Candida metabolites are the cause of Candida Related Complex and responsible for the chronic state of the syndrome.

In fact, the metabolites and fungal wastes are what affects the neuroendocrine system and remote organs.

One time the infection is established, the same organism is able to suppresses the immune response necessary to clear the infection. Mannan, a glycoprotein found in the fungal cell wall, is in fact an immune stimulant but when it reaches the blood, it binds with cooper creating a complex that catabolizes very slowly and is able to suppress cell-mediated immunity. It is also postulated that proteins linked to thryptophan metaboilism found in candida albicans cell wall neutralize Th 17 creating an state of immune suppression during the active overgrowth.

It is the same pathogen the biggest culprit regarding to the chronic immune suppression state candida sufferer have. It is the same fungus what neutralizes the necessary immune response to eradicate the infection.Candida Albicans also form Amyloids which inhibit neutrophil response.

All these reasons justify any effort to eliminate candida albicans cells present in the intestinal tract. Candida species are intruders and successful colonizers of the human tissues. The metabolic production and pathogenesis is confined to a single cell or a massive fungal colony. There isn't difference regarding to toxicity between a single cell or a mutated colony. The germination is only a phenotype change giving the elongate form more virulence and capacity of tissue invasion. ( cell penetration ) Any form is pathogenic and should be eliminated of the human tissues.

RESULTS: Amyloid was present on the cellular surface of fungi invading gut tissue. Moreover, SAP bound to the fungal cell walls, confirming the presence of amyloid. In vitro observations showed SAP bound avidly to fungi when amyloid formed in fungal cell walls. An unexpected result was the lack of host neutrophils in response to the invading fungi, not only in neutropenic patients but also in patients with normal or increased white blood counts.

CONCLUSIONS: We report the first demonstration of functional fungal amyloid in human tissue and the binding of SAP to invading fungi. It is postulated that fungal amyloid, SAP, or a complex of the proteins may inhibit the neutrophil response.

IL-17 is one of the key cytokines that stimulate host defense during a Candida infection. Several studies have demonstrated the capacity of Candida albicans to induce a Th17 response. Surprisingly, experiments employing live C. ablicans demonstrated a specific downregulation of host IL-17 secretion in human blood mononuclear cells (PBMCs). By avoiding the direct contact of live C. albicans and PBMCs, we demonstrate that this inhibition effect is mediated by a soluble factor released by live C. albicans. However, this effect is due neither to the releasing of C. albicans pathogen-associated molecular patterns nor to the alteration of different Th cell subtypes. Rather, we found that live C. albicans shifts tryptophan metabolism by inhibiting IDO expression away from kynurenines and toward 5-hydroxytryptophan metabolites. In addition, we show that these latter 5-hydroxytryptophan metabolites inhibit IL-17 production. In conclusion, live C. albicans inhibits host Th17 responses by modulatory effects on tryptophan metabolism.

Candida mannan: chemistry, suppression of cell-mediated immunity, and possible mechanisms of action.
R D Nelson, N Shibata, R P Podzorski, and M J Herron
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Abstract

The ability of Candida albicans to establish an infection involves multiple components of this fungal pathogen, but its ability to persist in host tissue may involve primarily the immunosuppressive property of a major cell wall glycoprotein, mannan. Mannan and oligosaccharide fragments of mannan are potent inhibitors of cell-mediated immunity and appear to reproduce the immune deficit of patients with the mucocutaneous form of candidiasis. However, neither the exact structures of these inhibitory species nor their mechanisms of action have yet been clearly defined. Different investigators have proposed that mannan or mannan catabolites act upon monocytes or suppressor T lymphocytes, but research from unrelated areas has provided still other possibilities for consideration. These include interference with cytokine activities, lymphocyte-monocyte interactions, and leukocyte homing. To stimulate further research of the immunosuppressive property of C. albicans mannan, we have reviewed (i) the relationship of mannan to other antigens and virulence factors of the fungus; (ii) the chemistry of mannan, together with methods for preparation of mannan and mannan fragments; and (iii) the historical evidence for immunosuppression by Candida mannan and the mechanisms currently proposed for this property; and (iv) we have speculated upon still other mechanisms by which mannan might influence host defense functions. It is possible that understanding the immunosuppressive effects of mannan will provide clues to novel therapies for candidiasis that will enhance the efficacy of both available and future anti-Candida agents.

This is a great article citing the interplay between the fungus and the host defenses :

http://courses.path.utah.edu/classes/path7310/Documents/WV-InfectionAndImmuni...