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Lactobacillus, Bifidobacteria, Bacteroides, Clostridia, Fusobacteria, Eubacteria, Peptococcus, Streptococcus, Escherichia and Veillonella. They regulate a myriad of host processes and provide several nutrients to their host and their symbionts within the microbial community. In healthy individuals, these relationships are thought to occur in equilibrium; however, the normal balance of gut microbiota can be altered by a number of factors and this is turn can contribute to certain functional disorders.[39] For example, the number of different commensal bacteria is altered in inflammatory bowel disease (IBD). IBD patients have increased bacteroides, adherent or invasive Escherichia coli, and enterococci, and reduced Bifidobacteria and Lactobacillus species.[40]
The composition of the gut microbiota can be altered by various factors including stress. Psychological stress alters the gut microbiota towards decreased numbers of Bifidobacteria and Lactobacilli.[41] Bifidobacteria are a group of bacteria that have been shown to reduce intestinal LPS levels and LPS-induced activation of nuclear factor-kappa B (NF-κB) in mice.[42] Inhibition of LPS-induced NF-κB activation was accompanied by a dose-dependent decrease of pro-inflammatory cytokines and cyclooxygenase 2.[42] Stress in neonatal Rhesus monkeys was reported to suppress the numbers of Lactobacilli in the fecal flora in association with increased susceptibility for opportunistic infections.[43]
Restraint conditions, acoustic stress and food deprivation have all been shown to negatively alter gut microbiota in various animal studies.[44,45] Interestingly, stress (e.g., psychological, physical exhaustion) is a well-established trigger factor for CFS.[12]
Investigations have documented that there are marked alterations in the gut microbiota of CFS patients, with lower levels of Bifidobacteria and higher levels of aerobic bacteria.[18] Dr. Henry Butt and colleagues from the University of Newcastle, Australia have been examining the intestinal microbiota of CFS patients for a number of years. In 1998, they presented the first evidence of altered fecal microbiota in CFS patients compared to normal, healthy controls.[46]
The mean distribution of the Gram negative Escherichia coli as a percentage of the total aerobic flora of control subjects was 92.3% compared to 49% in CFS patients. Among aerobes, the D-lactic acid producing Enterococcus and Streptococcus species were strongly over-represented in CFS patients. These findings were recently confirmed.[22] Among anaerobic bacteria, Prevotella was the most commonly overgrown bacteria. Moreover, it was shown that the higher the aerobic enterococcal count, the more severe the neurological and cognitive deficits including nervousness, memory loss, forgetfulness and confusion.[46] Consequently, high plasma LPS levels in CFS could result from an increased production of endotoxin upon changes in the gut microbiota.[47]
Mucosal Barrier Function
To protect itself from uncontrolled inflammatory responses, the intestinal epithelium has developed mechanisms to restrain bacterial growth, limit direct contact with the bacteria, and prevent bacterial dissemination into underlying tissue. The mucosal barrier, which consists of only a single layer of epithelial cells, is one of the most important components of the innate immune system, and all that separates the inside of the body from a very “dirty” outside environment. Thus, mucosal barrier function is a key component in the arsenal of defense mechanisms required to prevent infection and inflammation. Mucosal barrier function is maintained by several interrelated systems, including mucous secretion, chloride and water secretion, and binding together of epithelial cells at their apical junctions by tight junction proteins. Together, they act as the “gatekeeper” of the mucosal barrier.
Disruption of mucosal barrier function occurs in CFS as demonstrated by the increased serum concentrations of IgA and IgM to LPS of gram-negative enterobacteria.[12] Psychological stress disrupts the mucosal barrier allowing increased entry of antigens and microorganisms, which in turn is expected to stimulate hyperactive responses in the mucosal immune system. For example, chronic water avoidance stress in rats induces increases in the adherence of bacteria to intestinal epithelial cells, bacterial internalization into enterocytes and the appearance of bacteria in the lamina propria.[48] Consequently, mucosal barrier dysfunction causes alterations in gut motility, abnormal secretion, and changes in visceral sensation that could contribute to symptom generation. This may at least partially explain the link between stress and CFS. The relationship between IBS and CFS may also reflect in part disorders in gut permeability as altered gut microbiota (e.g., higher numbers of Veillonella and Lactobacillus than healthy controls) and a disrupted mucosal barrier are found in patients with IBS.[49,50] Furthermore, IBS patients with high acetic acid or propionic acid levels presented more severe symptoms, impaired quality of life and negative emotions.[50] Butt and colleagues reported that fatigue presentation in CFS patients with symptoms of IBS was more severe than in CFS patients without irritable bowel.[46] Furthermore, patients with both CFS and IBS had poorer appetite, increased abdominal pain, increased severity of loose stools, diarrhea, nausea, and gastric reflux. The gut microbiota influences the sensory, motor and immune system of the gut and interacts with higher brain centers even at extremely low levels.[50] So aberrant gut microbiota and gut barrier dysfunction may actually be creating an “irritable” bowel. Altered intestinal microbiota and gut barrier dysfunction could also contribute to the symptoms of CFS through increased translocation of LPS from gram-negative enterobacteria.
Therapeutic Restoration of Mucosal Barrier Function
Since altered intestinal microbiota and gut barrier dysfunction barrier are found in CFS,[18] they offer potential targets for intervention that would include modulation of the gut microbiota to correct an imbalance, as well as tightening of interepithelial junctions. Enhancement of barrier function by probiotic bacteria has been observed in both in vitro models and in vivo animal models.[51]
Probiotics are live microorganisms with a vast array of therapeutic potential for GI disease. They have a beneficial effect on the intestinal mucosa via several proposed mechanisms that include inhibition of the mucosal adhesion of pathogens, improvement of the barrier function of the epithelium, and alteration of the immune activity of the host.
They may also regulate intraluminal fermentation and stabilize the gut microbiota.[39] In addition, probiotics have recently emerged as promising adjunctive therapy in treating IBS, with B. infantis becoming the frontrunner for treatment (for review see [52]).
Probiotic bacteria are Lactobacilli spp., certain types of Streptococcus, and Bifidobacteria spp., but also other non-pathogenic bacilli such as E. coli-Nisle 1917 and yeasts such as Saccharamyces boulardii. They secrete short chain fatty acids, an action that results in decreased luminal pH and production of bactericidal proteins. Butyric acid, a byproduct of bacterial fermentation of fiber, has been shown to nourish colonic enterocytes, enhancing mucosal integrity.[53] In addition, probiotics may improve bowel dysmotility.[53]
Researchers have demonstrated the utility of probiotics for mood regulation in CFS patients.[54] Administration of Lactobacillus casei strain Shirota (LcS; 24 billion cfu/day) to adult patients meeting the formal diagnostic criteria for CFS, was found at eight weeks to cause a significant rise in both Lactobacillus and Bifidobacteria in those taking the LcS and there was also a significant decrease in anxiety symptoms.[54] The elevation of Bifidobacteria levels should be considered a positive finding, particularly when considering that Bifidobacteria levels may be low in CFS.[18]
Bifidobacteria appear to play an important role in maintaining the gut barrier. An increase in Bifidobacteria in ob/ob mice was associated with a significant improvement of gut permeability measured in vivo; this improvement was linked to an increase in tight junction mRNA expression and protein distribution.[47] In addition, the rise in Bifidobacteria was correlated with a decrease in plasma LPS concentrations; therefore, a significant reduction inmarkers of oxidative and inflammatory stress.[47]
Bifidobacterium infantis can boost serotonin levels in areas of the brain associated with anxiety and depression. Improvements in anxiety scores among those CFS patients consuming LcS bacteria are especially noteworthy.[54]