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I’ve found several studies regarding Crohn’s, IBD, diarrhea and e coli that might be of interest. Since e coli is also associated with SIBO as the most common aspirant you might also find mechanism of action so to speak appears to occur in the small intestine. 

Since Crohn’s is somewhat unique as compared to more common gut issues I only cover it briefly in my book.

Endotoxemia

Endotoxins are a toxin that is present inside a bacterial cell and is released when the cell disintegrates. It is sometimes responsible for the characteristic symptoms of a disease, e.g., in botulism.

Lipopolysaccharides (LPS), also known as lipoglycans and endotoxins, are large molecules consisting of a lipid and a polysaccharide composed of O-antigen, outer core and inner core joined by a covalent bond; they are found in the outer membrane of Gram-negative bacteria.

Endotoxemia is a critical component in the development of hemolytic uremic syndrome in a mouse model that closely mimics the condition in humans. Since this condition is caused by the ingestion of E. coli strains that express both a toxin (Shiga-like toxin 2) and LPS, oral administration of colostrum will treat and ameliorate the disease. Bovine colostrum ameliorates diarrhea in infection with diar- rheogenic E. coli, Shiga toxin-producing E. coli and E. coli expressing intimin and hemolysin it supports wound healing and also the regenera- tion of damaged intestinal mucosa.

*Traveler’s diarrhea is usually caused by Escherichia coli. Ac- cording to M. M. Levine (Travelers’ Diarrhea: Prospects for suc- cessful immune prophylaxis. Sand. J. Gastroentrol. 18:121-124, 1983, suppl. 84), this is the bacteria that causes 22-75% of the Travelers’ diarrhea cases that occur in 29-57% of the travelers to less-developed countries.

Mucosa-associated adherent, invasive Esch- erichia coli (E. coli), which are pro-inflammatory and resistant to killing by mucosal macrophages, may be associated with the pathogenesis of CD (Crohn’s Disease).

During malnutrition, endotoxemia impairs immune cell function leading to recurrent infections and accelerates the development of AIDS.

80% of ‘conditions’ are caused by 20% of  ‘issues’

Chance discovery links inflammatory bowel disease with common bacterial gut toxin
New research links common bacterial toxin with IBD.

New research has uncovered a surprise link between a common bacterial toxin found in the gut and inflammatory bowel disease (IBD).

IBD includes long-term conditions such Crohn’s disease and ulcerative colitis.

The John Innes Centre scientists, led by Professor Tony Maxwell, have been working with microcin B17 for several years in their search for new antibiotics. It is produced by E. coli (Escherichia coli) as a weapon against other bacteria in the gut.

“The bacteria that live inside us have a lot of impact on well-being and the twist here is that it’s not the E. coli bacteria but the toxin that’s produced by the bacteria that appears to have an effect,” explains Professor Maxwell.

“They produce these toxins to kill their neighbours in their fight for ecological niches but it appears that the breakdown products of the toxin can initiate gut inflammation,” he adds.

E. coli bacteria exploits Crohn’s disease inflammation

New research links common bacterial toxin with IBD.

A multi-year study of the role of E. coli gut bacteria in Crohn’s disease finds that intestinal inflammation liberates chemicals that nourish the bacteria’s growth and promotes their ability to cause inflammation.

A particular type of E. coli, called adherent and invasive E.coli (AIEC), which stick to and invade cultured epithelial cells from the intestine (the gut lining) and replicate in defensive white blood cells (macrophages), has been isolated in 21 to 63% of patients with ileal Crohn’s disease, leading researchers to suspect AIEC plays a key role in the disease process.

Genetic defects, diet and gut bacteria are all suspected to play roles in Crohn’s disease. Studies have shown that inflammation and the composition of the microbiome (gut bacteria populations) are interlinked, such that when the gut is inflamed, the microbiome switches from more beneficial bacteria to more unfriendly bacteria, such as E. coli.

Toxin provides clues to long-term effects of diarrhea caused by E. coli
Bacteria change surface of human intestine to benefit themselves

A study has found that a toxin produced by E. coli changes intestinal cells to benefit itself, an ability that could provide a clue to why the bacteria have been linked to nutritional problems such as malnutrition and stunted growth.

Fleckenstein and first author Alaullah Sheikh, PhD, a postdoctoral researcher, study enterotoxigenic E. coli (ETEC), a toxin-producing strain of E. coli that is a common cause of severe, watery diarrhea. The bacterium’s so-called heat-labile toxin causes ion channels on intestinal cells to open, triggering an outpouring of water and electrolytes into the digestive tract — in other words, diarrhea.

Since oral rehydration therapy was invented in the 1970s, deaths from diarrhea have dropped by more than 80% worldwide. While invaluable at helping people survive a bout of diarrhea, the therapy does nothing to reduce the number of cases. Worldwide, young children still develop diarrhea an average of three times a year, with the youngest and poorest children bearing the brunt of the caseload — and of the long-term health consequences.

Fleckenstein and Sheikh speculated that ETEC’s heat-labile toxin might be doing more than just causing acute diarrhea and dehydration. If so, it might explain the link between ETEC and malnutrition, stunting and other problems.

Gut reaction: Repeated mild food poisoning triggers chronic disease

Small bacterial infections that may go unnoticed and which the body easily clears without treatment, such as occurs during mild food poisoning, nevertheless can start a chain of events that leads to chronic inflammation and potentially life-threatening colitis.

Alternavita: All you need to know (critical info in a nutshell)..... by focusing exclusively on these foundational health and immune development issues up to 90% of chronic conditions can be eliminated.

WHO STATEMENTS: 2017 Millennium Goal

  1. Breastfeeding,
  2. food (security)
  3. and water security (sanitation)

are major protective factors against malnutrition and critical factors in the maturation of healthy gut microbiota, characterized by a transient bifidobacterial bloom before a global rise in anaerobes. Early depletion in gut Bifidobacterium longum, a typical maternal probiotic, known to inhibit pathogens, represents the first step in gut microbiota alteration associated with severe acute malnutrition (SAM). Later, the absence of the Healthy Mature Anaerobic Gut Microbiota (HMAGM) leads to deficient energy harvest, vitamin biosynthesis and immune protection, and is associated with diarrhea, malabsorption and systemic invasion by microbial pathogens. A therapeutic diet and infection treatment may be unable to restore bifidobacteria and HMAGM.

 

Researchers found that malnourished children’s microbiota failed to follow the healthy pattern they identified in healthy children. The microbiota of malnourished children is immature, lagging in development behind that of their healthy peers. Supplementing these children’s meals with widely used therapeutic foods that increase calories and nutrient density reduces deaths from malnutrition, but it does not fix their persistent microbiota immaturity.

“Perhaps more insidious than slowing growth is malnutrition’s effect on less visible aspects of health, including impaired brain development and dysfunctional immunity, which follow these children throughout their lives”.

The Father of The Microbiome

Dr. Jeffrey Gordon

SIBO

SIBO can cause severe malabsorption, serious malnutrition and immune deficiency syndromes in children (non breastfed) and adults. 

Prognosis is usually serious, determined mostly by the underlying disease that led to SIBO.

 

Immunizations

The WHO recommends that immunization or treatment be orally administered due to economic, logistical and security reasons. Furthermore, this route offers important advantages over systemic administration, such as reducing side effects, as the molecules are administered locally and have the ability to stimulate the GALT immune responses  (Levine and Dougan, 1998Neutra and Kozlowski, 2006Bermúdez-Humarán et al., 2011).

 

Infections

For ANY infectious or parasitic disease to start, it is ALWAYS a requisite that the host suffer IMMUNODEFICIENCY. At the same time, infectious and parasitic diseases themselves cause additional IMMUNE SUPPRESSION and more MALNUTRITION. This immune suppression is SECONDARY to the accumulation of free radicals, especially oxidizing species, that occurs during and after infectious and parasitic diseases.

Clinical Aspects of Immunology and Biochem J.

 

Current IBD Research 2016

Currently available treatments for IBD, which target the systemic immune system, induce immunosuppression, thereby exposing the patient to the risk of infections and malignancy. The interplay between the gut and the systemic immune system determines the final effect on target organs, including the bowel mucosa. Inflammatory bowel diseases (IBD) are associated with an altered systemic immune response leading to inflammation-mediated damage to the gut and other organs.

Clinical & Translational Immunology (2016)
Gastroenterology and Liver Units, Department of Medicine, Hebrew University-Hadassah Medical Center, Jerusalem, Israel

Most importantly, the immune modulatory agents used today for IBD do not achieve remission in many patients.

Not all IBD patients benefit from currently available drugs. Young people with IBD do not want to be on long-term drug therapy. Oral immune therapy, while not yet studied in large cohorts of patients, may provide an answer to this unmet need.

Clinical & Translational Immunology (2016)
Gastroenterology and Liver Units, Department of Medicine, Hebrew University-Hadassah Medical Center, Jerusalem, Israel

Tolerance

Tolerance is the ability of the immune system to ‘see’ and respond appropriately. Without galactose (a necessary sugar) the immune system can not 'see'. Your immune system would not be able to function without galactose Your body wouldn’t know which cells are “good” and what cells are “bad.” Your body wouldn’t know who the invaders were and which ones should be attacked by antibodies. As you will learn the importance of these ‘sugars’ in gut microbiota health is a rapidly expanding field of research, only recently discovered, including HMO's (human milk oligosaccharides).

Why galactose? Milk sugar aka lactose has been shown to be very beneficial for the human body though unlike sucrose, lactose is made up of glucose and galactose. There is no fructose in lactose. It is a healthy disaccharide sugar. Galactose is known as the “brain sugar” and supports brain development of babies and children. Galactose helps triggers long-term memory formation. Galactose has been shown to inhibit tumor growth and stop its spread, particularly to the liver. This beneficial sugar can also enhance wound healing, decrease inflammation, enhances cellular communication, and increases calcium absorption.
What does immune ‘tolerance’ mean in simple language?
Immune tolerance, or immunological tolerance, or immunotolerance, is a state of unresponsiveness of the immune system to substances or tissue that have the capacity to elicit an immune response in a given organism. The Th1 cytokine profile is vital for clearance of certain organisms and ancillary immune activity, and a limiting effect on this cytokine profile may result in reduced chances for overcoming infections especially intra-cellular organisms residing within macrophages. Effective clearance will depend on appropriate macrophage activation (which occurs through IFN≥ release by Th1 and NK cells) and production of nitric oxide. If this pathway is disrupted IFN≥ secretion is blocked, impairing macrophage activation. Persistent blockade of these inhibitory receptors has lead to the breakdown in immune self tolerance, thereby increasing susceptibility to autoimmune or auto-inflammatory side effects, including rash, colitis, hepatitis and endocrinopathies. Many drugs may cause checkpoint blockade toxicity including pharmaceutical drugs termed ‘immuno therapy’ by pharmaceutical companies, these include Mab drugs and cancer treatments. Checkpoint Inhibitor–Induced Colitis: A New Type of Inflammatory Bowel Disease? Madeline Bertha, MD MS, corresponding author1 Emanuelle Bellaguara, MD, Timothy Kuzel, MD, and Stephen Hanauer, MD ACG Case Rep J. 2017; 4: e112. Published online 2017 Oct 11. doi: 10.14309/crj.2017.112 PMCID: PMC5636906 PMID: 29043290

The Elderly

Mammal milk is required for enhanced phagocytosis as shown by research, especially in the elderly. Whole fat mammal milk can actually restore phagocytosis in senescent cells in the elderly. Phagocytosis, by which immune cells ‘eat’ bacteria or infected cells, is one of the mechanisms that help to resist infections. Lactic acid bacteria strains like acidophilus also increases phagocytosis.