
Contents
What Is Intestinal Dysbiosis?
[dropcap]I[/dropcap]ntestinal dysbiosis is an imbalance of the composition and quantity of microbe populations (called the microbiota), that naturally inhabit our human gut. Dysbiosis causes altered gut immunity, abnormal fermentation of undigested foodstuffs, and impaired production within the colon of certain necessary nutrients such as vitamin K and biotin.
There is growing evidence that dysbiosis of the gut microbiota is associated with the development of both intestinal and extra-intestinal disorders. Intestinal disorders include inflammatory bowel disease, irritable bowel syndrome (IBS), and celiac disease, while extra-intestinal disorders include allergy, asthma, metabolic syndrome, cardiovascular disease, and obesity.1
Microbiota Facts.
Our well-being is uniquely tied to the condition of our gut, which is commonly unhealthy at diagnosis of celiac disease. Our resident microbes which are called commensal, whether beneficial (probiotic) or harmful (pathogenic), play a decisive role in nourishing or damaging the cells that form the intestinal lining. To keep our gut healthy, we need to understand what happens there on a microscopic level.
- The microbiota consists of an estimated 100 trillion microorganisms (ten times the number of our own cells) comprising more than 40,000 species – mainly commensal called probiotic (maintain health) and some pathogenic ones (cause disease) according to metagenomic surveys.
- Probiotic microbiota have a symbiotic relationship with humans, meaning that we need each other for our mutual health. Again, the word describing these microbes is commensal.
- Probiotic microbiota inhibit colonization (invasion and growth) of pathogens by physically preventing them from adhering to the gut lining. Here are other important functions:
- Produce short chain fatty acids (SCFAs) such as propionic acid, acetic acid, i-butyric acid, and i-valeric acid. SCFAs are important and necessary energy byproducts formed during fermentation of undigested carbohydrates in the colon by microbes. SCFAs nourish the colonocytes, the cells that line the colon. They also help absorb salts and water from stool.
- Synthesize and supply vitamins. This is important since humans cannot make most vitamins and these must thus be provided in the diet or by probiotic microbes. Probiotic microbes produce a form of vitamin K and appreciable amounts of biotin, folate, riboflavin, and vitamin B12.2. Lactobacillus planterum and Lactobacillus fermentum particularly produce riboflavin.3 Genome studies show that Lactobacillus fermentum 3872 contains genes required for the synthesis of such vitamins as B1, B2, B5, B7 and B9. These genes may play a crucial role in providing the natural hosts with essential vitamins.4
- Reduce the presence of putrefactive enzymes.
- Protect against toxic substances, such as heavy metals by absorbing them from the intestine. Seven Lactobacillus plantarum and Lactobacillus fermentum strains were shown to remove cadmium and lead from culture medium and are advised for people at risk of cadmium and/or lead exposure.5 Conversely, these heavy metals proved toxic to other probiotics including Lactobacillus brevis, buchneri, and rhamnosus. Cadmium and/or lead are found in many chocolate products made from cocoa beans grown in parts of South America and Africa where the ground contains these metals.
- Contribute to normal bowel movements by adding bulk.
- Protect against invasion by pathogenic microbes (disease causing organisms). For example, Lactobacillus fermentum has been shown to have good anti-microbial features.6 An animal study showed that Lactobacillus paracasei protected against Candida albicans infection.7
- In dysbiosis, the numbers of pathogens increase while various populations necessary for our health decrease. Large scale shifts in commensal populations, rather than occurrence of particular microorganisms, are associated with disease such as obesity, inflammatory bowel disease, celiac disease, and cancer.8
- Nevertheless, mutual benefit exists only if the bacteria are luminally confined by intestinal barriers. Disruption of the gut barrier (tight junctions and brush border), followed by penetration of microbial products into the gut mucosa and circulatory bloodstream, predisposes the host (our bodies) to enterocolitis (inflammation of the intestinal mucosa), systemic inflammation, or septic complications.9
- Co-existing paracellular and transcellular barrier defect in intestinal epithelium was documented in inflammatory bowel disease, celiac disease, and intestinal obstruction.9
- Pathogenic bacteria cause inflammation by specific surface proteins called antigens or markers which trigger our immune system to react with them. Sydora et al. investigating whether live fecal bacteria were necessary for the initiation of an inflammatory response in inflammatory bowel disease or whether sterile fecal material would provoke a similar response found that while both dead and live pathogenic bacteria provoke inflammation, only live fecal bacteria also caused injury and a systemic immune response.10
- Small intestine bacterial overgrowth occurs when symptoms such as diarrhea are related to increased numbers of small bowel bacteria, that is more than 105 bacteria/mm3 in small bowel fluid culture. These bacteria are usually but not exclusively anaerobic (do not need oxygen to thrive).11
A sure indication of dysbiosis is a reduction in the amount of stool in a bowel movement. How so? It is estimated that a third of stool passed is made up of dead microbes that formerly inhabited the gut. That’s a lot of bacteria! It is estimated that the microbiota weigh between 3 and 5 pounds.
Q: So stress causes dysbiosis?
A: Yes. Studies suggest that the effect of psychological stress upon the microbiota is a universal process, as opposed to either an artifact or isolated finding. Think about this: just 2 hours of stress can kill a majority of our lactobacillus.
What Is Dybiosis In Celiac Disease and/or Gluten Sensitivity?
- Dysbiosis, or the imbalance of intestinal microbiota composition, is associated with celiac disease. Importantly, the severity of disturbances in intestinal balance of microbiota was found to depend on the gravity of the patient’s state.12 That is, the more damage there is to the small intestinal lining, the more dysbiosis is found.
- The metabolic activity of intestinal microbiota in celiacs is different from the general population.13
- Reductions in total Bifidobacterium and B. longum microbe populations were associated with both active and non-active celiac disease when compared to controls in an early study by Collado et al.14
- Bacteroides, Bifidobacterium and lactic acid bacteria (LAB) populations in the duodenum of children with typical celiac disease (active and treated) and controls were found to differ in diversity and species composition which could contribute to features of celiac disease.15
- Results of a study investigating intestinal microbiota (normal bacterial residents) in patients with celiac disease confirms earlier studies showing that with lower levels of the genus bifidobacteria, celiac patients have an imbalance in the intestinal microbiota even while on a gluten-free diet. This fact could favor the pathological process of the disorder. The concentration of bifidobacteria per gram of feces was significantly higher in healthy subjects (2.5, give or take 1.5, x 107 colony forming units [CFU]/gram) when compared to celiac patients (1.5, give or take 0.63, x 108 CFU/gram).16
- Among breast-fed infants, the prevalence of B. uniformis was higher in those with low genetic risk than in those with high genetic risk. Among formula-fed infants, the prevalence of Bacteroides ovatus and Bacteroides plebeius was increased in those with low genetic risk, while the prevalence of Bacteroides vulgatus was higher in those with high genetic risk. The results indicate that both the type of milk feeding and the HLA-DQ genotype (inherited genes) influence the colonization process of Bacteroides species, and possibly the disease risk.17
- Breast-feeding can be a significant source of lactic acid bacteria to the infant gut. Lactic acid bacteria present in milk may have an endogenous origin (arrives in milk) and may not be the result of contamination from the surrounding breast skin.18
- Dysbiosis could be involved in the pathogenesis of celiac disease.19
- Developmental aspects of the adaptive immune system are influenced by intestinal bacterial colonization, and this may underlie disorders such as celiac disease.20
- The gut microbiota shapes intestinal immune responses during health and disease. Evidence demonstrates the capacity of probiotic organisms to influence intestinal immune responses. The common feature of almost all bacterial species used as probiotics is the ability of these organisms to control inflammation. Bacterial species can act on several cell types (epithelial cells, dendritic cells, and T lymphocyte cells), but recent evidence suggests that induction of regulatory T cells by these organisms is crucial to limiting inflammation and disease.21
- It is possible that different classes (or even species) of bacteria induce diverse immunological functions. Therefore, the balance between inflammation and regulation in the gut may be due to the community structure of the microbiota.
- Impact of stressor exposure on the interplay between commensal microbiota and host inflammation. Psychological stress is produced in celiac disease both by the effects of gluten and by insufficiency of many nutrients. Such stress activates multiple physiological processes aimed at maintaining balance within the body. However, these physiological processes also have the capacity to influence the composition of microbial communities in the digestive tract, and research now indicates that exposure to stressful stimuli leads to gut dysbiosis.22While stress alters the relative abundance of many different bacterial types, findings in nonhuman primates and laboratory rodents, as well as humans, indicate that bacteria in the genus Lactobacillus are consistently reduced in the gut during stress.23
How Prevalent Is Dysbiosis In Celiac Disease and/or Gluten Sensitivity?
Intestinal enzyme deficiencies, sugar intolerances and associated dysbiosis appear commonly in persons with celiac disease.25
The concentration of bifidobacteria per gram of feces was significantly higher in healthy subjects (2.5 ± 1.5 x107 CFU/g) when compared to celiac patients (1.5 ± 0.63 x108 CFU/g).26
What Are The Symptoms Of Dysbiosis?
Symptoms depend on the cause of dysbiosis but generally include the following:
- Bloating.
- Brain fog (impaired thinking and memory).
- Diarrhea that may be urgent when the cause is poor carbohydrate digestion.
- Fatigue.
- Hard-to-control to explosive gas, abdominal cramps, and borborygmi (loud noises in belly) when the cause is carbohydrate malabsorption.
- Headache.
- Lingering stinky gas when the cause is fat malabsorption.
- Pale constipation and/or loose floating stools when the cause is fat malabsorption.
- Putrid gas when the cause is malabsorption of protein.
- Small and poorly formed stool.
How Does Dysbiosis Develop In Celiac Disease and/or Gluten Sensitivity?
- Inflammation. Gluten triggers inflammation on contact with intestinal mucosa via the adaptive immune system in celiac disease which harms the microbiota, causing dysfunction and destruction, and might play a primary role together with genetics and gluten intake.27 This same response reportedly occurs in non-celiac gluten sensitivity as well.
- Malabsorption. In this situation, microbial imbalances develop from excessive passage of undigested foodstuffs into the colon which include fat, carbohydrates and protein that results from pancreatic insufficiency, bile insufficiency and digestive enzymopathies (deficiencies). Undigested means unabsorbed.
- Pancreatic insufficiency is the deficiency of pancreatic digestive enzymes lipase, amylase, and protease needed for the digestion of fat, carbohydrates, and protein.
- Bile insufficiency includes the impaired secretion of bile by the liver, obstruction of the bile ducts and abnormal circulation of bile salts that impairs the digestion of fats.
- Deficiency of lactase, sucrase, maltase and protease enzymes results in failure to finish the digestion of sugars and protein required for absorption.
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Poor gut motility. In this situation, impaired movement of foodstuffs through the digestive tract and low stomach acidity commonly found in celiac disease promote fermentation in the large bowel and also overgrowth of yeast and bacteria in the small bowel.
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Nutrient deficiencies. The health and integrity of intestinal cells depends on adequate availability of niacin, zinc and vitamin A. Deficiency of these nutrients sets the stage for inflammation, infection and diarrhea that worsen gut function and induce overpopulation by pathogens.
- Stress. Exposure to stressful stimuli leads to gut dysbiosis.22 Celiac disease causes psychological stress which alters the relative abundance of many different bacterial types mainly due to nutritional deficiencies, but also the difficulty of maintaining a strict gluten-free diet after diagnosis. Bacteria in the genus Lactobacillus, such as acidophillus, are consistently reduced in the gut during stress.22
Does Dysbiosis Respond To Gluten-Free Diet?
Yes. Celiac disease-related dysbiosis responds to a nutritious, balanced gluten free diet. Supplementation with probiotics and/or addition to the diet of foods rich in probiotics is recommended to quickly restore healthy microbe populations. Acetic acid, such as found in unfermented apple vinegar, is an excellent choice to not only provide probiotic microbes but also to nourish cells that line the colon.
When milk and yogurt were used as food carriers, Lactobacillus plantarum and Lactobacillus fermentum strains displayed a significant ability to survive the upper digestive tract and arrive safely in the colon.28
Many probiotic strains decrease toxic microbial metabolic activities.29
6 Steps To Improve Dysbiosis In Celiac Disease and/or Gluten Sensitivity:
- [dropcap]1[/dropcap]Remove the Trigger. Maintain a Strict, Nutritious Gluten Free Diet:
[box type=”shadow” ]Treatment. This condition responds to the complete elimination of gluten, which is the required treatment that improves both dysbiosis and gut health.
- Gut health is the foundation to restore ALL health. Restored health will enable you to maintain a strict gluten free diet, just as other life tasks will be easier.
- A strict gluten free diet means removing 100% of wheat, barley, rye and oats from the diet.
- Cutting out bread and other obvious sources of gluten is not good enough for recovery. Even 1/8th teaspoon of flour or bread crumb is enough to sustain the inflammation that is damaging your small intestine, causing increased permeability (leaky gut) and allowing undigested gluten to enter your body where it can damage structures and function, and instigate immune inflammatory responses.
Correct Your Individual Nutritional Needs.
- Eat foods that can replenish missing nutrients. Find them under NUTRIENT DEFICIENCIES.
- Take nutritional supplements as needed. Find them under NUTRIENT DEFICIENCIES.
Recovery. You should begin to feel better within a week and notice more energy as inflammation subsides and the absorbing cells that make up the surface lining of your small intestine are better able to function.
- Intestinal lining cells are replaced every 5 days. The healing process is like sunburn where the damaged surface layer of skin sloughs off and is replaced with new normal cells.
- Leaky gut normally resolves in two month after starting a gluten free diet and brings about a big improvement in health. Improvement in intestinal permeability precedes morphometric recovery (cell appearance and structure) of the small intestine in celiac disease.30
- The intestinal lining may take up to a year to heal. Dysbiosis definitely inhibits normal recovery. [/box]
- [dropcap]2[/dropcap] Reduce Inflammation. Foods to Eat and Foods Not to Eat:
Because gluten is inflammatory, eliminate OTHER inflammatory foods from your diet to reduce an additive effect to gluten. At the same time, try to eat foods that reduce inflammation (anti-inflammatory).
[box type=”shadow” ]Here Are Major Inflammatory Food Types That Reduce Healing:
- Damaging Foods. In susceptible persons, includes corn, dairy (cow), and soy. Lactose, the sugar in any animal milk, disrupts intestinal permeability causing leaky gut.31
- Allergenic Foods. Includes foods that trigger the immune sytem to produce IgE antibodies. Allergy testing is the usual way to discover these offending foods.
- Shelf Stable Processed Foods. Includes any that contain additives and preservatives. Look for them on the nutrition label of the box or package. Additives and preservatives also disrupt intestinal permeability causing leaky gut.31
- Fats. Limit deep fried foods, trans-fats, saturated fats (animal fat/butter), and EXCESSIVE omega-6 fatty acid oils like corn oil. Rancid fats, sodium caprate (a medium chain fat), and sucrose monester fatty acid (a food grade surfactant) induce significant disruption of the intestinal barrier that causes leaky gut.31.
- Excessive Refined White Flours (bran layer removed). Includes products made from them such as cookies, bread, cakes, pies. Bran contains the vitamins and minerals that metabolize grains and slows the otherwise rapid entry of sugar from their digestion into the bloodstream. Also disrupt intestinal permeability causing leaky gut.31
- Refined Sugars. Includes white sugar, corn fructose and high fructose corn syrup.
- Certain Spices. Includes paprika and cayenne pepper which disrupt intestinal permeability causing leaky gut.31
- Alcohol and Caffeine. Disrupt intestinal permeability causing leaky gut.31
- Cocoa and Black Tea increase blood sugar.
- Rosemary. Increases blood sugar levels and should not be used by persons with insulin resistance or diabetes. [/box]
[box type=”shadow” ]Here Are Important Anti-Inflammatory Food Types to Promote Health:
- Fruits. Contain ample amounts of vitamins, minerals and phytochemicals which are naturally occuring components in plants that detoxify toxins, carcinogens (reducing the risk by 50%) and mutagens. This includes unfermented apple cider and apple cider vinegar.
- Non-Starchy Vegetables. Support intestinal integrity and provide ample amounts of vitamins, minerals and phytochemicals. Includes green leafy vegetables such as lettuce and kale, also onion, broccoli, garlic, and others.
- High Quality Complex Carbohydrates. Provide vitamins, minerals, and fiber while boosting serotonin levels to help you relax and feel calm. Includes whole grains, legumes, and root vegetables such as carrots, parsnips, sweet potatoes, turnips, red beets, and others.
- Antioxidants. Protect the body from inflammatory oxidant molecules that continually occur and help us handle stress and reduce irritability. Includes vitamin C-containing foods such as lemon, grapefruit, apricot, Brussels sprouts and strawberries, and others. Also, includes vitamin E-containing foods such as nuts, seeds, avocado, olive oil, and others. Cocoa is good, too.
- Omega-3 Fatty Acids. Balance opposing omega-6 fatty acids and bad fats. Fish sources includes tuna, salmon, cod, and others. Plants sources include flax, chia seeds, canola oil, and others.
- Probiotics. Supply normal microbes needed for colon health and health of the body. These are found in such fermented foods as these: yogurt, kefir, and unpasteurized apple cider vinegar and rice vinegar. Note: most yogurts are pasteurized which kills organisms, so that if live bacterial cultures (probiotics) are not added after the heat treatment, such yogurts would not be a source of probiotics. Sheep and goat yogurts a excellent sources of probiotics for people who cannot have dairy.
- Prebiotics/ High Fiber Foods. Food with fiber keeps our population of colonic microbes healthy.
- Protective Herbs and Spices. See below #6 below for examples.[/box]
- [dropcap]3[/dropcap] Information Sheet You Can Take to Your Doctor or Other Health Professional:
Click here.
- [dropcap]4[/dropcap] Manage Your Medications Safely:
[box type=”shadow” ]
Certain medications cause leaky gut and/or dysbiosis along with depleting various nutrients important for gut health. Ask your doctor or pharmacist about this possible adverse effect if you are taking any of the drugs listed below. Do not stop prescribed medications without supervision.
This is not a complete listing.
ANTIBIOTICS disrupt intestinal permeability which complicates celiac disease and deplete probiotic microbes.
- Gentomycin, Neomycin, Streptomycin, Cephalosporins deplete B Vitamins, Vitamin K, Probiotics, Vitamin C.
- Tetracyclines deplete Coenzyme Q10, Calcium, Magnesium, Iron, Vitamin B6, Zinc, Probiotics, Riboflavin.
- Cipro depletes Coenzyme Q10, Zinc.
- Dapsone depletes vitamin K.
- Penicillins deplete Vitamin B2, Folic Acid, Vitamin B12, Biotin, Vitamin K, Probiotics.32
- Erythromycin depletes Vitamin B2, Folic Acid, Vitamin B12, Biotin, Vitamin K, Probiotics.33
ANTI-INFLAMMATORIES disrupt intestinal permeability which complicates celiac disease.
- Corticosteroids (Prednisone, Medrol®, Aristocort®, Decadron) deplete Calcium, Vitamin D, Magnesium, Zinc, Vitamin C, Vitamin B6, Vitamin B12, Folic Acid, Selenium, Chromium, Phosphorus.
- NSAIDS (Motrin®, Aleve®, Advil®, Anaprox®, Dolobid®, Feldene®, Naprosyn® and others) deplete Folic acid.
- Aspirin and Salicylates deplete Calcium, Folic acid, Vitamin C, Iron, Pantothenate (vitamin B5).
FEMALE HORMONES disrupt intestinal permeability which complicate celiac disease.
- Oral Contraceptives (Norinyl®, Ortho-Novum®, Triphasil®, and others) deplete Vitamin B2, Vitamin B3, Vitamin B6, Vitamin B12, Vitamin C, Folic Acid, Magnesium, Selenium, Zinc, Phosphorus. Correlation analysis shows significant association between some trace elements and the duration of contraception and body mass index of the study participants.34
- Oral Estrogen/Hormone Replacement (Evista®, Prempro®, Premarin®, Estratab® and others) deplete Vitamin B2, Vitamin B6, Vitamin B12, Vitamin C, Folic Acid, Magnesium, Zinc.
[/box]
- [dropcap]5[/dropcap]Nutritional Supplements To Help Correct Deficiencies:
[box type=”shadow” ]
- Multivitamin/mineral combination that provides 100% once a day is useful to improve overall nutrient levels. This is a safe dose, but always check with your doctor to avoid interactions with medications.
- Probiotics that deliver live bacteria.
Storage Note: Store container tightly sealed, away from heat, moisture and direct light to avoid loss of potency. That is, in a safe kitchen cabinet – not in the bathroom or on the kitchen table. Probiotics should be refrigerated.[/box]
- [dropcap]6[/dropcap]Manage Natural Remedies:
[box type=”shadow” ]Hydration:
- Eight glasses of water are recommended per day unless there is a contraindication such as kidney or heart disease. The Institute of Medicine recommends approximately 2.7 liters (91 ounces) of total water, from all beverages and foods, each day for women and 3.7 liters (125 ounces) daily of total water for men.
- If you are thirsty, drink water. Add fresh, squeezed lemon to water. Lemon is anti-inflammatory, alkalizing and provides vitamin C.
- Hydration Test: Urine should be pale yellow. Fingertips should be plump, without pruning but this may not be reliable when fingers are swollen with edema. Lips should be plump, without puckering. The feeling of thirst can be unreliable.
- What is wrong with soda, coffee, tea, and alcohol? These drinks are dehydrating, increase acid, and deplete nutrients.[/box]
[box type=”shadow” ]Carminatives. The following anti-inflammatory plant sources called carminitives help heal the digestive tract. They also tone the digestive muscles which improves peristalsis, thus aiding in the expulsion of gas from the stomach and intestine to relieve digestive colic and gastric discomfort.
Carminative Food Remedies:
- Raspberry.
- Carrot is also a cleansing digestive tonic.
- Grape is also bile stimulating and a cleansing remedy for sluggish digestion and laxative.
- Redbeets also stimulate and improve digestion and are easily digested.
- Cabbage also stimulates and improves digestion and is also a liver decongestant.
- Lettuce also stimulates and improves digestion and is also an alterative, meaning it improves the function of organs involved with the digestion and excretion of waste products to bring about a gradual change.
- Potatoes are antispasmodic (due to atropine like properties) and a liver remedy.
Carminative Herb Remedies:
- Sage is also a digestive, astringent, bile stimulant and energy tonic that heals the mucosa. Drink as tea or use in cooking.
- Chamomile, lemon balm, and fennel, (as a tea) also help relieve nervous tension.
- Parsley also relieves indigestion.
- Rosemary as a tea and in cooking also is a nervous system tonic for stress and fatigue, bile stimulant, and can relieve headaches and indigestion. However, because it increases blood sugar levels, it should not be used by persons with insulin resistance or diabetes.
- Thyme is also soothing remedy useful for stimulating digestion of rich, fatty foods.
Carminative Spice Remedies:
- Cloves are also antispasmodic.
- Nutmeg is also useful for indigestion.
- Ginger.[/box]
[box type=”shadow” ]Exercise Helps:
Exercise improves circulation and rids the body of toxins.
- Walking is aerobic exercise that reconditions the whole body to improve stamina. Read more about Exercise and Fitness.
- Weight training builds muscle. Read more about Exercise and Fitness.
- Stretching improves flexibilty. Read more about Exercise and Fitness.
Note: Exercise is important, but the amount and type of exercise undertaken depends on your health. Your first priority is to heal. [/box]
What Do Medical Research Studies Tell About Dybiosis In Celiac Disease and/or Gluten Sensitivity?
RESEARCH STUDY SUMMARIES
“Lower bifidobacteria counts in adult patients with celiac disease on a gluten-free diet.” This study investigated the concentration of fecal bifidobacteria (normal gut bacteria) and pH (acid/alkaline level) of patients with celiac disease on gluten-free diet and control subjects in order to identify if the imbalance on fecal microbiota still remain during the treatment of celiac disease and identify the necessity of dietary supplementation with pre- or probiotics. Results suggest that with lower levels of bifidobacteria, celiac patients have an imbalance in the intestinal microbiota, regardless of pH, even while on a gluten-free diet. This fact could favor the pathological process of the disorder.
Feces of 42 healthy subjects and 14 celiac patients were analyzed. The bifidobacteria count in feces was done in selective medium BIM-25. Microscopic analysis of the colonies was performed by Gram stain. The identification of the genus Bifidobacterium was performed by determination of fructose-6-phosphate phosphoketolase. Fecal pH was measured using a pH meter.
The concentration of bifidobacteria per gram of feces was significantly higher in healthy subjects (controls) (2.5 ± 1.5 x107 CFU/g) when compared to celiac patients (1.5 ± 0.63 x108 CFU/g). The fecal pH was not different between celiac patients (7.19 ± 0.521) and controls (7.18 ± 0.522).35
“Duodenal-mucosal bacteria associated with celiac disease in children.” This study aimed to characterize the composition and diversity of the cultivable duodenal mucosa-associated bacteria of celiac disease patients and control children. Duodenal biopsy specimens from patients with active disease on a gluten-containing diet (n = 32), patients with nonactive disease after adherence to a gluten-free diet (n = 17), and controls (n = 8) were homogenized and plated on plate count agar, Wilkins-Chalgren agar, brain heart agar, or yeast, Casitone, and fatty acid agar. The isolates were identified by partial 16S rRNA gene sequencing. Renyi diversity profiles showed the highest diversity values for active celiac disease patients, followed by nonactive celiac disease patients and control individuals.
Members of the phylum Proteobacteria were more abundant in patients with activeceliac disease than in the other child groups, while those of the phylum Firmicutes were less abundant. Members of the familiesEnterobacteriaceae and Staphylococcaceae, particularly the species Klebsiella oxytoca, Staphylococcus epidermidis, and Staphylococcus pasteuri, were more abundant in patients with active disease than in controls. In contrast, members of the family Streptococcaceae were less abundant in patients with active celiac disease than in controls. Furthermore, isolates of the Streptococcus anginosus and Streptococcus mutans groups were more abundant in controls than in both celiac disease patient groups, regardless of inflammation.36
“Intestinal Bacteroides species associated with coeliac disease.” This study seeking to characterize the predominant species of bacterial populations associated with duodenal biopsies of pediatric patients with active and treated coeliac disease found that Bacteroides, Bifidobacterium and lactic acid bacteria populations in the duodenum of Spanish children with typical coeliac disease (active and treated) and controls differ in diversity and species composition.20 biopsy specimens from patients with active coeliac disease, 12 from patients with treated coeliac disease, and eight from age-matched controls were evaluated for comparative purposes. Bacteroides, Bifidobacterium and lactic acid bacteria (LAB) populations were analysed by PCR-denaturing gradient gel electrophoresis using group-specific primers.
RESULTS: Bacteroides diversity was higher in biopsy specimens from controls than in those from patients with active and treated coeliac disease. Bacteroides distasonis, Bacteroides fragilis/Bacteroides thetaiotaomicron, Bacteroides uniformis and Bacteroides ovatus were more abundant in controls than in patients with coeliac disease (p<0.05). Bacteroides vulgatus was more frequently detected in controls than in patients with treatedcoeliac disease (p<0.01). Bacteroides dorei was more common in patients with active coeliac disease than in those with treated coeliac disease and control children (p<0.01). Bifidobacterium diversity was higher in patients with coeliac disease than in controls. Bifidobacterium adolescentis and Bifidobacterium animalis subsp lactis were more prevalent in patients with active celiac disease than in patients with treated coeliac disease and control children.
A higher LAB diversity was found in patients with treated celiac disease and controls than in patients with active celiac disease. Weissella spp and Lactobacillus fermentum were more frequently detected in patients with treated celiac disease than in controls and patients with active celiac disease.37
“Imbalances in faecal and duodenal bifidobacterium species composition in active and non-active coeliac disease.” This study investigating the possible relationships between the gut bifidobacteria composition and coeliac disease (CD) in children found reductions in total Bifidobacterium and B. longum populations were associated with both active and non-active CD when compared to controls.
A total of 48 faecal samples (30 and 18 samples from active and no active CD patients, respectively) and 33 duodenal biopsy specimens of CD patients (25 and 8 samples from active and non-active CD patients, respectively) were analysed. Samples (30 faecal samples and 8 biopsies) from a control age-matched group of children were also included for comparative purposes. Gut Bifidobacterium genus and species were analyzed by real-time PCR.
Results: Active and non-active CD patients showed lower numbers of total Bifidobacterium and B. longum species in faeces and duodenal biopsies than controls, and these differences were particularly remarkable between active CD patients and controls. B. catenulatum prevalence was higher in biopsies of controls than in those of active and non-active CD patients, whereas B. dentium prevalence was higher in faeces of non-active CD patients than in controls. Correlations between levels of Bifidobacteriumand B. longum species in faecal and biopsy samples were detected in both CD patients and controls.38
“Bacterial antigens alone can influence intestinal barrier integrity, but live bacteria are required for initiation of intestinal inflammation and injury.” This study in mice investigating whether live fecal bacteria were necessary for the initiation of an inflammatory responseor whether sterile fecal material w ould provoke a similar response found that while both dead and live bacteria provoke inflammation, only live fecal bacteria initiated mucosal inflammation and injury and a systemic immune response. Fecal bacterial antigens in the presence of live bacteria and sterile fecal bacterial antigens have different effects on the initiation and perpetuation of intestinal inflammation.
Three preparations of fecal material were prepared: (1) a slurry of live fecal bacteria, (2) a sterile lysate of bacterial antigens, and (3) a sterile filtrate of fecal water. Each preparation was introduced via gastric gavage into the intestines of axenic interleukin-10 gene-deficient mice genetically predisposed to develop inflammatory bowel disease. Intestinal barrier integrity and degrees of mucosal and systemic inflammations were determined for each preparation group.
Intestinal barrier integrity, as determined by mannitol transmural flux, was altered by both live fecal bacterial and sterile lysates of bacterial antigens, although it was not altered by sterile filtrates of fecal water.39
“Human milk is a source of lactic acid bacteria for the infant gut.” This study investigating whether human breast milk contains potentially probiotic lactic acid bacteria, and therefore, whether it can be considered a synbiotic food found that Breast-feeding can be a significant source of lactic acid bacteria to the infant gut. Lactic acid bacteria present in milk may have an endogenous origin and may not be the result of contamination from the surrounding breast skin.
Lactic acid bacteria were isolated from milk, mammary areola, and breast skin of eight healthy mothers and oral swabs and feces of their respective breast-fed infants. Some isolates (178 from each mother and newborn pair) were randomly selected and submitted to randomly amplified polymorphic DNA (RAPD) polymerase chain reaction analysis, and those that displayed identical RAPD patterns were identified by 16S rDNA sequencing.
RESULTS: Within each mother and newborn pair, some rod-shaped lactic acid bacteria isolated from mammary areola, breast milk, and infant oral swabs and feces displayed identical RAPD profiles. All of them, independently from the mother and child pair, were identified as Lactobacillus gasseri. Similarly, among coccoid lactic acid bacteria from these different sources, some shared an identical RAPD pattern and were identified as Enterococcus faecium. In contrast, none of the lactic acid bacteria isolated from breast skin shared RAPD profiles with lactic acid bacteria of the other sources.40
- Carding S, Verbeke K3, Vipond DT, Corfe BM, Owen LJ. Dysbiosis of the gut microbiota in disease. Microb Ecol Health Dis. 2015 Feb 2;26:26191. doi: 10.3402/mehd.v26.26191. eCollection 2015. [↩]
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