Healing, Nutrient Availability in Illness, NO Synthesis, Functional Foods, Priming

[Guest guest]

These are useful review articles, the full papers are available..

http://www.ebmonline.org/cgi/content/full/226/11/1003

MINIREVIEW

Inflammatory Mediators in Gastrointestinal Defense and Injury

L. Wallace,1 and Li Ma

Mucosal Inflammation Research Group, Faculty of Medicine, University

of Calgary, Calgary, Alberta, T2N 4N1, Canada

http://www.ajcn.org/cgi/content/full/75/5/789

American Journal of Clinical Nutrition, Vol. 75, No. 5, 789-808, May 2002

Review Article

Protective nutrients and functional foods for the gastrointestinal tract1,2,3

Also, more on mechanisms involved in inflammatory priming:

http://ndt.oxfordjournals.org/cgi/content/full/21/8/2057

Nephrology Dialysis Transplantation 2006 21(8):2057-2060; doi:10.1093/ndt/gfl281

Intestinal bacterial microflora—a potential source of chronic

inflammation in patients with chronic kidney disease

This paper on the gut bacteria has a good description of how

lipopolysaccharide endotoxins can cross from the GI tract into the

blood, causing that inflammatory priming that has been shown by Drs.

Islam, Dearborn and others to make people MUCH more sensitive to cell

and immune system damage caused by some of the most destructive common

mycotoxins.

Excerpt:

" Bacterial translocation

'Bacterial translocation' describes the passage of viable resident

bacteria and of macro-molecules such as lipopolysaccharide endotoxin

across the intestinal barrier to the blood. There are two pathways for

the passage of substances from the intestinal lumen to the blood, a

paracellular and a transcellular route. Specific membrane pumps and

channels govern the transcellular transport, whereas tight junctions

control the paracellular pathway [5].

Numerous insults, such as infections, both in the intestinal tract and

in other sites (such as pneumonia), inflammatory bowel disease,

parenteral nutrition, malnutrition, surgical stress, burns, shock,

obstructive jaundice, thermal injury, stress, circulatory compromise,

congestion in heart failure and hypoxia, bacterial overgrowth and

reduced intestinal motility may be causative of impaired intestinal

barrier function [2]. Endotoxin concentrations were shown to be higher

in oedematous than in stable congestive heart failure (CHF) patients.

Gut-derived endotoxin may trigger immune activation and inflammatory

responses in CHF patients during oedematous episodes [6].

Pathogens impair the integrity of the intestinal barrier with a number

of different virulence factors. Escherichia coli, Salmonella

typhimurium, Clostridium perfringens, Bacteroides fragilis, Vibrio

cholerae and rotavirus directly disrupt tight-junction proteins [5].

Transcellular migration of E. coli and Proteus mirabilis have been

visualized within intact enterocytes [7]. Host factors have an effect

on bacterial proliferation and mucosal adhesion. Stress mediators such

as norepinephrine and adrenocorticotropic hormone have been shown to

directly enhance the virulence characteristics and adherence of

enterohaemorrhagic E. coli to the colonic mucosa [8,9]. It is

conceivable that sympathetic overactivity, as observed in uraemia, may

also alter intestinal susceptibility to bacterial translocation.

The cellular processes underlying bacterial translocation have been

studied in the rat common bile duct ligation model. In this model

xanthine oxidase (XO) is activated presumably by translocated

bacterial products and XO-derived reactive oxygen species (ROS) are

significantly increased. Inhibition or inactivation of XO by

allopurinol or by a tungsten-supplemented diet normalized the mucosal

ROS and attenuated bacterial translocation significantly [10]. ROS

activate nuclear factor kappa B (NFkB) and the expression of genes

encoding cytokines such as tumour necrosis factor-{alpha}

(TNF{alpha}), interleukin-2 (IL2), IL8, intercellular adhesion

molecule-1 (ICAM-1), and others. Some of these cytokines may promote a

disruption of tight junctions and facilitate bacterial translocation

[11]. "