Collegamento tra candida e morbo di chron ?

Alcuni estratti da "Publimed"

Carbohydrate Elimination or Adaptation Diet for Symptoms of Intestinal Discomfort in IBD: Rationales for "Gibsons' Conundrum".

THERAPEUTIC USE OF CARBOHYDRATES IN INFLAMMATORY BOWEL DISEASES (IBDS) IS DISCUSSED FROM TWO THEORETICAL, APPARENT DIAMETRICALLY OPPOSITE PERSPECTIVES: regular ingestion of prebiotics or withdrawal of virtually all carbohydrate components. Pathogenesis of IBD is discussed connecting microbial flora, host immunity, and genetic interactions. The best studied genetic example, NOD2 in Crohn's disease, is highlighted as a model which encompasses these interactions and has been shown to depend on butyrate for normal function. The role of these opposing concepts in management of irritable bowel syndrome (IBS) is contrasted with what is known in IBD. The conclusion reached is that, while both approaches may alleviate symptoms in both IBS and IBD, there is insufficient data yet to determine whether both approaches lead to equivalent bacterial effects in mollifying the immune system. This is particularly relevant in IBD. As such, caution is urged to use long-term carbohydrate withdrawal in IBD in remission to control IBS-like symptoms.

Eliminazione dei carboidrati e/o assunzione di prebiotici per controllare IBD e IBS.

La patogenesi delle malattie infiammatorie croniche intestinali (IBD) comporta un’interazione tra la flora microbica dell’intestino, l’immunità dell’ospite e le interazioni genetiche.

L'esempio più studiato in genetica, è il NOD2 nel morbo di Crohn.

Entrambi gli approcci possono alleviare i sintomi sia di IBD che IBS.

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Candida albicans and Saccharomyces cerevisiae induce interleukin-8 production from intestinal epithelial-like Caco-2 cells in the presence of butyric acid.

Intestinal epithelial cells (IEC) are important in initiation and regulation of immune responses against numerous foreign substances including food, microorganisms and their metabolites in the intestine. Since the responses of IEC against yeasts have not yet been well understood, we investigated the effects of Candida albicans, Saccharomyces cerevisiae, and their cell wall components on interleukin-8 (IL-8) secretion by the IEC-like Caco-2 cells. Live cells of both yeast species stimulated Caco-2 cells to produce IL-8 only in the presence of butyric acid, which is a metabolite produced by intestinal bacteria. S. cerevisiae zymosan and glucan also enhanced IL-8 secretion. Treatment of Caco-2 cells with butyric acid increased the expression of mRNAs coding for Toll-like receptor 1 (TLR1), TLR6 and dectin-1, which recognize zymosan. C. albicans induced more IL-8 secretion and also decreased transepithelial electrical resistance more rapidly than S. cerevisiae. These results suggest that both yeasts in the intestine stimulate the host's mucosal immune systems by interacting with IEC.

Cellule epiteliali intestinali (IEC) sono importanti in avvio e regolazione delle risposte immunitarie contro numerose sostanze estranee tra cui alimentari, microrganismi e loro metaboliti a livello intestinale.

Poiché le risposte di IEC contro lieviti non sono ancora stati ben compresi, abbiamo studiato gli effetti di Candida albicans, Saccharomyces cerevisiae, e dei loro componenti della parete cellulare di interleuchina-8 (IL-8), la secrezione dalle IEC-simili cellule Caco-2.  Questi risultati indicano che entrambi i lieviti nell'intestino stimolano il sistema immunitario mucosale dell'ospite interagendo con IEC.

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Saccharomyces cerevisiae and Candida albicans stimulate cytokine secretion from human neutrophil-like HL-60 cells differentiated with retinoic acid or dimethylsulfoxide.

We investigated whether non-pathogenic Saccharomyces cerevisiae and human commensal opportunistic pathogenic Candida albicans stimulate cytokine responses of human neutrophil-like HL-60 cells pre-treated with either 1 microM retinoic acid or 1.25% dimethyl sulfoxide (DMSO). Intact and heat-killed S. cerevisiae enhanced secretion of interleukin (IL)-1beta, IL-6, IL-8, IL-12, IL-18, MCP-1/CCL2 and TNF-alpha from retinoic acid-treated HL-60 cells, accompanied by alterations in mRNA expression of the cytokines. Heat-killed C. albicans promoted secretion of IL-6, IL-8, IL-12, MCP-1 and TNF-alpha, while intact C. albicans slightly enhanced secretion of IL-1beta, IL-8 and IL-18. In response to yeast stimuli, retinoic acid-treated HL-60 cells generally secreted cytokines more strongly than DMSO-treated HL-60 cells. Gene expression levels of Toll-like receptor (TLR)1, TLR2, TLR4, TLR6 and dectin-1 in HL-60 cells were additionally affected by retinoic acid or DMSO and by co-culturing with S. cerevisiae or C. albicans. Our results suggest that both intact and heat-killed S. cerevisiae and C. albicans induce cytokine responses of neutrophils in the intestine, and stimulate host immune function.

Saccharomyces cerevisiae e Candida albicans stimolano la secrezione di citochine da neutrofili umani.

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Anti-glycan antibodies establish an unexpected link between C. albicans and Crohn disease. Candida albicans colonization and ASCA in familial Crohn's disease.

Almost 80 % of the dry weight of the yeast cell wall is composed of glycans including mannans, glucans and chitin. Within this variable and complex edifice, glycans play a major role in their relation with the environment. Experimental antibodies allowed to define the localization, the variability of expression and the biological role of numerous natural oligosaccharidic sequences. These glycans and their synthetic analogues were used to study the human humoral response during invasive candidiasis (IC) determined by Candida albicans and Crohn's disease (CD) where antibodies against the dietary yeast Saccharomyces cerevisiae have been reported. On these bases, it was established experimentally and clinically that a large panel of CD biomarkers consisting in anti glycans antibodies were also generated during IC establishing a link never suspected between C. albicans and CD. We describe here the principle of this serological analysis and its perspectives related to the use of multianalyte profiling technology for a a better understanding of IC and CD pathophysiology. This may contribute to improve disease management in terms of diagnosis and therapy.

Gli anticorpi anti-glicani stabiliscono un legame inaspettato tra C. albicans e la malattia di Crohn.

Circa l'80% del peso secco della parete cellulare del lievito è composto di glicani compresi mannans, glucani e chitina.

Questi glicani e loro analoghi sintetici sono stati usati per studiare la risposta umorale umana durante la candidiasi invasiva (IC) determinato da Candida albicans e malattia di Crohn (MC) in cui sono stati riportati anticorpi contro il lievito Saccharomyces cerevisiae.

Su queste basi, si è stabilito sperimentalmente e clinicamente che un grande pannello di biomarcatori CD consiste negli anticorpi anti-glicani che sono stati generati anche durante la IC, questo porta a stabilire un legame mai sospettato tra C. albicans e CD.

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Anti ASCA and Candida albicans

Anti-Saccharomyces cerevisiae antibodies (ASCAs) are present in 50-60% of patients with Crohn's disease (CD) and in 20-25% of their healthy relatives (HRs). The yeast, Candida albicans, has been shown to generate ASCAs, but the presence of C. albicans in the digestive tract of CD patients and their HRs has never been investigated. Therefore, we studied C. albicans carriage in familial CD and its correlation with ASCAs.

Study groups consisted of 41 CD families composed of 129 patients and 113 HRs, and 14 control families composed of 76 individuals. Mouth swabs and stool specimens were collected for isolation, identification, and quantification of yeasts. Serum samples were collected for detection of ASCAs and anti-C. albicans mannan antibodies (ACMAs).

C. albicans was isolated significantly more frequently from stool samples from CD patients (44%) and their HRs (38%) than from controls (22%) (P<0.05). The prevalence of ACMAs was similar between CD patients, their HRs, and controls (22, 19, and 21%, respectively, P=0.845), whereas the prevalence of ASCAs was significantly increased in CD families (72 and 34% in CD and HRs, respectively, in contrast to 4% in controls, P<0.0001). AMCA levels correlated with C. albicans colonization in all populations. ASCA levels correlated with C. albicans colonization in HRs but not in CD patients.

CD patients and their first-degree HRs are more frequently and more heavily colonized by C. albicans than are controls. ASCAs correlate with C. albicans colonization in HRs but not in CD. In HRs, ASCAs could result from an altered immune response to C. albicans. In CD, a subsequent alteration in sensing C. albicans colonization could occur with disease onset.

Gli anticorpi anti-Saccharomyces cerevisiae (ASCA) sono presenti nel 50-60% dei pazienti con malattia di Crohn (CD), e nel 20-25% dei loro parenti sani (HR).

Il lievito, Candida albicans, ha dimostrato di generare ASCA, ma la presenza di C. albicans nel tratto digestivo di pazienti con MC e loro HRs non è mai stata studiata. Pertanto, abbiamo studiato C. albicans trasporto in famigliare CD e la sua correlazione con ASCA.

RISULTATI:

C. albicans è stata isolata significativamente più frequentemente da campioni di feci di pazienti CD (44%) e HR (38%) che dai controlli (22%) (P <0.05).

La prevalenza di ASCA era significativamente aumentata in famiglie di CD (72 e 34% in CD e HR, rispettivamente, in contrasto al 4% nei controlli, p <0,0001).

Livelli ASCA correlato con C. albicans colonizzazione in HR ma non nei pazienti con CD.

CONCLUSIONI:

Pazienti CD e HRs di primo grado sono più frequenti e più pesantemente colonizzate da C. albicans che sono i controlli. ASCA correlano con C. albicans colonizzazione in HR, ma non in CD. In HR, ASCA potrebbe derivare da una risposta immunitaria alterata da C. albicans. In CD, una successiva alterazione nella percezione C. albicans colonizzazione potrebbe verificarsi con l'insorgenza della malattia.

Conclusione mia personale

Pertanto, sulla base di questi estratti, si potrebbe ipotizzare un possibile collegamento tra una suscettibilità genetica personale alla candida albicans e alla successiva comparsa di un'infiammazione permanente come il morbo di Chron. 
Se, come suggerito nel primo articolo, una "cura" per le malattie infiammatorie croniche intestinali e la sindrome del colon irritabile è togliere tutti i carboidrati (cereali, zuccheri, ecc.) questo comporta anche un'eliminazione del lievito candida albicans dall'intestino, o perlomeno, un suo drastico abbassamento e quindi i sintomi sono tenuti sotto controllo più facilmente.