulardii depend mainly on the inhibition of some bacterial toxins, anti-inflammatory effects, and on stimulating effects on the intestinal mucosa such as trophic effects on the brush border enzymes and immunostimulatory effects. At present, in pediatric populations, there is evidence that S. boulardii is beneficial for the treatment of acute gastroenteritis and the prevention of antibiotic-associated diarrhea. More data are needed in other indications such as traveller's diarrhea, Helicobacter pylori eradication, and inflammatory bowel disease. S. boulardii is a yeast strain that has been extensively studied in vitro and in vivo. Recent data have opened the door for new therapeutic indications.
J Surg Res. 2009 Mar 9. [Epub ahead of print]
Probiotic Agent Saccharomyces boulardii Reduces the Incidenceof Lung Injury in Acute Necrotizing Pancreatitis Induced Rats.
Karen M, Yuksel O, Akyürek N, Ofluo?lu E, Ca?lar K, Sahin TT, Pa?ao?lu H, Memi? L, Akyürek N, Bostanc? H.
Department of Surgery, Gazi University Medical School, Ankara, Turkey.
BACKGROUND: Acute necrotizing pancreatitis is a severe acute inflammatory disease of the pancreas that can lead to extrapancreatic organ involvement. Supervening lung injury is an important clinical entity determining the prognosis of the patient. Probiotics are dietary supplements known to reduce or alter inflammation and inflammatory cytokines. In the present study, we hypothesize that probiotics may reduce lung injury by reducing bacterial translocation, which results in reduced infection, inflammation, and generation of proinflammatory cytokines in an experimental model of acute necrotizing pancreatitis. METHODS: Pancreatitis was induced by concomitant intravenous infusion of cerulein and glycodeoxycholic acid infusion into the biliopancreatic duct. Saccharomyces boulardii was used as the probiotic agent. Rats were divided into three groups: sham, pancreatitis-saline, which received saline via gavage at 6 and 24 h following the pancreatitis, pancreatitis-probiotics, which received probiotics via gavage method at 6 and 24 h following the pancreatitis. The rats were sacrificed at 48 h, venous blood, mesenteric lymph node, pancreatic and lung tissue samples were obtained for analysis. RESULTS: Serum pancreatic amylase, lactate dehydrogenase, secretory phospholipase A(2), and IL-6 were found to be increased in pancreatitis-saline group compared with the other groups (P < 0.05). Histological analyses revealed that edema, inflammation, and vacuolization as well as polymorphonuclear leukocyte infiltration in the lung tissue was significantly reduced in the probiotic treated group. Bacterial translocation was significantly reduced in the probiotic treated group compared with the other groups (P < 0.05). CONCLUSION: These results suggest that Saccharomyces boulardii reduce the bacterial translocation. As a result of this, reduced proinflammatory cytokines and systemic inflammatory response was observed, which may be the reason underlying reduced lung injury in acute necrotizing pancreatitis.
J Infect. 2009 Jun;58(6):403-10. Epub 2009 Apr 5.
Recurrent Clostridium difficile infection: a review of risk factors, treatments, and outcomes.
Infectious Disease Section, Loyola University Medical Center, Stritch School of Medicine, Maywood, IL 60153, USA. firstname.lastname@example.org
Episodes of recurrent Clostridium difficile infection (CDI) are difficult to treat for several reasons. Foremost, data are lacking to support any particular treatment strategy. In addition, treatment of recurrent episodes is not always successful, and repeated, prolonged treatment is often necessary. Identification of subgroups at risk for recurrent CDI may aid in diagnosing and treating these patients. Two likely mechanistic factors increasing the risk of recurrent CDI are an inadequate immune response to C. difficile toxins and persistent disruption of the normal colonic flora. Important epidemiologic risk factors include advanced age, continuation of other antibiotics, and prolonged hospital stays. Current guidelines recommend that the first recurrent episode be treated with the same agent (i.e., metronidazole or vancomycin) used for the index episode. However, if the first recurrence is characterized as severe, vancomycin should be used. A reasonable strategy for managing a subsequent episode involves tapering followed by pulsed doses of vancomycin. Other potentially effective strategies for recurrent CDI include vancomycin with adjunctive treatments, such as Saccharomyces boulardii, rifaximin "chaser" therapy after vancomycin, nitazoxanide, fecal transplantation, and intravenous immunoglobulin. New treatment agents that are active against C. difficile, but spare critical components of the normal flora, may decrease the incidence of recurrent CDI.
Gastroenterology. 2009 Sep;137(3):914-23. Epub 2009 May 29.
Saccharomyces boulardii inhibits EGF receptor signaling and intestinal tumor growth in Apc(min) mice.
Chen X, Fruehauf J, Goldsmith JD, Xu H, Katchar KK, Koon HW, Zhao D, Kokkotou EG, Pothoulakis C, Kelly CP.
Division of Gastroenterology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA.
BACKGROUND & AIMS: Saccharomyces boulardii (Sb) is a probiotic yeast with anti-inflammatory and anti-microbial activities and has been used for decades in the prevention and treatment of a variety of human gastrointestinal disorders. We reported previously that Sb modulates host inflammatory responses through down-regulation of extracellular signal-regulated kinase (Erk)1/2 activities both in vitro and in vivo. The aim of this study was to identify upstream mediators responsible for extracellular signal-regulated kinase (Erk)1/2 inactivation and to examine the effects of Sb on tumor development in Apc(Min) mice. METHODS: Signaling studies of colon cancer cells were done by western blot. Cell proliferation was measured by MTS and BrdU assay. Apoptosis was examined by flow cytometry, tunel assay and caspase assay. Apc(Min) mice were orally given Sb for 9 weeks before sacrifice for tumor analysis. RESULTS: We found that the epidermal growth factor receptor (EGFR) was deactivated upon exposure to Sb, leading to inactivation of both the EGFR-Erk and EGFR-Akt pathways. In human colonic cancer cells, Sb prevented EGF-induced proliferation, reduced cell colony formation, and promoted apoptosis. HER-2, HER-3, and insulin-like growth factor-1 receptor were also found to be inactivated by Sb. Oral intake of Sb reduced intestinal tumor growth and dysplasia in C57BL/6J Min/+ (Apc(Min)) mice. CONCLUSIONS: Thus, in addition to its anti-inflammatory effects, Sb inhibits EGFR and other receptor tyrosine kinase signaling and thereby may also serve a novel therapeutic or prophylactic role in intestinal neoplasia.
PMID: 19482027 [PubMed - indexed for MEDLINE]
Med Oncol. 2009;26(3):350-7. Epub 2008 Dec 9.
The effect of Saccharomyces boulardii on reducing irinotecan-induced intestinal mucositis and diarrhea.
Sezer A, Usta U, Cicin I.
Department of General Surgery, Faculty of Medicine, Trakya University, Edirne, Turkey.
To investigate the efficiency of Saccharomyces boulardii on irinotecan-induced mucosal damage and diarrhea in rats, fifty rats were randomized into three groups with 20 rats in two study groups and 10 rats in the control group. Control group did not receive any treatment. Irinotecan (60 mg/kg) alone was administered intravenously once a day for four consecutive days to the rats of Group A. Throughout the experiment, Group B rats were additionally given Saccharomyces boulardii (800 mg/kg) for 3 days before administration of irinotecan and 7 days throughout the experiment. Delayed diarrhea was more severe in Group A than Group B (P = 0.009). The weight loss was 34.7 +/- 3.8 mg for Group A, while it was 17.4 +/- 1.7 mg for Group B (P < 0.001). Findings of mucositis most clearly appeared in the jejunum. Regarding edema (P = 0.003), leukocyte migration (P = 0.038), and inflammation (P = 0.006) significant recovery was detected in the mucosa of rats receiving Saccharomyces boulardii. Villous thickness was significantly greater in Group A than Group B (P < 0.001). The results indicate that Saccharomyces boulardii provided significant improvement in irinotecan-induced diarrhea and mucositis.
FEMS Yeast Res. 2009 Dec;9(8):1312-21. Epub 2009 Aug 5.
The antagonistic effect of Saccharomyces boulardii on Candida albicans filamentation, adhesion and biofilm formation.
Krasowska A, Murzyn A, Dyjankiewicz A, ?ukaszewicz M, Dziadkowiec D.
Faculty of Biotechnology, Wroc?aw University, Wroc?aw, Poland.
The dimorphic fungus Candida albicans is a member of the normal flora residing in the intestinal tract of humans. In spite of this, under certain conditions it can induce both superficial and serious systemic diseases, as well as be the cause of gastrointestinal infections. Saccharomyces boulardii is a yeast strain that has been shown to have applications in the prevention and treatment of intestinal infections caused by bacterial pathogens. The purpose of this study was to determine whether S. boulardii affects the virulence factors of C. albicans. We demonstrate the inhibitory effect of live S. boulardii cells on the filamentation (hyphae and pseudohyphae formation) of C. albicans SC5314 strain proportional to the amount of S. boulardii added. An extract from S. boulardii culture has a similar effect. Live S. boulardii and the extract from S. boulardii culture filtrate diminish C. albicans adhesion to and subsequent biofilm formation on polystyrene surfaces under both aerobic and microaerophilic conditions. This effect is very strong and requires lower doses of S. boulardii cells or concentrations of the extract than serum-induced filamentation tests. Saccharomyces boulardii has a strong negative effect on very important virulence factors of C. albicans, i.e. the ability to form filaments and to adhere and form biofilms on plastic surfaces.
Aliment Pharmacol Ther. 2009 Oct 15;30(8):826-33. Epub 2008 Jul 23.
Review article: anti-inflammatory mechanisms of action of Saccharomyces boulardii.
Division of Digestive Diseases, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, CA 90095, USA. email@example.com
BACKGROUND: Saccharomyces boulardii, a well-studied probiotic, can be effective in inflammatory gastrointestinal diseases with diverse pathophysiology, such as inflammatory bowel disease (IBD), and bacterially mediated or enterotoxin-mediated diarrhoea and inflammation. AIM: To discuss the mechanisms of action involved in the intestinal anti-inflammatory action of S. boulardii. METHODS: Review of the literature related to the anti-inflammatory effects of this probiotic. RESULTS: Several mechanisms of action have been identified directed against the host and pathogenic microorganisms. S. boulardii and S. boulardii secreted-protein(s) inhibit production of proinflammatory cytokines by interfering with the global mediator of inflammation nuclear factor kappaB, and modulating the activity of the mitogen-activated protein kinases ERK1/2 and p38. S. boulardii activates expression of peroxisome proliferator-activated receptor-gamma (PPAR-gamma) that protects from gut inflammation and IBD. S. boulardii also suppresses 'bacteria overgrowth' and host cell adherence, releases a protease that cleaves C. difficile toxin A and its intestinal receptor and stimulates antibody production against toxin A. Recent results indicate that S. boulardii may interfere with IBD pathogenesis by trapping T cells in mesenteric lymph nodes. CONCLUSIONS: The multiple anti-inflammatory mechanisms exerted by S. boulardii provide molecular explanations supporting its effectiveness in intestinal inflammatory states.
Clin Exp Immunol. 2009 Apr;156(1):78-87. Epub 2009 Jan 21.
Saccharomyces boulardii inhibits lipopolysaccharide-induced activation of human dendritic cells and T cell proliferation.
Thomas S, Przesdzing I, Metzke D, Schmitz J, Radbruch A, Baumgart DC.
Department of Medicine, Division of Gastroenterology and Hepatology, Charité Medical Center-Virchow Hospital, Medical School of the Humboldt-University of Berlin, Berlin, Germany.
Saccharomyces boulardii (Sb) is a probiotic yeast preparation that has demonstrated efficacy in inflammatory and infectious disorders of the gastrointestinal tract in controlled clinical trials. Although patients clearly benefit from treatment with Sb, little is known on how Sb unfolds its anti-inflammatory properties in humans. Dendritic cells (DC) balance tolerance and immunity and are involved critically in the control of T cell activation. Thus, they are believed to have a pivotal role in the initiation and perpetuation of chronic inflammatory disorders, not only in the gut. We therefore decided to investigate if Sb modulates DC function. Culture of primary (native, non-monocyte-derived) human myeloid CD1c+CD11c+CD123(-) DC (mDC) in the presence of Sb culture supernatant (active component molecular weight < 3 kDa, as evaluated by membrane partition chromatography) reduced significantly expression of the co-stimulatory molecules CD40 and CD80 (P < 0.01) and the DC mobilization marker CC-chemokine receptor CCR7 (CD197) (P < 0.001) induced by the prototypical microbial antigen lipopolysaccharide (LPS). Moreover, secretion of key proinflammatory cytokines such as tumour necrosis factor-alpha and interleukin (IL)-6 were notably reduced, while the secretion of anti-inflammatory IL-10 increased. Finally, Sb supernatant inhibited the proliferation of naive T cells in a mixed lymphocyte reaction with mDC. In summary, our data suggest that Sb may exhibit part of its anti-inflammatory potential through modulation of DC phenotype, function and migration by inhibition of their immune response to bacterial microbial surrogate antigens such as LPS.
Int Arch Allergy Immunol. 2009;150(2):133-43. Epub 2009 May 11.
Effects of live and inactivated VSL#3 probiotic preparations in the modulation of in vitro and in vivo allergen-induced Th2 responses.
Mastrangeli G, Corinti S, Butteroni C, Afferni C, Bonura A, Boirivant M, Colombo P, Di Felice G.
Department of Infectious, Parasitic and Immune-Mediated Diseases, Istituto Superiore di Sanità, Rome, Italy.
BACKGROUND: The immunological mechanisms responsible for the immunomodulatory and anti-allergic effects of probiotic bacteria are still poorly defined. The combined effects of mixtures of different species of probiotic bacteria have been explored only in part. The present study describes the immunomodulatory activity of the VSL#3 probiotic preparation in in vitro and in vivo systems. METHODS: The activation and cytokine production by in vitro probiotic-stimulated bone-marrow dendritic cells (BM-DCs) and spleen cells isolated from naïve or Par j 1-sensitized mice were investigated. Mice were intranasally administered a sonicate preparation of VSL#3 before immunization with rPar j 1. Serum antibody levels and cytokine expression in the lung were determined. RESULTS: Both live and sonicated VSL#3 preparations induced maturation and cytokine production by BM-DCs. Cytokine production by spleen cells from naïve or Par j 1-sensitized mice was modulated by the probiotic preparations towards a Treg/Th0 profile, characterized by increased IL-10 and IFN-gamma production. In vivo prophylactic treatment with VSL#3 induced a significant reduction of serum specific IgG1. At lung level, VSL#3 pre-treatment remarkably reduced IL-13 and IL-4 mRNA expression and increased IL-10 expression. CONCLUSIONS: The VSL#3 preparations have not only the capacity to bias primary immune responses towards a Treg/Th0-type profile, but also to modify in the same way the functional characteristics of established in vitro Th2 responses. In vivo studies on a mouse model of Par j 1 sensitization indicate that the prophylactic intranasal treatment with probiotic bacteria is able to modulate the development of Th2-biased responses. (c) 2009 S. Karger AG, Basel.