What is lactobacillus gg

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You are here Home » lactobacillus rhamnosus GG. Top of the page. What is the most important information I should know about lactobacillus rhamnosus GG? What is lactobacillus rhamnosus GG? What should I discuss with my healthcare provider before taking lactobacillus rhamnosus GG? You may not be able to use lactobacillus rhamnosus GG if you have certain medical conditions, especially: short bowel syndrome; or weak immune system caused by disease or by using certain medicine.

Ask a doctor before using this product if you are pregnant or breast-feeding. How should I take lactobacillus rhamnosus GG? Lactobacillus rhamnosus GG may be taken with or without food. You may also store this product in the refrigerator. Do not freeze. Do not use this product if the blister foil covering the capsules is torn.

What happens if I miss a dose? What happens if I overdose? Seek emergency medical attention or call the Poison Help line at What should I avoid while taking lactobacillus rhamnosus GG?

What are the possible side effects of lactobacillus rhamnosus GG? As SpaC is distributed not only at the tip, but also over the pilus length [ 26 ], it is thought that a zipper-like mechanism can facilitate a close interaction with the host after the first interaction is initiated by a SpaC subunit, enabling other SpaC subunits along the tip, but also other cell surface adhesins on the LGG surface to adhere step by step, resulting in a more stable interaction.

As key adhesive components, the immunomodulatory capacity of the pili is also of high interest, although current data are very limited. Moreover, in a comparison between LGG and other commercial probiotic L.

As part of our ongoing research, we are investigating whether the pili have a direct effect as MAMP interacting with PRRs, such as TLR2, like has been shown for the type I pilus of Streptococcus pneumonia [ 40 ], or whether they mainly act indirect by mediating a close interaction with the host cells and other LGG exposing surface-bound ligands. Recent data suggest that it is not specifically the presence or absence of SpaCBA pili that mediate immune status. Rather, the pili appear to play an indirect modulating role by promoting close interactions with host cells such as epithelial cells, probably by the zipper-like mechanism discussed above, so that other effector molecules can exert their immune modulating activities [ 14 ].

It will be very interesting to substantiate this indirect immunomodulatory role in human volunteers, e. However, the bio-active concentration of LTA is typically in de micromolar range, while LPS is active in nanomolar concentrations [ 41 ].

The glycolipid moiety contains 2 fatty acid chains with an average length of C14, with one double bound per fatty acid [ 12 , 43 ]. To investigate the in situ role of LTA in live bacteria, a mutant of LGG that showed a modified LTA structure lacking D-alanine residues and an altered glycolipid anchor, was created by mutating the dltD gene. This gene encodes a membrane protein that facilitates the ligation of the D-alanyl carrier protein with D-alanine [ 12 ].

Furthermore, the dltD mutant significantly improved DSS- induced colitis in treated mice compared to buffer control, while the wild type strain showed actually detrimental effects in that model [ 44 ]. Interestingly, similar effects were observed with LTA mutants in other lactobacilli [ 45 ]. This shows that LTA is not an LGG-specific effector molecule, but that it is an important molecule in understanding Lactobacillus -host interactions and is a crucial factor to take into account when investigating anti-inflammatory effects.

They found that the survival-promoting effect was also present in other probiotic strains such as L. Consequently, two proteins from the LGG supernatans were found to cause the antiapoptic effect [ 49 ]. Each of the purified proteins was shown to activate the Akt signaling peptide, inhibit cytokine-induced IEC apoptosis and reduce tumor necrosis factor TNF - induced epithelial damage.

The proteins also promoted cell growth in human and mouse colon IECs and cultured mouse colon explants [ 51 ]. Moreover, they were shown to protect the intestinal epithelial barrier function from hydrogen peroxide-induced damage through blocking of MAP kinases [ 52 ].

The importance of EGF-R in the mechanism was confirmed in the in vivo tests [ 53 ]. Nevertheless, the exact PRR could not be identified. For instance, the homologous proteins of L. However, there exists some heterogeneity between the homologues. Msp1 was characterized in LGG as a D-glutamyl-L-lysyl endopeptidase with an important role in daughter cell separation [ 15 ].

Intriguingly, we could also show that the Msp1 protein is glycosylated in LGG with Con-A reactive residues [ 56 ], which could explain the apparent discrepancy previously seen between the predicted molecular weight and the molecular weight shown on Western blot [ 51 ]. The serine-rich glycosylation site was not found in homologues of Msp1 in several L.

The glycosylation does not impede enzyme activity and was suggested not to interfere with activation of Akt, although a the glycan chain appears to have a modulating role as shield.

The glycosylation seems to play a role in increasing protein stability and protein binding to the cell wall [ 56 ]. The Msp2 protein, on the other hand, appears not to be glycosylated.

The exact function of LGG Msp2 remains unclear since its hydrolytic peptidoglycan PG degrading activity is limited and an msp2 knock-out mutant could not be constructed, possibly because of its essential role in LGG.

Immunofluorescence analysis suggests a possible role in early stage cell septum formation [ 15 ]. Because of their action as PG hydrolases, it also remains to be studied whether Msp1 and Msp2 could have immunomodulatory functions by release of PG fragments. Intriguingly, a recent study showed that PG might be a central mediator for the beneficial effect of certain probiotic lactobacilli, such as Lactobacillus salivarius Ls33 in inflammatory bowel disease with NOD-2 as a key receptor [ 58 ].

An extracellular polysaccharide EPS layer is commonly found in lactobacilli. Of interest, EPS molecules show a large structural diversity [ 60 ], so that they are clearly strain-specific molecules. We could yet identify the operon responsible for galactose-rich EPS synthesis [ 62 ]. A knock-out mutant of the welE gene, encoding the priming glycosyltransferase, is completely devoid of the long galactose-rich EPS but shows a higher concentration of short glucose-rich EPS [ 62 ].

In addition, this type of galactose-rich EPS appears to be an important adaptation factor for LGG as the welE mutant shows a reduced in vivo survival in the murine gastrointestinal tract GIT [ 63 ]. More specifically, the long galactose-rich EPS were shown to protect the cell against complement-mediated lysis and cathelicidins, specific cationic antimicrobial peptides [ 63 ]. It thus seems important that this type of EPS production is balanced between optimal protection and optimal adhesion.

Results obtained in our lab indicate that isolated galactose-rich EPS are not principal inducers of cytokines in the Caco-2 intestinal epithelial cell line [ 14 ].

However, as low concentrations of the major secreted proteins have an anti-apoptotic effect in IECs [ 51 ], it remains to be ruled out that protein contaminants in the purified EPS are not interfering with the results. A recent network based in silico analysis of the glycosyltranferase genes of LGG could identify the putative gene cluster involved in their biosynthesis [ 65 ], which opens perspectives for functional analyses with mutants.

Apart from EPS, other genes and molecules play a role as factors that promote the adaptation of LGG to the human host and gastro-intestinal tract in particular. For instance, an elegant study combining transcriptomics and proteomics in LGG identified putative adaptation factors involved in the bile stress response of LGG.

Among the identified functions were general stress responses as well as cell envelope-related functions, including pathways affecting fatty acid composition, cell surface charge, and thickness of the EPS layer [ 66 ]. Several in vitro studies have shown the efficacy of LGG against the viability, adherence or infection of GIT pathogens. Indeed, LGG was shown to reduce the viability of Salmonella enterica subsp.

In vivo mice experiments confirmed that LGG pretreatment reduces S. Typhimurium infection parameters [ 74 ]. However, there is some controversy concerning the results obtained with S.

Typhimurium, as not all studies could detect a reduction in viability [ 74 , 75 ] or reduced adherence to human intestinal mucus [ 75 , 76 ]. Unfortunately, to our knowledge no human trials have been carried out focusing on Salmonella specifically. There have been a number of studies trying to identify the antibacterial compounds, mostly focusing on S. Typhimurium SL in a pH-dependent manner [ 76 ].

Interestingly, lactic acid was identified as the main antimicrobial compound in different conditions [ 69 , 71 , 72 ], which is clearly not a specific factor for LGG. As lactic acid permeabilizes the Gram-negative outer membrane, it might facilitate antibacterial action of other compounds, such as organic acids or bacteriocins [ 77 ].

These compounds might indeed participate as a recent study showed that the antimicrobial effect appears not to be dependent on lactic acid concentration alone [ 68 ].

Seven heat-stable peptides with antibacterial activity against enteroaggregative E. Unfortunately, these peptides have not yet been identified, to the best of our knowledge. Of note, the genome sequence of LGG encodes several bacteriocin-related genes [ 9 ]. Despite several attempts, we and others were not yet able to shown bacteriocin production under laboratory conditions and coculture with possible inducing strains, although a bacteriocin locus was found to be induced in the murine gastro-intestinal tract after R-IVET Sarah Lebeer et al.

Bacterial cell-cell communication through quorum sensing QS might also interfere with pathogen infection as strains present in the gut microbiota are thought to communicate to coordinate adaptive processes such as competition and cooperation for nutrients and adhesion sites [ 2 ].

LGG was reported to produce autoinducer-2 AI-2 , which is suggested to be an important interspecies QS molecules, produced by both Gram-positive and Gram-negative bacteria [ 79 ]. However, the role of QS in pathogen exclusion is difficult to investigate since the AI-2 synthase LuxS also interferes with the cell metabolism. Indeed, a luxS knock-out mutant of LGG was shown to have numerous pleiotropic effects, which could not be complemented by exogenous addition of synthetic AI-2 molecules [ 10 ].

For instance, McCormick and colleagues could nicely show that cyclic dipeptides of strain Lactobacillus reuteri RC quench agr -mediated expression of toxic shock syndrome toxin- 1 in staphylococci [ 80 ], highlighting that QS could play a role in antipathogenic mechanisms of probiotics. Targeting TLR9 with CpG or ODN has been a strategy for a number of clinical trials studying the effect on cancer treatment, allergy and infection diseases, reviewed in [ 82 ]. It is important to note that TLR9 function in the intestinal epithelial layer is thought to be polarized as IECs respond differently to apical or basolateral exposure to CpG.

This mechanism is thought to play an important role in epithelial homeostasis [ 83 ]. A bioinformatic analysis of the frequency of CpG motifs in the genomes of gut commensals demonstrated a correlation with genomic GC content [ 84 ]. The genome of LGG, but also of other lactobacilli such as L. ID35 isolated form LGG genome even seems to be beneficial in allergy prevention in an ovalbumin-sensitized mouse model, by inducing the T H 1-response and suppressing ovalbumine-specific IgE production [ 88 ].

The above mentioned LGG molecules and their corresponding mutants are studied one-by- one but it should be highlighted that in situ the host interaction towards LGG will be an integrated sum of different interactions. A combination of all MAMP-PRR interactions decides how the immune system is triggered, while also various metabolites such as lactic acid can be envisaged to modulate host responses. Until now, these host responses towards LGG have been mainly characterized by transcriptomics methods, but also other approaches such as proteomics and metabolomics show great potential, especially if methods are integrated and combined with network biology approaches [ 90 ].

For instance, a gene expression analysis of the small bowel mucosa from patients treated with LGG compared with placebo treatment, showed that LGG affected genes involved in immune response and inflammation, apoptosis, cell-cell signaling, cell growth and cell differentiation, cell adhesion and signaling. It should be noted that these analyses were done at a rather late time point, i.

A more recent in vivo transcriptome analysis compared the mucosal responses towards LGG 1. Interestingly, even after only 6 h, the mucosal response to LGG was also mainly characterized by the induction of T H 1 development via the IFN-STAT4 signal transducer and activator of transcription 4 axis and affected pathways include cellular growth and proliferation pathways, wound healing, angiogenesis, interferon mediated responses, calcium signaling and ion homeostasis [ 92 ].

The same method was also used to investigate whether humans respond differently to different growth stages of L. They indeed observed clear differences in the transcriptional response to exponentially growing or stationary phase bacteria, and between viable and heat-killed stationary bacteria.

It will be very interesting to use the same analyses to investigate the transcriptional responses towards LGG wild type and spontaneous non-GMO food-grade mutants, such as spontaneous pili mutants, to explore their relative contribution to the human host response. In addition, ex vivo and in vitro models such as the porcine small intestinal epithelial cell line IPEC-J2 appear to be good models for the study of innate immune responses to probiotics [ 95 ].

Molecular interactions of LGG with intestinal epithelial cells. A recent human duodenal transcriptome study indicates that JUN and STAT4 transcription factors play a central role in downstream signaling after consumption of LGG, leading to mainly T H 1 cytokine production and activating pathways involved in cellular growth and proliferation, wound healing, angiogenesis, interferon-mediated responses, calcium signaling and ion homeostasis [ 92 ].

Adapted from [ 96 ]. Nevertheless, and probably most importantly, the abovementioned duodenal transcriptome studies of Kleerebezem and coworkers showed a remarkable large distance of the transcriptome profiles between the human participants. As all participants were healthy, the large inter-person variation indicates that mucosal tissues have multiple mucosal solutions to accomplish healthy homeostasis, which is suggested to be a molecular "bandwidth of human health" [ 96 ]. Clearly, this complicates the selection of the most appropriate biomarkers to monitor probiotic intervention in human study subjects and the possibility for stratification of responders and non-responders.

In the next paragraphs, we tried to summarize some well documented clinical benefits and explain some of the findings with the molecular framework we provided above, although this association should be taken with caution. As mentioned before, LGG has been shown to colonize the gut of newborns significantly better than adults [ 18 ].

Interestingly, prenatal supplementation with LGG 1. Others showed that postnatal application of LGG 10 9 CFU daily, lyophilized powder mixed with breast milk appears to affect neonatal intestinal colonization patterns causing a higher species diversity compared to placebo [ ], although the analysis was not done at detailed level.

How exactly LGG could promote the colonization of bifidobacteria in vivo remains to be further explored. Given its excellent intestinal mucus adherence capacities, LGG has also been often selected as candidate probiotic for the prevention and treatment of gastro-intestinal infections and diarrhea, although the efficacy is not uniformly proven.

Three subsequent meta-analysis studies have discussed the use of LGG for the treatment of acute diarrhea in children [ - ]. Overall, the current data suggest that LGG can reduce the duration of diarrhea with 1. LGG 10 9 CFU daily in fermented milk product was also shown to reduce the risk of acquiring nosocomial gastrointestinal infections when administered daily in hospitalized children [ ]. Effects were the largest in non-breastfed children [ ].

However, long-term consumption of milk containing LGG 10 8 CFU daily in children attending day care centers in Finland could not show an effect on the incidence of gastro-intestinal symptoms [ ]. It is important to note that the unsuccessful trial tested a fold lower daily concentration, although other factors such as probiotic formulation and study subject heterogeneity could of course also play a role. A recent meta-analysis concluded that LGG treatment can also reduce pain frequency and intensity in children with abdominal pain-related disorders, particularly among irritable bowel syndrome IBS patients.

However, it is important to mention that the clinical effects were significant but moderate [ ], which is not unexpected if you consider the large subject heterogeneity in IBS patients.

In other conditions, LGG effects were better stratified. Furthermore, application of a commercial yoghurt with LGG to renal patients during 8 weeks has been shown to succeed in clearing vancomycin-resistant enterococci in all patients in an double-blind, randomized, placebo-controlled trial [ ].

Clearly, experiments with non-GMO pili deficient variants of LGG would be highly interesting to study their role in the gastro-intestinal and pathogen exclusion effects of LGG. For instance, LGG has been shown to reduce oral counts of Streptococcus mutans , a bacterium correlated with caries formation, respectively in yogurt, milk and lozenges [ - ]. Importantly, LGG appears not to ferment sucrose to a significant level [ 9 ], indicating that it is itself not cariogenic, a property which is sometimes attributed to lactobacilli due to lactic acid production.

Others have investigated the effect of LGG consumption on respiratory health. For instance, Hojsak and colleagues [ ] showed that fermented milk containing LGG was efficient in reducing the risk on respiratory tract infections RTIs that lasted longer than three days in hospitalized children.

Also, preterm infants treated daily with 10 9 CFU LGG in capsules starting within one week after birth, appear to have significantly lower incidence of RTIs and rhinovirus-induced episodes in the first 2 months [ ]. Furthermore, capsulated LGG 10 9 CFU was shown to protect hospitalized patients against ventilator-associated pneumonia, mainly when caused by Gram-negative pathogens like Pseudomonas aeruginosa [ ].

Moreover, in cystic fibrosis patients colonized with P. Unfortunately, this study did not evaluate P. Clearly this area requires further research, because probably a combination of LGG's antipathogenic and immune modulating capacities determines its potential in RTIs. The potential immunomodulatory effects of LGG that have yet received most attention include its widely discussed effects against allergic disease.

However, allergic rhinitis and asthma tended to be more common in the LGG treated group and no significant differences were found in incidence of cow milk allergy.

Moreover, Kopp and colleagues [ ] could not repeat the beneficial results against eczema using a similar protocol and concentration. The reason for these different outcomes is unknown, however it is thought that the different genetic background of the tested populations Finnish versus German might play a role.

Also, the German trial had more infants with older siblings, which could be a potential cofounder [ , ]. In addition, it seems that different probiotic products have been used for these studies, so that also differences in probiotic formulation, and for instance pili presence, cannot be ruled out.

However, in these trails there was a consistent but not significant effect of LGG in the IgE-sensitized subgroup. This is probably a good example that patient stratification is important to identify potential responders, but more research is necessary to determine the effect of LGG in IgE-sensitized infants. In milk-hypersensitive adults, LGG 2.

Another perhaps more elegant way to investigate the immunomodulatory effects of LGG is by studying its capacity to ameliorate humoral responses to vaccines when applied as an adjuvant. LGG in milk 10 10 CFU daily, 1 week before vaccination, 4 weeks after was also shown to increase the poliovirus neutralizing antibody titer with a fourfold increase in poliovirus-specific IgA in adults receiving an oral vaccine against polio 1, 2 and 3 [ ].

Moreover, LGG treatment 10 10 CFU in a capsule, daily, 28 days starting at vaccination increased protection rates after an oral life attenuated influenza vaccine. The effect was viral strain-dependent as antibody titers against H1N1 and B strains were low for placebo and LGG-treated groups.

However, there was no influence on the effect of an oral S. In addition, a recent study even showed that maternal supplementation with LGG 1. Moreover, van Baarlen et al. Is LGG a better probiotic strain than other probiotics on the market? This question is difficult to answer, since the answer largely depends on the host response that is aimed for by the application. As mentioned before, the host response is dependent on the combination of several bacterial effectors, including MAMPs interacting with PRRs.

However, it is also apparent that not all reported health effects of LGG are univocal. Nevertheless, one of the clear advantages of LGG is that this probiotic is well characterized and so widely used that it has a very good safety track record.

LGG has been consumed in over 40 countries worldwide and is especially popular in Finland with a yearly per capita consumption rate of 6L in [ ]. To support the safety of LGG, it was shown that despite increasing LGG consumption in Finland and Sweden respectively, the rate of Lactobacillus bacteremia remained constant [ , ]. Moreover, the use of LGG in a wide variety of clinical trials without serious adverse events confirmed its safety.

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