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admin | Cure Bv Naturally | 06.11.2015
Our amazing body, as much a work of art as it is advanced biology, is made up of 100 trillion cells – give or take 10 to 20 trillion. The largest numbers of bacteria in the body are in the gut (aka the large intestine or colon), and mostly in the fecal biotic environment. Bacteria make up most of the flora in the gut; there are between 300 and 1000 different species living in the large intestine. For adults, indigestible and fermentable dietary substances, called prebiotics, are necessary in large amounts to support probiotic populations and activity. The starting point for a healthy gut is eliminating refined foods and consuming a diet containing enough quality prebiotics. There are many health advantages of taking probiotics, including alleviating symptoms of food allergies, decreasing lactose intolerance, increasing resistance to infection, suppressing cancer, and improving digestion and elimination. A healthy diet contains a balanced mix of carbohydrates, fats and oils, protein, and fiber. We’ve recently created a selection of programs based on his work, to help you get real, tested and effective natural solutions. These programs include how to improve thyroid function, how to read your blood tests, and how to support your adrenals naturally.
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People who receive acupuncture – a needling technique used as an alternative medicine treatment – may sometimes develop infections, according to a new case report. In the new case report – published December 11 in the journal BMJ Case Reports – a man in Australia developed a severe bacterial infection after a five-week course of acupuncture that was meant to treat his cervical spondylosis also known as neck arthritis (condition that affects the discs and joints in your neck). The man had experienced even worse neck pain, and had felt ill and feverish for several days, before he went to the emergency room (ER) at Geraldton Regional Hospital in Western Australia. Doctors examined the man’s neck and saw that he had developed cellulitis, a bacterial infection involving the inner layers of the skin which can be dangerous if not treated promptly. Further investigations using magnetic resonance imaging (MRI) showed that the man had developed a painful infection in a joint, known as septic arthritis.
Public-health officials in Australia were sent to investigate the acupuncture clinic where the man was treated. Enter your email address to subscribe to this blog and receive notifications of new posts by email.
Mucosal Immunology - Regulatory T cells promote a protective Th17-associated immune response to intestinal bacterial infection with C.
Top of pageAbstractIntestinal infection with the mouse pathogen Citrobacter rodentium induces a strong local Th17 response in the colon. This microbiome of flora have beneficial effects on resisting viral and bacterial infection, lowering cholesterol, exerting anti-tumor properties, improving food intolerance, and supporting immunity.
The degree of metabolic activity performed by this legion of bacteria in the large intestine is equal to that of any organ in the body! However, since refined foods and over use of antibiotic drugs has weakened our gut environment, replacing bad bacteria with friendly species (probiotics) is important. However, it’s very difficult to recolonize the gut with only oral probiotics, since most are killed in the acid environment of the stomach and then cannot survive in a gut environment with an imbalanced pH, excessive unfriendly and pathogenic bacteria, and not enough prebiotic substances to act as a medium for friendly bacteria to thrive. For health, we need at least 25 grams of fiber each day, but for optimal health and cancer prevention, we’re better off pushing our fiber intake up to 55 grams daily. The infection was detected in the atlanto-axial joint (located in the upper part of the neck). Mark Fisher, a rheumatologist at Massachusetts General Hospital in Boston who treats people with arthritis, said that that infection began in the skin on the man’s neck. Fisher, the Staphylococcus aureus bacteria first entered the man’s bloodstream, and then settled in his neck joint. He was hospitalizes for eight days, and for about six weeks, he was given intravenous antibiotics until his infection cleared. Fisher advises patients to first try taking nonsteroidal anti-inflammatory drug (such as ibuprofen) or acetaminophen. Although this inflammatory immune response helps to clear the pathogen, it also induces inflammation-associated pathology in the gut and thus, has to be tightly controlled.
However, sustained activation of Th17 cells can lead to inflammation-associated immunopathology and pathogen-induced Th17 responses have, thus, to be tightly controlled. Asian countries,[18] United States (including Hawaii), Canada ,[19] and Scotland)[20] due to bacterial resistance. In terms of immune health, the colon, often called the ‘forgotten organ’ is perhaps the most important system of the body.
A probiotic is a live microbial food supplement that beneficially affects the host by improving the intestinal microbial pollution of commensals and restores healthy micobiome balance. Since 1967, he has lived and worked with indigenous tribes, and spends as much time in the high Andean wilderness and deep Amazonian rainforest as possible. We encourage you to make your own health care decisions based upon your research and in partnership with a qualified health care professional.
Lab tests and blood tests also showed the presence of the bacterium Staphylococcus aureus, the doctors said.
Infections may occur any time there is a break in the skin – in this case due to acupuncture – Dr. The bacteria could have severely damaged the man’s neck bones, had the doctors not diagnosed the infection in time, Dr. In fact, the acupuncturist was using all the right procedures to prevent infections of this nature. In this project, we therefore studied the impact of Foxp3+ regulatory T cells (Treg) on the infectious and inflammatory processes elicited by the bacterial pathogen C.
Th17 cells at the crossroads of innate and adaptive immunity against infectious diseases at the mucosa.


In the biological milieu of natural evolution, created over hundreds of thousands of years, it makes sense to reconsider who we are, and how this relates to health and disease.
The relationship between gut flora and human health is not merely commensal (of a non-harmful coexistence), but is also a mutually beneficial, symbiotic relationship greatly important to health. Breast milk has important prebiotic function in the development of a healthy immune system in infants. Consume enough complex carbohydrates, at about 40 to 50 percent of your total calories, in order to have enough energy and fiber.
Williams has over 30 years of clinical experience in the natural health world and has had over 100,000 patient visits over that time.
In 2010, he founded Ayniglobal, a non-profit organization dedicated to protecting indigenous cultures, environments, and intellectual rights.
Using an infection model with the Th17-inducing pathogen Citrobacter rodentium,9 we show in this study that the absence of Treg during the initial phase of infection impairs bacterial clearance, the induction of a protective Th17 response and leads to an enhanced bacterial dissemination to systemic sites. In other words, bacteria have been around a long time and even though very small, they count big when it comes to bodily function. This human microbiome of gut flora have beneficial effects on resisting viral and bacterial infection, improving blood lipid (lowering cholesterol) levels, exerting antitumor properties, improving food intolerance (like sensitivity to gluten or lactose), and supporting immunity. The modern refined food diet contains too many acidic foods, shifting the blood pH towards the acid side. His current work is mainly with the Q’ero people of the Peruvian Andes, and where he teaches Earth-based wisdom and heart-centered spirituality. Surprisingly, we found that depletion of Treg by diphtheria toxin in the Foxp3DTR (DEREG) mouse model resulted in impaired bacterial clearance in the colon, exacerbated body weight loss, and increased systemic dissemination of bacteria. This demonstrates that Treg can help to establish an effective Th17 response in the gut environment, although this comes at the cost of (transient) immunopathology at the site of infection.Top of pageRESULTSTreg depletion enhances susceptibility toward intestinal infection with C.
Nutritional modulation of gut micro-ecology with diet and supplements is one of the most important keys to optimal health.
Consistent with the enhanced susceptibility to infection, we found that the colonic Th17-associated T-cell response was impaired in Treg-depleted mice, suggesting that the presence of Treg is crucial for the establishment of a functional Th17 response after the infection in the gut. The tuber is composed of water and fructo-oligosaccharides, an important prebiotic, sold as yacon syrup. As a consequence of the impaired Th17 response, we also observed less inflammation-associated pathology in the colons of Treg-depleted mice.
Interestingly, anti-interleukin (IL)-2 treatment of infected Treg-depleted mice restored Th17 induction, indicating that Treg support the induction of a protective Th17 response during intestinal bacterial infection by consumption of local IL-2. Formerly from San Diego, he now practices in Sarasota, Florida and teaches at NOVA Southeastern University and also at Emperor’s College of Oriental Medicine in Los Angeles. IL-22 is expressed by Th17 cells in an IL-23-dependent fashion, but not required for the development of autoimmune encephalomyelitis.
This enhanced susceptibility of Treg-depleted mice was accompanied by a markedly increased amount of C. Interleukin-22, a T(H)17 cytokine, mediates IL-23-induced dermal inflammation and acanthosis. Interleukin (IL)-22 and IL-17 are coexpressed by Th17 cells and cooperatively enhance expression of antimicrobial peptides.
One representative shown out of at least five individual experiments with 3–7 mice per group. Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells. Data are one representative of three individual experiments, each with five mice per group. Later, the intensity of bioluminescence signal increased from day 1 to 5 in control as well as Treg-depleted mice. TGFbeta in the context of an inflammatory cytokine milieu supports de novo differentiation of IL-17-producing T cells. Further analysis confirmed that WT controls were able to clear the pathogen after 3 weeks of infection (Figure 1e). However, Treg-depleted mice that survived were able to eventually clear the infection, although with a delayed kinetic compared with control animals (Figure 1e).
Together, these data suggest that depletion of Treg rendered the hosts more susceptible to C. As shown in Supplementary Figure S3, we could detect a substantial frequency of IL-22-producing ILCs in the colon, however with no significant differences between control and Treg-depleted mice. Also, in accordance with the infection kinetics shown in Figure 1d, there was no difference in the bacterial burden in the feces at this time point (Figure 1e and data not shown). This indicates that Treg have no influence on the function of ILC during the early phase of intestinal infection with C.
TGF-beta-induced Foxp3 inhibits T(H)17 cell differentiation by antagonizing RORgammat function. In contrast, we observed a striking defect in Th17 cell induction in Treg-depleted mice at the peak of the adaptive immune response between day 9–12, when these animals started to become moribund. At this time point, the frequency of IL-17-producing T cells in the lamina propria of the colon was reduced by more than 50% (Figure 2a). In addition, we found that this cytokine was significantly reduced on the protein as well as on the transcription level in Treg-depleted mice in anti-CD3 stimulated colonic lamina propria lymphocytes (LPLs) (Figure 2c and d). Similarly, the expression levels of other Th17-associated factors like IL-17F, IL-23r, and CCR6 were significantly reduced in restimulated colonic LPLs from Treg-depleted mice (Figure 2d).
Data shown in the graphs represent mean, pooled from three individual experiments, each with 3–5 mice per group (lower panel). Data are pooled from two individual experiments (lower panel), each with 2–4 mice per group. Cell culture supernatants were collected for IL-22 enzyme-linked immune sorbent assay (ELISA), and (d) cells were harvested and analyzed for gene expression by RT-PCR.
Gene expression was normalized to expression of β-actin and is shown as fold difference.


Data, shown as mean, represent one representative out of three individual experiments, each with 2–4 mice per group. Bar chart represents total number of neutrophils in the colons of mice from different groups (right panel). Direct analysis of the intestine on day 11 after infection revealed high bioluminescent signals in the colon of Treg-depleted mice, whereas the C. Taken together, we conclude that after Treg depletion and the consequent loss of an Th17-associated immune response, the pathogen can expand in parts of the gastrointestinal tract that are usually not colonized.
In addition, a strong bioluminescent signal was also detectable in the livers of Treg-depleted mice, whereas it was below the detection limit observed in control mice (Figure 3d).
The enhanced bacterial load in this organ in Treg-depleted mice was further validated by counting the bacterial colony forming units (Figure 3e), together showing that Treg depletion resulted in an impaired pathogen containment to the colon and elevated systemic bacterial spread.Reduced immunopathology in the colon of treg-depleted miceOral infection with C.
Although Treg-depleted mice showed similar signs of colon crypt hyperplasia (Figure 4, red arrows), suggesting that the turnover of epithelial cell layer was uninfluenced by Treg-cell depletion, we observed significantly less cellular infiltration and signs of tissue structure destruction in Treg-depleted mice compared with infected WT controls (Figure 4).
Red stars indicate severe infiltration and epithelial injury; Red arrows represent crypt hyperplasia. Hence, one mechanism how Treg influence on the development of T-helper cells responses is by depriving T-helper cells of their IL-2.33 Since IL-2 can inhibit the differentiation of Th17 cells,17 this implicated that Treg might promote colonic Th17 induction after C. However, further analysis of the downstream effects of IL-17 revealed that the antibody-mediated IL-2 neutralization failed to restore the recruitment of neutrophils to the colon of Treg-depleted mice (Figure 5c). Accordingly, anti-IL-2 mAb treated, Treg-depleted mice also failed to clear the pathogen as effectively as WT controls (Figure 5d). This discrepancy might be explained by the fact that despite the observed induction of Th17 cells, the total number of IL-17-producing cells per colon was still significantly reduced in anti-IL-2 mAb treated mice (Figure 5e). Data display one representative out of three individual experiments, each with 3–5 mice per group (upper panel). Lower right panel represents total number of neutrophils in the colons of mice from different groups.
Data are pooled from at least four individual experiments, each with 2–3 mice per group. In our model, IL-2 neutralization already leads to an enhanced systemic Th1 response in infected WT controls (Supplementary Figure S7). In accordance with our data, antibody-mediated depletion of CD25+ Treg impaired the downstream recruitment of neutrophils and reduced the local inflammatory response. Our data now indicate that this mechanism is also operational under highly infectious conditions in the gut. Of note, IL-2 neutralization in the absence of Treg resulted in restored Th17 cell frequencies at the local site of infection, but also resulted in systemic side effects during infection, showing that IL-2 neutralization is not a therapeutic option to enhance anti-bacterial immune responses in vivo. More importantly, total numbers of colonic IL-17-producing T cells were still reduced after anti-IL-2 treatment of Treg-depleted mice.
This failure to fully restore the phenotype might be explained by a more complex action of IL-2 on Th17 cells. As outlined by the studies of Pandiyan and Chen,15, 16 the inhibitory effect of IL-2 on the Th17 development is likely to be only functional during the early induction period. Whether this reflects the small increase in the amount of Th17 cells or if other cells types are recruited after IL-2 neutralization is, however, not clear and remains to be studied.Finally, the question remains if this surprising capacity of Treg to support local Th17 induction is of any physiological relevance? Considering the high frequencies of Treg in mucosal tissues, especially the colon (Supplementary Figure S1 and unpublished observations) under normal homeostatic conditions, this might favor the induction of an appropriate Th17 immune response at the initial phase of a mucosal infection.
Thus, the ability of Treg to promote Th17 cells might represent an important mechanism of immune regulation especially in the gut.Top of pageMethodsMice and bacterial strains. BAC transgenic DEREG mice have been described previously.18 All control mice used in experiments were nontransgenic litter of heterogenic DEREG breeding pairs.
Mice were bred and maintained under specific pathogen-free condition in our animal facilities (TWINCORE, Hannover, Germany; Helmholtz Center for Infection Research, Braunschweig, Germany).
All animal experiments were performed in compliance with the German animal protection law (TierSchG BGBl. The mice were housed and handled in accordance with good animal practice as defined by FELASA and the national animal welfare body GV-SOLAS. Citrobacter rodentium (previously known as Citrobacter freundii, biotype 4280) strain ICC180 expressing bioluminescent signal was described previously by Wiles et al.20Reagents and antibodies.
DT (isolated from Corynebacterium diphtheriae) was obtained from Sigma-Aldrich (St Louis, MO). For bacterial burden in colonic feces, stools from infected mice were collected into a preweighed Luria Bertani medium containing tube. Mice were anesthetized with isoflurane carried in 2% O2 and placed in a supine position in a chamber for imaging with an IVIS Spectrum CT (PerkinElmer, Waltham, MA). Uninfected DT-intraperitoneal-injected nontransgenic mice were served as baseline controls. Luminescence emitted from region of interest with the same size in individual mouse was quantified as total flux and pseudocolor images representing intensity from bacteria-derived luminescence were generated. For detection of three-dimensional bioluminescent signal, anesthetized mice were first scanned by computed tomography under the mode of medium resolution and then C. Collected epithelial cells were resuspended in 1 ml of TRIzol (Life Technologies, Darmstadt, Germany) for further RNA extraction. RNA was obtained from cultured LPLs with Qiagen (Hilden, Germany) RNeasy Micro Kit (Qiagen) and further quantified using NanoDrop-1000 spectrophotometer (Peqlab, Erlangen, Germany). Samples were analyzed on a LightCycler 480 II (Roche, Mannheim, Germany).Cytokine production detection by enzyme-linked immunosorbent assay. Tissues were then stained with haematoxylin and eosin (H&E) and were examined by a trained blinded observer.



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