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Candida and LPS

Most children with autism have both a yeast and bacterial overgrowth. It was found that they have abnormal levels of gram negative bacterias, the kind of bacterias that contain LPS as well as candida albicans.

We will give you seven reasons as to why it is more important to eliminate the bacteria first and how this will result in improving the yeast problem.

1 The bacterial toxin, LPS, that makes the candida more toxic.

In laboratory research, it was found that the bacterial toxin, LPS, makes the candida more toxic. More mice died if they got injections with LPS three hours after being infected with candida albicans.[1] This means that children with autism will get more hurt by the candida if they have high levels of LPS due to the overgrowth of gram negative bacteria .

2 Bacterias are more harmful than yeast:

Many experts define autism as an auto immune disease because the abberant immune reaction of autistic children is so harmful to their condition. Both yeast and bacteria are destructive to children with autism because they provoke an extreme immune response but the immune reaction from candida is less potent than the immune reaction from LPS, the very common bacterial toxin. Moreover, the immune reaction from candida is predominantly anti-inflammatory as compared to the pro-inflammatory response from LPS. In other words, LPS, the bacterial toxin produces more inflammation and a stronger immune response.[2]

3 Candidiasis is more easily cured in people who are not immunocompromised.

Children with autism are immunocompromised because they have an autoimmunity disorder. There are many research articles that state that LPS plays a key role in the development of autoimmune syndrome. The influence of LPS is so powerful that it can even overcome genetics. Mice who are genetically resistant to autoimmunity may develop autoimmune diseases if they are given a high dose of LPS.

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4 The bacteria protect the yeast from anti fungals.

Many candida and bacteria species live together in biofilms in nature and in the human body. As a matter of fact, the majority of bacteria and yeast grow in matrix-enclosed biofilms. The candida are surrounded by layers of bacteria who form a kind of shield from anti fungals. In the biofilm, the the bacteria protect candida from the anti fungals.[3]

The next three benefits are related to the fact that Bacterias have better ability to form biofilms than yeast therefore Biofilms that contain bacterias offer more protection than biofilms that only contain yeast. [5]The bacterias have the capacity to make bigger biofilms due to their quorum sensing ability; a bigger biofilm offers more protection than a smaller one.

One article, from the website of University College in Dublin, explains the reason:

"The big difference between yeast and bacteria biofilms, said Geraldine, is in how individual cells communicate. Researchers now understand that the cells communicate using what are called quorum sensing molecules. In yeast, if the concentration of quorum sensing molecules is increased, the yeast don't make biofilms, but the opposite is the case for bacteria." [4]

6 One research article suggests that multiple species biofilms may be bigger because of enzyme complementation by some of the species. The article also suggests that the various species in the biofilm can survive longer in times of food shortage if they are not all needing the same nutrients. [] 7 References Increasing the Number of Viable Candida Albicans

View this article in PubMed

1: J Infect Dis. 1995 Jun;171(6):1539-44.
Mortality of Candida albicans-infected mice is facilitated by superinfection of Escherichia coli or administration of its lipopolysaccharide.

* Akagawa G, * Abe S, * Yamaguchi H.

Department of Microbiology and Immunology, Teikyo University School of Medicine, Tokyo, Japan.

Pathogenesis of complex infection with Candida albicans and gram-negative bacteria was studied by determining the influence of infection with Escherichia coli or injection of E. coli lipopolysaccharide (LPS) on mortality of C. albicans-infected mice. Mice were infected intravenously with lethal doses of C. albicans, then treated intravenously at various times with viable E. coli or E. coli LPS, which individually were not lethal. Treatments 3 h after C. albicans infection clearly facilitated the death of the mice. Corresponding to this facilitated death, production of tumor necrosis factor (TNF) in sera was augmented 2 h after LPS injection into the infected mice. Similar increased production of TNF was also observed in mice treated with a nonlethal combination of heat-killed C. albicans and LPS. The number of viable C. albicans in kidneys of the infected mice was increased by LPS treatment, which was assumed to be the main cause of the greater mortality rate.

PMID: 7769289 [PubMed - indexed for MEDLINE]

Click here to view this article on NLM Gateway A service of the U.S. National Institutes of Health

Mannans are Major Immunostimulators of Candida albicans Characterized by an Anti-Inflammatory Cytokine Pattern.

ZIMMERMANN M, WENDEL A, HARTUNG T; Interscience Conference on Antimicrobial Agents and Chemotherapy.
Abstr Intersci Conf Antimicrob Agents Chemother Intersci Conf Antimicrob Agents Chemother. 1999 Sep 26-29; 39: 554 (abstract no. 696).

Univ. of Konstanz, Konstanz, GERMANY.

BACKGROUND: Candida infection is characterized by subacute inflammatory responses and often inefficient host defense. Mannoproteins (mannans) from Candida have been shown to activate human leukocytes.METHODS: Candida blastospores and their mannans prepared according to Kocourek and Ballou induced cytokine release in human whole blood. The pattern of mediators released was compared to bacterial endotoxins (LPS) from Salmonella abortus equi, E. coli, Klebsiella pneumoniae and Salmonella enteriditis.RESULTS: Candida spores even after heat inactivation as well as their mannan at microg levels induced similar amounts of IL-1beta in whole blood incubations. The kinetic of cytokine release induced by mannan compared to LPS was delayed by 4 h. The mannan was negative in the limulus assay for endotoxins and not inhibited by the LPS binding component polymyxin B. Mannan inducible but not LPS inducible cytokine release was inhibited by alpha -D-methyl-mannopyranosid or beta -mannosidase. Compared to the Candida mannan 10[3] to 10[6] times less LPS was required to induce similar amounts of IL-1beta. When equipotent concentrations of all stimuli with regard to IL-1beta stimulation were employed, the mannan induced twice as much TNFalpha , 5 to 10 times more IL-6 and 10 to 100 times more of the anti-inflammatory factors IL-10, prostaglandin E[2] and G-CSF. In contrast, the mannan failed to induce any IFNg . Inhibition of IL-10 by antibodies or prostaglandin E[2] formation by indomethacin significantly increased IL-1beta and TNFalpha formation 2- to 3-fold.CONCLUSIONS: Mannan appears to be a major immunostimulatory component from Candida albicans acting via the mannose receptor. Compared to LPS, mannan was less potent and induced predominantly anti-inflammatory factors which contribute to the poor induction of pro-inflammatory cytokines.