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Candida, Bacterias and Immunosuppression.

Research shows that bacteria have the capacity to trigger immunosuppression, thus hindering the body's defense against candida.

This section contains two versions: an easy to understand one for parents and another version for scientists with references.

For Parents

Bacteria has the ability to suppress your immune system. Some children with autism are likely to have an overgrowth of yeast because of their weakened immune systems.

Children with autism have been shown to have very high numbers of bacteria that are able to cause disease. Being infected with these bacteria can cause suppression of the immune system. This might be due to the loss of Dendritic cells (cells that regulate the immune system). This can happen when the toxins from the bad bacteria get into the blood or tissues.

LPS is a bacterial toxin. Research has found that LPS can decrease the number of Dendritic cells (those good cells that regulate the immune system!).

When your immune system is suppressed, you are much more likely to have an overgrowth of candida (bad yeast). Studies of mice have shown a 100 fold increase in yeast in mice that had weakened immune systems.

By eliminating bad bacteria, it will help to strengthen the immune system.

Adapted by Diane D.

Scientific Version

Some children with autism are vulnerable to Candida because they are immunocompromised. Autism researcher, Teresa Binstock, wrote: "Autism is associated with a variety of immune atypicalities whose documentation indicates that a subgroup of autism- spectrum children is at least to some extent immune impaired (eg, 17-19), thereby increasing the likelihood of significant Candida." [1] Teresa Binstock provides links in her article to prove her assertion that children on the ASD spectrum have immune impairment.[1]

We see the role of bacteria for producing the condition of being immunocompromised. It has been shown that children with autism have very high numbers of pathogenic bacterias. There is evidence that sepsis (microbial infection) causes immunosuppression and that this might be due to the dramatic loss of Dendritic cells (DCs) and later dysfunction in DC activity that occurs with sepsis. [2][3]

LPS, a bacterial toxin, has been implicated for causing depletion in Dendritic cells (DCs) numbers and a later dysfunction in DC activity.

There is a research article that explains how LPS affects Dendritic cells (DCs). "48 hours after LPS injection, the number of splenic DC decreased markedly, an observation that correlates with an impaired capacity to activate naive T lymphocites in vitro and vivo."[5] LPS also affects the maturation of Dendritic cells and renders them mature. [6] This is not a good thing since "Immature DC have been shown to take up and process antigen, a property that can be lost in mature DC."[5A]

The endotoxin (LPS) from gram negative bacteria are not the only culprit; components from gram positive bacteria are also capable of this damage.[7].

Being immunosuppressed makes a mammal very vulnerable to systemic candidosis. An experiment was done to assess the difference between immunocompromised mice and non-immunocompromised controls after an inoculation with Candida albicans. The results were dramatic: "Cultures of the homogenized stomach showed a 100-fold increase in colony forming units (c.f.u.) of C. albicans compared with stomach homogenates of infected but non-immunocompromised controls." Moreover, there was another important difference: the candida of non immunocompromised mice, was primarily localized in the stomach and intestines while the immunocompromised mice had candida in many parts of their body including the esophagus, liver and occasionally in the lungs and kidneys.[8]

This experiment illustrates how important it is to eliminate the bacteria that cause immunosuppression.


[1] Click here to view the article by Teresa Binstock

[2] Click here to view this article on PubMed

1: J Immunol. 2002 Mar 1;168(5):2493-500.

Depletion of dendritic cells, but not macrophages, in patients with sepsis.

Hotchkiss RS, Tinsley KW, Swanson PE, Grayson MH, Osborne DF, Wagner TH, Cobb JP, Coopersmith C, Karl IE.

Department of Anesthesiology, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110, USA.

Dendritic cells (DCs) are a group of APCs that have an extraordinary capacity to interact with T and B cells and modulate their responses to invading pathogens. Although a number of defects in the immune system have been identified in sepsis, few studies have examined the effect of sepsis on DCs, which is the purpose of this study. In addition, this study investigated the effect of sepsis on macrophages, which are reported to undergo apoptosis, and MHC II expression, which has been noted to be decreased in sepsis. Spleens from 26 septic patients and 20 trauma patients were evaluated by immunohistochemical staining. Although sepsis did not decrease the number of macrophages, sepsis did cause a dramatic reduction in the percentage area of spleen occupied by FDCs, i.e., 2.9 +/- 0.4 vs 0.7 +/- 0.2% in trauma and septic patients, respectively. The number of MHC II-expressing cells, including interdigitating DCs, was decreased in septic, compared with trauma, patients. However, sepsis did not appear to induce a loss of MHC II expression in those B cells, macrophages, or DCs that were still present. The dramatic loss of DCs in sepsis may significantly impair B and T cell function and contribute to the immune suppression that is a hallmark of the disorder.

PMID: 11859143 [PubMed - indexed for MEDLINE]

[3] Click here to view this article on PubMed

1: J Leukoc Biol. 2008 Mar;83(3):439-46. Epub 2007 Nov 16.

Dendritic cells at the interface of innate and acquired immunity: the role for epigenetic changes.

Wen H, Schaller MA, Dou Y, Hogaboam CM, Kunkel SL.

University of Michigan Medical School, 109 Zina Pitcher Place, Ann Arbor, MI 48109-2200, USA.

Dendritic cells (DC) are known to be essential immune cells in innate immunity and in the initiation of adaptive immunity. The shaping of adaptive immunity by innate immunity is dependent on DC unique cellular functions and DC-derived effector molecules such as cytokines and chemokines. Thus, it is not surprising that numerous studies have identified alterations in DC number, function, and subset ratios in various diseases, such as infections, cancers, and autoimmune diseases. Recent evidence has also identified that immunosuppression occurring after severe systemic inflammation, such as found in sepsis, is a result of depletion in DC numbers and a later dysfunction in DC activity. This correlation suggests that the sustained DC dysfunction initiated by life-threatening inflammation may contribute to the subsequent immunoparalysis, potentially as a result of the long-term maintenance of an abnormal gene expression pattern. In this review, we summarized the present information regarding altered DC function after a severe, acute inflammatory response and propose a mechanism, whereby epigenetic changes can influence long-term gene expression patterns by DC, thus supporting an immunosuppression phenotype.

PMID: 17991763 [PubMed - indexed for MEDLINE]

[5]De Smedt, T., B. Pajak, E. B., L. Muraille, E. Lespagnard, P. Heinen, J. De Baetselier, O. Urbain, O. Leo, M. Moser. 1996. Regulation of dendritic cell numbers and maturation by lipopolysaccharide in vivo J. Exp. Med. 184:1413.

To view a brief summary:

Click here to view this article.

Second paragraph after introduction.

[5A] Last Paragraph of the article mentioned in the link above.

Click here to view this article.

"Immature DC have been shown to take up and process antigen, a property that can be lost in mature DC."


Click here to view this article on PubMed

1: J Immunol. 1998 Nov 1;161(9):4476-9.

Antigen-specific T lymphocytes regulate lipopolysaccharide-induced apoptosis of dendritic cells in vivo.

De Smedt T, Pajak B, Klaus GG, Noelle RJ, Urbain J, Leo O, Moser M.

Département de Biologie Moléculaire, Université Libre de Bruxelles, Rhode-Saint-Genèse, Belgium.

The potent accessory properties of dendritic cells (DC) develop sequentially during a process termed "maturation." Splenic DC undergo functional maturation in vivo in response to the bacterial product LPS and migrate from the marginal zone to the T cell areas. The redistribution of fully mature DC, which present Ags encountered in the periphery, in the T cell area is likely to result in T cell priming. Unexpectedly, we found that DC rapidly die by apoptosis once they have entered the T cell zone. Injection of OVA peptide in OVA-specific, TCR-transgenic mice strongly delays the LPS-induced apoptosis of DC in situ. We conclude that mature DC are programmed to die unless they receive a survival signal from T cells and that the regulation of DC survival may be a mechanism aimed at controlling the initiation and the termination of the immune response.

PMID: 9794369 [PubMed - indexed for MEDLINE]

[7]Click here to view this article

Scroll down to the lower 3/5 of the article. It is the second paragraph of the section called: DISCUSSION)

From the full article:

"A variety of components released from Gram-negative as well as Gram-positive bacteria has been shown to induce maturation of DC [18 19 20 21 ].

[8] Click here to view this article

1: J Med Vet Mycol. 1989;27(6):363-80. Gastrointestinal and systemic candidosis in immunocompromised mice.

Cole GT, Lynn KT, Seshan KR, Pope LM.

Department of Botany, University of Texas, Austin.

Oral-intragastric inoculation of 6-day-old outbred Crl:CFW(SW) BR mice with Candida albicans can lead to colonization of the gastrointestinal (GI) tract. We have shown that in the absence of an immunocompromising treatment, Candida is primarily localized in the stomach and intestines of mice at 20 days post-inoculation. Cultures of homogenates of the esophagus of most animals tested, and homogenates of the liver, lungs, spleen and kidneys of all animals tested, proved negative for C. albicans. Previous histological examinations of the GI tract of these colonized, non-immunocompromised mice showed hyphal elements associated with the stratified, squamous epithelium of the stomach in the region of the cardial-atrium fold. In this study, mice were immunocompromised by intraperitoneal injection of cyclophosphamide and cortisone acetate 11-14 days after oral-intragastric challenge with C. albicans and then sacrificed 20 days post-challenge. A high density of invasive hyphae was observed in the same, cardial-atrium region of the stomach of these animals. Cultures of the homogenized stomach showed a 100-fold increase in colony forming units (c.f.u.) of C. albicans compared with stomach homogenates of infected but non-immunocompromised controls. In addition, homogenates of the esophagus and selected body organs of most immunocompromised mice examined were positive for C. albicans by plate culture. When the immunocompromising drug treatment was delayed 3-5 weeks after oral-intragastric challenge, proliferation of C. albicans in the stomach and intestines was still evident, although fewer mice showed systemic spread and lower numbers of c.f.u. were recovered from body organ homogenates. Abscesses which contained both C. albicans hyphae and yeast cells were frequently observed in the liver and occasionally in the lungs and kidneys of immunocompromised mice sacrificed 20 days post-inoculation. The frequent occurrence of abscesses in the liver simulates a clinical variant of this mycosis, referred to as focal hepatic candidosis, which has been recognized with increasing frequency in immunocompromised patients. We suggest that the animal model described here may be particularly useful both for exploring methods which may prevent dissemination of C. albicans from localized foci of colonization in the GI tract after exposure of the host to immunocompromising drugs, and for testing the efficacy of anti-Candida drugs in clearance of the pathogen from body organs with established fungal abscesses.

PMID: 2628558 [PubMed - indexed for MEDLINE]

Other Important Information about Candida and Bacteria.

Click here to read how bacteria help candida to live in biofilms.

Click here to view more articles about candida and bacteria.