Interaction between Candida and Lactobacillus.!

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  • #116831

    dvjorge
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    This is a fragment of an article I have read many times. Yeah, 5 years collecting articles about it. I never thought this could be part of my life.

    Very interesting, by the way.!

    DISCUSSION
    This study focuses on C. albicans gastric colonization of mice during the postantibiotic recovery phase. Using culture-independent and culture-dependent approaches, we demonstrated here that cefoperazone causes long-term disturbances to the gastric bacterial microbiome, including a significant reduction in the numbers of lactobacilli and the outgrowth of enterococci. The introduction of C. albicans into this disrupted community antagonizes the regrowth of Lactobacillus (directly or indirectly) and promotes increased Enterococcus levels, implicating that C. albicans can antagonize Lactobacillus in vivo. Most importantly, these findings begin to address the factors involved in C. albicans switching from a commensal to a pathogen and identify that the indigenous microbiome plays a critical role in this process, both through colonization resistance and through an unknown mechanism that inhibits gastric inflammation.

    This is one of the first reports to use culture-independent analysis to analyze antibiotic-mediated disruption of the murine gastric microbiome. Our group has previously demonstrated that disturbances of the cecal microbiome by cefoperazone can be detected 6 weeks after the cessation of the antibiotic (1). Culture-based studies of the murine gastric microbiota have revealed a diverse, but limited community (just over 20 culturable genera), including lactobacilli (10). Cefoperazone is a poorly absorbed broad-spectrum cephalosporin with excellent activity against anaerobic organisms (18). It can promote C. albicans overgrowth in mice and humans, suggesting that its spectrum of activity encompasses bacteria that are critical for colonization resistance against C. albicans outgrowth or invasion (24, 36, 44). Although the exact mechanisms still remain to be determined, it has been suggested that lactobacilli are critical (22, 23). The results from in vitro studies implicate the bacterial microbiome in blocking yeast adhesion to the epithelium and producing inhibitor substances (such as volatile fatty acids and secondary bile acids) that can reduce C. albicans adhesion, hyphal transformation, and invasion (22, 23, 31, 32, 47, 48). It is well documented that mice lacking a bacterial microbiome are readily colonized by C. albicans, whereas conventional mice are highly resistant (3, 16). We have demonstrated that the effects of oral cefoperazone on the gastric bacterial microbiota can last at least 3 weeks after the cessation of the antibiotic, allow colonization by C. albicans, and promote C. albicans-induced gastritis.

    One unexpected result from these studies was that the well-documented interaction between Lactobacillus and C. albicans, whereby Lactobacillus antagonizes the growth, adhesion, and hyphal transformation of C. albicans, can be a bidirectional process. Previous studies have demonstrated the ability of Lactobacillus to displace Candida from the epithelial layer of the stomach (37), inhibit hyphal invasion (37, 47), and prevent germ tube formation (31, 32), but the novel observation from these studies is that Lactobacillus-Candida antagonism can be a two-way process whereby the presence of Candida can prevent the regrowth of Lactobacillus after antibiotics. This could be via direct microbe-microbe interactions or indirectly through the induction of mucosal inflammation. Dietary modulation can also create a temporary Lactobacillus-deficient state, which has been shown to predispose a host to C. albicans overgrowth (48). Feeding mice lactobacilli can reduce the numbers of C. albicans in the stomachs of colonized mice (45–47). Thus, it is likely that a major contributing factor underlying C. albicans colonization and the ensuing gastritis is a reduction in lactobacilli in the stomachs of cefoperazone-treated mice.

    In addition to changes in Lactobacillus numbers, the presence of C. albicans during antibiotic recolonization promoted the persistence of another lactic acid bacterium, Enterococcus. This bacterium, especially E. faecalis (the predominant species isolated from our treated mice), is a major concern in critical care settings, both due to its pathogenicity and to concern regarding antibiotic resistance (6, 7, 35, 40). Enterococcus is well adapted to survival along the mucosa: it can adhere to different epithelial and extracellular matrix proteins (13) and survive in a broad range of pH environments (29). Little is known about lactic acid bacterium niche competition on the human mucosa (e.g., Lactobacillus-Enterococcus antagonism) or C. albicans-Enterococcus antagonism. However, since both C. albicans and Enterococcus are concerns in critical care settings, our studies suggest that dissecting their potential symbiosis may provide new insights for treatments.

    T-RFLP does not provide exact identities of the bacteria in a complex, undefined community, such as found in the murine stomach; rather, it generates a TRF profile or “fingerprint” that represents the community, and changes in that fingerprint serve as a surrogate measurement for changes in bacterial community structure. T-RFLP cannot differentiate between abundance changes within a community and additions/loss of new membership. If the bacterial community is a defined community, i.e., the identities of all of the members are known, then T-RFLP is often used to approximate changes in this known membership and specific TRFs assigned to specific bacterial species. This assignment of TRFs to a specific species of bacteria relies upon knowledge of the 16S rRNA gene sequence of that bacteria (which can usually be obtained through a database such as the RDP). In our studies, it is very unlikely that the number of enterococci is sufficient to generate an observable TRF. However, the lactobacilli are likely numerous enough to generate a T-RFLP signal; however, all of them would need to contain the exact same site for the T-RFLP restriction enzyme to generate the same TRF. There are some candidate peaks that may indeed be lactobacilli, but we cannot say with certainty that these are indeed the TRFs. Thus, we have decided not to overinterpret our T-RFLP results and simply use them as a culture-independent methodology to identify that changes in the bacterial community structure of the stomach microbiota occur after oral cefoperazone therapy.

    In the studies presented here, we presented separate sets of experiments demonstrating that both strain CHN1 and SC5314 were able to induce gastric inflammation at the limiting ridge. No histologically evident inflammation was observed in the duodenum, jejunum, ileum, cecum, or colon (data not shown). This is consistent with previous studies, which have demonstrated, using other C. albicans strains, that the limiting ridge is a primary site of hyphal invasion and inflammation in mice with an altered microbiota following oral inoculation of C. albicans (4, 16, 34, 37, 38). While the function of the limiting ridge is unknown, it is the physical junction between the keratinized epithelium of the murine forestomach and the glandular body. The limiting ridge is comparable to the junction between the esophagus (squamous epithelium) and the stomach in humans. This anatomical resemblance of the murine limiting ridge and the human esophageal-gastric junction, combined with the evidence that C. albicans has a predilection to colonize and cause inflammation of the ridge, finds human parallels in the medical literature, where there are reports of esophageal ulcers related to Candida infections (8, 15).

    In humans, gastric ulcers associated with C. albicans colonization is a well-documented condition, although generally unappreciated in terms of etiologic agents of gastric ulceration. In one study of 293 patients aged 20 to 80 years, >50% patients with gastric ulcers and >10% with chronic gastritis had fungal colonization of the stomach, with C. albicans being the most frequently isolated fungus (50). In three separate studies of 188, 66, and 42 adult patients with benign gastric ulcers, C. albicans infiltration into the gastric lesions were identified in 7, 9, and 36% of the patients, respectively (12, 14, 26). The general conclusion of these studies was that the yeast were a secondary infection of the ulcer site, although causation versus secondary colonization were never actually examined in these studies. Finally, in another study of >150 patients, Candida spp. were found in the gastric mucosa of 17% of patients, and two-thirds of those samples were cocolonized with both H. pylori and Candida (19). Additional analysis identified a link between coexistence of H. pylori with Candida and gastric ulcers, suggesting synergism of these microbes in the development of gastric pathology. In subjects with gastric colonization by C. albicans, but no H. pylori, colonization levels on the gastric mucosa were low (<103 CFU/ml). Thus, while the pathogenesis of C. albicans in the mouse versus human gastric mucosa may be different, this yeast exerts a tropism for this tissue site that is very likely influenced by the microbiota.

    In support of this general concept, we observed a dichotomy between C. albicans colonization and gastric disease, which was bacterial microbiome dependent. Gastric colonization is known to be independent of the T cell status of the host, while gastritis involves the generation of a Th1 response, neutrophil infiltrates, and local production of indoleamine 2,3-dioxygenase (5, 9, 11, 16). Germfree mice C57BL/6 mice can respond to colonization and gastric candidiasis by increasing the expression of defensins and innate inflammatory cytokines (39). Some Candida species, such as C. pintolopesii, can exist in the murine microbiome without inducing inflammation (38). However, studies of C. albicans in mice have largely focused on its pathogenic potential, rather than on its ability to exist as a commensal or mutualist in the microbiome. Thus, little is known about the microbiome-derived interactions that control this switch. Our results predict that the bacterial community in cefoperazone-treated mice changes between days 7 and 21, thereby allowing the already established colonization by C. albicans to become an inflammatory stimulus for the gastric mucosa, similar to that in mice that completely lack a microbiota. Future kinetic studies, using culture-independent techniques such as pyrosequencing of 16S amplicons or high-throughput sequencing of metagenomic transcripts will provide some insights into this process. The role of the microbiome in regulating inflammatory responses to members of the indigenous microbiome is an area of current interest for a number of diseases. The potential ramification of understanding the process of C. albicans colonization is illustrated by research from our lab and others that has demonstrated that gastrointestinal colonization by C. albicans in mice can promote sensitization against intranasally and orally delivered antigens, such as food (30–32, 49). Further, our data provide new insights into the development and potential management of gastric ulcers and C. albicans-induced gastritis.

    #116833

    dvjorge
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    This article mentions effectiveness of antagonistic Lactobacillus therapy against candida colonization.

    Effectiveness of the association of 2 probiotic strains formulated in a slow release vaginal product, in women affected by vulvovaginal candidiasis: a pilot study.
    Vicariotto F1, Del Piano M, Mogna L, Mogna G.
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    Abstract
    BACKGROUND:
    Vulvovaginal candidiasis (VVC) is the second most common cause of vaginitis after bacterial vaginosis, and it is diagnosed in up to 40% of women with vaginal complaints in the primary care setting. Among Candida spp., Candida albicans is the most common infectious agent. The treatment of choice for uncomplicated VVC is achieved with single-dose or short-course therapy in over 90% of cases. Several topical and oral drugs are available, without evidence for superiority of any agent or route of administration. In any case, most classic treatments are unable to significantly offer a protection against possible recurrences. In recent years, probiotics are emerging as a new strategy to counteract VVC. In fact, they are well known for their ability to lower intravaginal pH, thus establishing a barrier effect against many types of yeasts. Some strains are also able to exert additional and more focused antagonistic activities mediated by specific molecules such as hydrogen peroxide and bacteriocins. For example, Lactobacillus fermentum LF5 (CNCM I-789) was successfully tested in 4 human trials involving a total of 340 women reporting VVC at enrollment. In any case, the way used to deliver probiotics to the vaginal environment represents a crucial point. The aim of this work was to first select 1 or more probiotic strains in vitro with an antagonistic activity on Candida yeasts and then to perform an in vivo human pilot study using an association of the most promising and active bacteria.
    METHODS:
    For this purpose, 2 probiotic strains Probiotical S.p.A (Italy) were selected based on their strong in vitro inhibition activity toward 4 particular Candida species, namely C. albicans, Candida glabrata, Candida parapsilosis, and Candida krusei and subsequently tested in a human intervention pilot trial involving 30 women with VVC. The probiotics used, L. fermentum LF10 (DSM 19187) and Lactobacillus acidophilus LA02 (DSM 21717), were administered by means of slow release effervescent vaginal tablets (ActiCand 30 product). The main endpoint was the assessment of the establishment and maintenance of a barrier effect against Candida yeasts in women suffering from VVC. Thirty female subjects who were diagnosed with VVC by both microscopic examination and yeast culture were enrolled in the study and directed to apply a vaginal tablet once a day for 7 consecutive nights, followed by 1 tablet every 3 nights for a further 3-week application (acute phase) and, finally, 1 tablet per week to maintain a long-term vaginal colonization against possible recurrences. A medical examination of each patient was performed at enrollment (d₀), at the end of the first 4 weeks of treatment (d₂₈), and at the end of the second month of relapse prevention (d₅₆). The visual and microscopic examination was always accompanied by microbiological analyses of vaginal swabs to assess the presence of Candida. A statistical comparison was made between d₂₈, or d₅₆, and d0, and between d₅₆ and d₂₈ to quantify the efficacy against possible recurrences.
    RESULTS:
    The administration of the product ActiCand 30 was able to significantly solve Candida yeast symptoms after 28 days in 26 patients out of 30 (corresponding to 86.6%, P<0.001). At the end of the second month, recurrences were recorded, albeit not particularly serious, in only 3 out of 26 patients (11.5%, P=0.083) who were found to have fully healed at the end of the first month of treatment. This is a further confirmation of the long-term barrier effect exerted by the product.
    CONCLUSIONS:
    VVC has a very high incidence as 70% to 75% of women report at least 1 episode during the life. Many treatments are currently available but, despite a relatively high effectiveness in the relief of symptoms typically associated with acute infections, they are generally unable to offer a long-term protective barrier against possible recurrences. This study demonstrated the ability of ActiCand 30 to not only solve Candida infections in a very high percentage of women, but also to exert a long-term physiological defense due to the colonization of vaginal microbiota and adhesion of the mucosa to the epithelial cells. The special formulation of ActiCand 30, consisting of slow release effervescent vaginal tablets, is able to mediate 2 types of barrier effects, the first represented by the formation of an anaerobic environment due to the release of CO₂ and the second guaranteed by the colonization and adhesion to the vaginal epithelium of the 2 probiotics L. fermentum LF10 and L. acidophilus LA02.

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