Gut Microorganisms and Autism: the Latest Research

LPS and Autism

LPS and Mercury

Treatments for LPS

LPS and Behavior

LPS and Detox

LPS and the Brain LPS and Thyroid LPS and GI System LPS and Immunity Other Effects of LPS
LPS and Inflammation LPS and Opioids LPS and Oxidative Stress LPS and Leaky Gut LPS and Candida
Anorexia and LPS NF-κB and LPS Mitochondria and LPS Liver and LPS Ammonia and LPS
Hypoglycemia and LPS Kidney and LPS Allergy and Bacteria Copper, Zinc and LPS Glutathione and LPS

Candida, Bacterias and Biofilms.

While some bacterias inhibit the growth of candida other bacteria assist the candida in ways that are essential for initiating infection.

There were hints that there might be cooperation between bacteria and candida when bacteria were found inside human fungal urinary infections about 40 years ago. [1]

Some types of bacteria assist candida by helping them to adhere to the human body[2]; assistance with adhesion is the biggest favor you can give to a fungi who is seeking to invade the human body.

Research from all over the world support the fact that adherence (AKA attachment) is an extremely important factor. A researcher from Tel Aviv writes in a paper from Microbiol Science: "Adhesion of microorganisms to various mucosal surfaces appears to be essential for initiating infection. The role of adhesion to host surfaces in pathogenesis of human mycoses, particularly the various manifestations of candidiasis, has been shown experimentally and correlated with epidemiological data."[3]

A research paper found that the attachments of Candida Albicans to human cells were low without bacteria.[4] However when the yeast was preincubated with piliated strains of bacteria the number of yeasts attaching to epithelial cells was either tripled or doubled depending on the type of bacteria used.[4]

Attachment is very important for several reasons; one extremely important advantage for attachment (some scientists use the term adhesion) is the ability to form biofilms, a special type of microbial colony. An organism cannot be part of a biofilm if it cannot adhere to the host cell or to another microbe that is attached to the host cell.

If an organism has the ability to attach to a certain type of material or host cell, then that organism will be more likely to form a colony or a biofilm on that surface.

A study was done to see if bacterias who had good adherence to plastic would be more likely to form large colonies on a polymer (plastic) surface. The study found that plastic-adherent bacterias were significantly more likely to be located in large cell clusters exceeding 50 cells on a plastic surface.[7]

Adhesion is a prerequisite for several key processes that need to happen in a biofilm

A research paper declares:

"This initial attachment is critical for the formation of a bacterial biofilm, as all other cells within a biofilm structure rely on the interaction between surface and bacterial cell for their survival."[5]

The microorganisms that are anchored inside the biofilm are significantly different from their counterparts who wander freely.[6] (The wanderers are referred to as planktons, from the Greek word that means wanderer.) The microorganisms inside the biofilm need to have their genes surpressed so that they can adapt to the conditions that are needed for maintaining a biofilm. Attachment triggers these genetic changes.[6]

The biofilm is covered with a very slimmy substance that offers protection from the outside world.. When microorganisms form a biofilm, they attach to surfaces and produce extracellular polysaccharides [8]. These extracellular polysaccharides have several names: matrix, slime or extracellular slime. [9]

This slime hinders the body's efforts to fight infection.[9][10] One of the reasons for protection is that the body's defense mechanisms cannot penetrate very well through the thick slime.

Biofilms confer microorganisms with many advantages. The microorganisms living inside biofilms are at least 500 times more resistant to antibacterial agents[6] and are phenomenally resistant to the defense mechanisms of our immune system. [11]

References

[1] Click here to view this article

Last paragraph of the article, just before the references.


[2] Click here to view this article

1: Infect Immun. 1983 Mar;39(3):1354-60.

Modulation of Candida albicans attachment to human epithelial cells by bacteria and carbohydrates.

Centeno A, Davis CP, Cohen MS, Warren MM.

The effects of carbohydrates (mannose and dextrose). Escherichia coli 07KL. and Klebsiella pneumoniae on Candida albicans attachment to epithelial cells was studied. Dextrose had no effect on yeast attachment to epithelial cells. Conversely, mannose significantly decreased both yeast and piliated bacterial attachment (E. coli 07KL, heavily piliated K. pneumoniae) whereas having no effect on nonpiliated K. pneumoniae attachment to epithelial cells. The number of yeasts attaching to epithelial cells was enhanced by preincubation of epithelial cells with piliated strains of bacteria, whereas preincubation with nonpiliated strains of bacteria had no effect on yeast attachment. Scanning electron microscopy showed that piliated bacteria and yeasts were juxtaposed on the epithelial cell surface. These data suggest that certain piliated strains of bacteria can enhance C. albicans attachment to epithelial cells and that type 1 pili of bacteria can be a factor in the enhanced attachment of C. albicans to epithelial cells.


[3] Click here to view this article

1: Microbiol Sci. 1987 Nov;4(11):344-7.Links Pathogenesis of human mycoses: role of adhesion to host surfaces. Segal E.

Department of Human Microbiology, Sackler School of Medicine, Tel Aviv University, Israel.

Adhesion of microorganisms to various mucosal surfaces

appears to be essential for initiating infection. The role of adhesion to host surfaces in pathogenesis of human mycoses, particularly the various manifestations of candidiasis, has been shown experimentally and correlated with epidemiological data.

PMID: 3153600 [PubMed - indexed for MEDLINE]


[4]Click here to view this article


[5] Click here to view this article

1: J Ind Microbiol Biotechnol. 2007 Sep;34(9):577-88. Epub 2007 Jul 6.

Bacterial cell attachment, the beginning of a biofilm. Palmer J, Flint S, Brooks J.

Institute of Food Nutrition and Human Health, Massey University, Palmerston North, New Zealand. J.S.Palmer@massey.ac.nz

The ability of bacteria to attach to surfaces and develop into a biofilm has been of considerable interest to many groups in numerous industries, including the medical and food industry. However, little is understood in the critical initial step seen in all biofilm development, the initial bacterial cell attachment to a surface. This initial attachment is critical for the formation of a bacterial biofilm, as all other cells within a biofilm structure rely on the interaction between surface and bacterial cell for their survival. This review examines what are believed to be some of the most important aspects involved in bacterial attachment to a surface.

PMID: 17619090 [PubMed - indexed for MEDLINE]


[6] Click here to view this article

1: Annu Rev Microbiol. 1995;49:711-45.

Microbial biofilms. Costerton JW, Lewandowski Z, Caldwell DE, Korber DR, Lappin-Scott HM.

Center for Biofilm Engineering, Montana State University, Bozeman 59717, USA.

Direct observations have clearly shown that biofilm bacteria predominate, numerically and metabolically, in virtually all nutrient-sufficient ecosystems. Therefore, these sessile organisms predominate in most of the environmental, industrial, and medical problems and processes of interest to microbiologists. If biofilm bacteria were simply planktonic cells that had adhered to a surface, this revelation would be unimportant, but they are demonstrably and profoundly different. We first noted that biofilm cells are at least 500 times more resistant to antibacterial agents. Now we have discovered that adhesion triggers the expression of a sigma factor that derepresses a large number of genes so that biofilm cells are clearly phenotypically distinct from their planktonic counterparts. Each biofilm bacterium lives in a customized microniche in a complex microbial community that has primitive homeostasis, a primitive circulatory system, and metabolic cooperativity, and each of these sessile cells reacts to its special environment so that it differs fundamentally from a planktonic cell of the same species.

PMID: 8561477 [PubMed - indexed for MEDLINE]

Click here to view this article on PubMed


[7] 1: Infect Immun. 1992 May;60(5):2048-57.

Parallel induction by glucose of adherence and a polysaccharide antigen specific for plastic-adherent Staphylococcus epidermidis: evidence for functional relation to intercellular adhesion.

Mack D, Siemssen N, Laufs R.

Institute for Medical Microbiology and Immunology, University Hospital Eppendorf, Hamburg, Germany.

The initial attachment and the accumulation of Staphylococcus epidermidis on polymer surfaces in multilayered cell clusters embedded in amorphous slime, which together lead to the plastic-adherent phenotype detected by the adherence assay used in this study, have been proposed to be major virulence factors of these bacteria. An antigen specific for plastic-adherent S. epidermidis strains was detected by an indirect immunofluorescence test using absorbed antiserum raised against the strongly plastic-adherent S. epidermidis 1457. A coagglutination assay was established, which allowed the quantitation of the antigen in bacterial extracts under different physiologic growth conditions. Expression of the antigen and of plastic adherence depended significantly on the presence of glucose in the growth medium. Parallel to increased plastic adherence, a 32- to 64-fold increase in the amount of the antigen was detected in bacterial extracts of cells grown in tryptone soya broth (TSB) compared with that in extracts of cells grown in TSB lacking glucose. A parallel time-dependent increase of plastic adherence and expression of the antigen was observed after stimulation by glucose of stationary-phase cultures of plastic-adherent S. epidermidis strains grown in TSB lacking glucose. The antigen consisted most probably of polysaccharide, because its immunologic reactivity was completely abolished by periodate oxidation but was resistant to protease digestion. A significant proportion of cells of plastic-adherent as compared with nonadherent S. epidermidis strains grown in TSB were located in large cell clusters exceeding 50 cells, which completely disintegrated after periodate oxidation of the cell preparations. Periodate oxidation of adherent bacterial films in situ led to release of the adherent cells from the plastic surface. These results strongly indicate a functional relation of the antigen to adherence of S. epidermidis to polymer surfaces, most probably by mediating intercellular adhesion of cells leading to accumulation in multilayered cell clusters.

PMID: 1314224 [PubMed - indexed for MEDLINE]

PMCID: PMC257114


[8] Click here to view this article

1: Clin Infect Dis. 2001 Oct 15;33(8):1387-92. Epub 2001 Sep 20.

Biofilm formation: a clinically relevant microbiological process.

Donlan RM.

Biofilm Laboratory, Centers for Disease Control and Prevention, Atlanta, GA 30333, USA. rld8@cdc.gov

Microorganisms universally attach to surfaces and produce extracellular polysaccharides, resulting in the formation of a biofilm. Biofilms pose a serious problem for public health because of the increased resistance of biofilm-associated organisms to antimicrobial agents and the potential for these organisms to cause infections in patients with indwelling medical devices. An appreciation of the role of biofilms in infection should enhance the clinical decision-making process.

PMID: 11565080 [PubMed - indexed for MEDLINE]


[9] Click here to view this article on PubMed

1: Epidemiol Infect. 1996 Oct;117(2):267-80.

Virulence of Staphylococcus epidermidis in a mouse model: significance of extracellular slime. Deighton MA, Borland R, Capstick JA.

Department of Applied Biology and Biotechnology, Royal Melbourne Institute of Technology, Melbourne, Australia.

The ability to produce large quantities of biofilm on solid surfaces in vitro is believed to distinguish potentially pathogenic strains of Staphylococcus epidermidis from commensals. Biofilm consists of staphylococcal cells encased in a matrix of extracellular polysaccharide (also referred to as slime), firmly adherent to each other and to the underlying surface structure. The association of slime with colonization of catheter surfaces in vivo has been examined extensively. Less attention has been paid to the contribution of slime to infections that occur in the absence of an inserted device. In a mouse model of subcutaneous infection without an implanted device 10 S. epidermidis strains (5 slime-positive, 5 slime-negative) produced abscesses; thus a foreign body is not essential for the expression of virulence by S. epidermidis. Biofilm-positive strains produced significantly more abscesses, that persisted longer than biofilm-negative strains. In these chronic infections, large numbers of staphylococci were associated with macrophages and viable staphylococci were cultured from specimens of pus collected at autopsy. Thus slime or components of slime appear to delay the clearance of S. epidermidis from host tissues, possibly by interfering with intracellular killing mechanisms. However, differences in the capacity to produce abscesses, within both the slime-positive and slime-negative groups, indicate that other factors also contribute to the virulence of S. epidermidis.

PMID: 8870624 [PubMed - indexed for MEDLINE]


[10] Click here to view this article

1: Microbiol Immunol. 1998;42(1):33-40.Links The inhibitory effect of Staphylococcus epidermidis slime on the phagocytosis of murine peritoneal macrophages is interferon-independent.

Shiau AL, Wu CL.

Department of Microbiology, National Cheng Kung University Medical College, Tainan, Taiwan.

The extracellular slime produced by Staphylococcus epidermidis has been shown to interfere with several human neutrophil functions in vitro, such as chemotaxis, degranulation and phagocytosis. Slime production has been suggested as a useful marker for clinically significant infections with coagulase-negative Staphylococcus. Since the main role of macrophages in defense mechanisms is phagocytosis, the effect of slime on the phagocytic activity of macrophages was investigated. The phagocytic activity of murine peritoneal macrophages treated with slime in vitro decreased in a dose-dependent fashion. A similar decrease was also observed in macrophages isolated from mice that had previously received intraperitoneal injection of slime. To investigate whether interferon also plays a role in this process, mice were treated with interferon or an interferon inducer, polyinosinic-polycytidylic acid (poly I:C), together with slime before macrophage isolation. The slime-suppressed phagocytic activity of macrophages was partially relieved by both agents, and the recovery effect of poly I:C in slime-suppressed phagocytosis of macrophages in vivo might be attributed to the increased interferon level in peritoneal fluid and sera. However, when slime was given to poly I:C-pretreated mice, the phagocytic activity remained suppressed. Thus, it appears that slime is able to suppress the phagocytic activity of macrophages regardless of the state of macrophage activation by poly I:C. The results suggest that the inhibition of phagocytosis by S. epidermidis slime may be independent from the activation of interferon.

PMID: 9525777 [PubMed - indexed for MEDLINE]


[11] Click here to view this article

(Fourth paragraph after introduction.)

Once we concede that bacteria lack a complex nervous system that could enable them to determine their location vis--vis the animal body, we deduce that they have certain basic survival strategies that they employ wherever they are. In natural and industrial systems, they form biofilms, within which they are protected from antibacterial chemicals (including natural antibiotics), environmental bacteriophages, and phagocytic amoebae. For these reasons, it should come as no surprise that chronic biofilm infections resist antibiotic therapy and are phenomenally resistant to host clearance mechanisms such as antibodies and phagocytes.