Oral probiotic administration induces interleukin-10 production and prevents spontaneous autoimmune diabetes in the non-obese diabetic mouse

Calcinaro, Filippo; Dionisi, S.; Marinaro, Mariarosaria; Candeloro, Paola; Bonato, V.; Marzotti, Stefania; Corneli, R. B.; Ferretti, Elisabetta; Gulino, Alberto; Grasso, Felicia; Simone, Claudio De; Mario, U. Di; Falorni, Alberto; Boirivant, Monica; Dotta, Francesco

doi:10.1007/s00125-005-1831-2

Cited by 304 publications

(246 citation statements)

References 58 publications

(65 reference statements)

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“…Other studies have also reported that probiotics induce IL-10 production. 34,35 Interestingly, mice pretreated with probiotics did not demonstrate an increased IL-10 response to LPS challenge. This may be due to a primary effect of probiotics in preventing an LPS-induced rise in proinflammatory cytokine secretion, or alternatively, a pretreatment with probiotics induces a maximal up-regulation of IL-10.…”

Section: Discussionmentioning

confidence: 97%

Probiotic bacteria prevent hepatic damage and maintain colonic barrier function in a mouse model of sepsis

et al. 2007

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A breakdown in intestinal barrier function and increased bacterial translocation are key events in the pathogenesis of sepsis and liver disease. Altering gut microflora with noninvasive and immunomodulatory probiotic organisms has been proposed as an adjunctive therapy to reduce the level of bacterial translocation and prevent the onset of sepsis. The purpose of this study was to determine the efficacy of a probiotic compound in attenuating hepatic and intestinal injury in a mouse model of sepsis. Wild-type and interleukin-10 (IL-10) gene-deficient 129 Sv/Ev mice were fed the probiotic compound VSL#3 for 7 days. To induce sepsis, the mice were injected with lipopolysaccharide (LPS) and D-galactosamine (GalN) in the presence and absence of the peroxisome proliferator-activated receptor gamma (PPAR␥) inhibitor GW9662. The mice were killed after 6 hours, and their colons were removed for the measurement of the cytokine production and epithelial function. The functional permeability was assessed by the mannitol movement and cyclic adenosine monophosphate-dependent chloride secretion in tissue mounted in Ussing chambers. The livers were analyzed for bacterial translocation, cytokine production, histological injury, and PPAR␥ levels. The tissue levels of tumor necrosis factor alpha, interferon gamma, IL-6, and IL-12p35 ribonucleic acid were measured by semiquantitative reverse transcription polymerase chain reaction. L iver dysfunction and failure contribute to the high mortality rates seen in patients with Gram-negative sepsis. The presence of lipopolysaccharide (LPS) from Gram-negative bacteria in the systemic circulation results in the activation of the innate immune system and the secretion of high levels of proinflammatory cytokines. In animal models, LPS challenge can induce a systemic reaction resulting in a sepsis-like condition characterized by fever, hypotension, and widespread tissue damage. D-Galactosamine (GalN) increases the susceptibility of mice to LPS-induced shock by impairing liver metabolism. 1 Challenging mice with low doses of LPS in conjunction with GalN results in massive liver apoptosis and increased mortality.Tumor necrosis factor alpha (TNF-␣) plays a central role in the overwhelming systemic inflammatory response to LPS. 2 However, the complete blockade of TNF-␣ production does not improve survival in animals or humans 3 The activation of nuclear factor kappa B (NF-B) has been shown to play a key role in the pathogenesis of sepsis and is a pivotal step in the regulation of several immune and proinflammatory genes, including TNF-␣. 4 The modulation of NF-B activity has been proposed as a strategy for reducing the mortality associated with sepsis. Peroxisome proliferator-activated receptor gamma (PPAR␥) is a nuclear hormone receptor and transcription

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Section: Discussionmentioning

confidence: 97%

Probiotic bacteria prevent hepatic damage and maintain colonic barrier function in a mouse model of sepsis

et al. 2007

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“…[191][192][193] However, other probiotic strains are capable of ameliorating EAE, 194 and other experimental autoimmune diseases that are known to be Th1 mediated, such as various models of rheumatoid arthritis [195][196][197] or type 1 diabetes. 198 Together, these fi ndings highlight the need for care in choosing appropriate probiotic strains for particular applications. In this process, it needs to be taken into account that the response to probiotic supplementation depends on the immunological status of the host, as demonstrated by in vitro 98,199 and in vivo experiments.…”

Section: Final Comments and Thoughtsmentioning

confidence: 99%

Probiotics and immunity

et al. 2009

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Probiotics are defi ned as live microorganisms that, when administered in adequate amounts, confer a health benefi t on the host, including the gastrointestinal tract. While this benefi cial effect was originally thought to stem from improvements in the intestinal microbial balance, there is now substantial evidence that probiotics can also provide benefi ts by modulating immune functions. In animal models, probiotic supplementation is able to provide protection from spontaneous and chemically induced colitis by downregulating infl ammatory cytokines or inducing regulatory mechanisms in a strain-specifi c manner. In animal models of allergen sensitization and murine models of asthma and allergic rhinitis, orally administered probiotics can straindependently decrease allergen-specifi c IgE production, in part by modulating systemic cytokine production. Certain probiotics have been shown to decrease airway hyperresponsiveness and infl ammation by inducing regulatory mechanisms. Promising results have been obtained with probiotics in the treatment of human infl ammatory diseases of the intestine and in the prevention and treatment of atopic eczema in neonates and infants. However, the fi ndings are too variable to allow fi rm conclusions as to the effectiveness of specifi c probiotics in these conditions.

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“…Selective decontamination of the gastrointestinal tract may prevent this response in a similar manner in which it prevents translocation of bacteria. Accordingly, we are seeing an increase in investigational efforts involving the use of probiotics [8] to modulate type 1 diabetes. In addition, in the context of antibiotic usage, the identification of unquestionable linkages between an autoimmune disorder, gut flora and antibiotics would add important information to the ongoing debate regarding appropriate versus spurious use of these agents.…”

Section: To the Editormentioning

confidence: 99%

Comment on: Brugman S et al. (2006) Antibiotic treatment partially protects against type 1 diabetes in the Bio-Breeding diabetes-prone rat. Is the gut flora involved in the development of type 1 diabetes? Diabetologia 49:2105–2108

et al. 2006

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Oral probiotic administration induces interleukin-10 production and prevents spontaneous autoimmune diabetes in the non-obese diabetic mouse

Abstract: Orally administered VSL#3 prevents autoimmune diabetes and induces immunomodulation by a reduction in insulitis severity. Our results provide a sound rationale for future clinical trials of the primary prevention of type 1 diabetes by oral VSL#3 administration.

Cited by 304 publications

References 58 publications

Probiotic bacteria prevent hepatic damage and maintain colonic barrier function in a mouse model of sepsis

Probiotic bacteria prevent hepatic damage and maintain colonic barrier function in a mouse model of sepsis

Probiotics and immunity

Comment on: Brugman S et al. (2006) Antibiotic treatment partially protects against type 1 diabetes in the Bio-Breeding diabetes-prone rat. Is the gut flora involved in the development of type 1 diabetes? Diabetologia 49:2105–2108

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