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A healthy Microbiota is an indispensable ally in all the various stages of life.
Eye OphthalResearch, in collaboration with Allergoline, offers you the opportunity to evaluate the Microbiota of your patients.
Single shipping method, valid for both swabs, genetic analyzes, and blood samples for food intolerance investigations.
Shipping to be paid by Allergoline:
book collection in ASSIGNED PORT using the subscription code 107676 in the name of Allergoline Biotech & Research , with delivery in Via delle Caravelle, 11, 56021, Cascina (PI) , using the web page www.sda.it (by clicking on the image) - > BOOK A RETREAT and filling in the fields as shown in the image
In the case of sending multiple withdrawals, please combine everything in a single shipment. Insert in the envelope both the exam request (complete in all its signed parts) and the sample to be analyzed on which the patient's name must be written.
Shipping with ORDINARY MAIL
It is also possible to send the withdrawal by ordinary mail, in this case the shipment is charged to the sender who can choose the most appropriate form (priority mail - registered mail - registered mail 1, etc ...).
The shipping address is Allergoline Biotech & Research - Via delle Caravelle, 11, 56021, Cascina (PI)
FECAL SAMPLING INSTRUCTIONS:
The kit is used to take stool samples to be sent to the laboratory for genetic analysis of the fecal microbiota. Once sealed, the swab protects the integrity of the microbial DNA for months when kept at room temperature. Withdrawal is simple, fast, safe and can also be done easily from home. The stools must be early in the morning, at least seven days after the last antibiotic therapy, do not take laxatives, antidiarrheals, antacids. The test consists of a metagenomic analysis of the intestinal microflora and is performed using Next Generation Sequencing (NGS) technology. The DNA analysis of the fecal microbiota allows to identify a series of bacterial and fungal phylums capable of influencing the composition and balance of the intestinal microbiota, correlating them with the main physiological functions of the host and identifying and characterizing any situations of intestinal dysbiosis .
The kit contains:
The test is very useful for preventive purposes, but also in subjects in which certain problems have already arisen, as well as in patients in particular stages of life such as infancy and aging, pregnancy, breastfeeding, to direct a precise food plan and / or an approach therapeutic
IMPORTANT INFORMATION:
read the instructions carefully before using the kit.
In order to obtain reliable results, only use samples taken from fresh stool.
Empty your bladder before taking the sample.
Collect a stool sample free of urine or water from the toilet.
You may need to use some toilet paper or tissue.
Samples not collected with the methods and quantities indicated may not be analysable
Intended for the collection of microbial cells.
The swab is for single use and for external use only.
Store at room temperature.
Use only if the package is intact and sealed.
In case of need, or if the kit is missing some component, please contact customer service:
ATTENTION:
Do not ingest the stabilizer solution.
If the stabilizing solution comes into contact with the skin or eyes, repeatedly rinse with plenty of water.
The kit should only be used by adults.
Keep out of reach of children - the casing could be a potential choking hazard.
Instructions for fecal sampling
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Instructions for buccal sampling
The sampling is performed with CYTOBRUSH to recover more material from which to extract DNA for the execution of genetic tests.
The withdrawal method is as follows:
Open the pouch and remove the sterile brush.
Pass the brush inside the right and left cheeks for about 30 seconds per side.
Place the brush in the same case and write the patient's surname and first name on the back.
If possible close with adhesive tape, otherwise it is sufficient to fold the flap of the case.
The sample can be kept for a long time at room temperature. It is therefore not necessary to put in place any particular method of conservation even if the sample is sent after several days.
For any doubt and / or further clarification send an email here:
Examples of reports and results
Insights on Polymorphisms
MICROBIOTA-INFLUENCE OF DNA
PTPN2- PROTEIN TIROSIN PHOSPHATASE N2
Chronic intestinal inflammation
The gut microbiota is critical to our health, and well-balanced interactions between the host's immune system and the microbiota are essential to prevent chronic inflammatory bowel disease (IBD).
Genomic association studies have identified several genes related to greater susceptibility to these diseases. Among these, a variant of the non-receptorial protein tyrosine phosphatase (PTP) of tpo 2 (PTPN2) is associated with a reduced risk of developing IBD.
PTPs are proteins involved in the response of B and T lymphocyte receptors and play an important role in immune cell function and intestinal homeostasis.
The loss of PTPN2 functionality is associated with a greater induction of T helper lymphocytes, which play a fundamental role in the immune system, producing a specific response for each type of substance considered foreign. The alteration in the production of T helper lymphocytes leads to an increased susceptibility to intestinal inflammation predisposing to the development of IBD.
The dysfunction of the non-receptor tyrosine phosphatase protein type 2 (PTPN2) also contributes to alterations in the composition of the intestinal microbiota, a condition which in turn predisposes to the pathogenesis of inflammatory bowel disease (IBD).
Recent scientific studies (Sharp et al., 2015 and Yilmaz et al, 2018), in fact, have shown how subjects with the presence of the genetic variant PTPN2 have an altered intestinal bacterial composition, especially as regards the Clostridialeceae and Lachnospiraceae families, which correlates with IBD.
Specifically, the studies report an increase in Roseburia spp. (Lachnospiraceae) and Ruminococcus spp. (Lachnospiraceae) in patients with ulcerative colitis (UC), compared to controls (healthy individuals). In patients with Crohn's disease (CD), however, a reduction of Faecalibacterium spp was identified. (Clostridiaceae), Bilophila spp. (Desulfovibrionaceae), Coprococcus spp. (Lachnospiraceae) and species belonging to the Erysipelotrichaeceae, Clostridiaceae and Ruminococcaceae families, while bacterial species belonging to the Bacteroidaceae family were increased compared to controls (healthy individuals).
In conclusion, the genetic variant PTPN2 was found in association with alterations of the intestinal microflora and an increased risk of developing conditions such as Crohn's disease, diabetes, obesity, colitis and rheumatoid arthritis.
PTPN22 - PROTEIN THYROSIN PHOSPHATASE N22
Predisposition to autoimmune diseases (Type 1 diabetes)
The immune system is finely regulated by a series of enzymatic reactions: the effectiveness of the immune system results in a rapid activation, but also in a fine regulation of the shutdown mechanism, in order not to damage the organism itself.
The cells mainly involved in the immune response are lymphocytes, in particular regulatory T lymphocytes, a dysfunction of which could be one of the contributing causes of the onset of autoimmunity and therefore potentially also of type 1 diabetes mellitus. In practice, the ineffectiveness of this control system could favor the emergence of immune responses against proteins (called antigens) that are expressed by insulin-producing cells and thus eventually trigger their destruction.
Recent studies indicate that a variant of the gene encoding non-receptor protein tyrosine phosphatase type 22 (PTPN22) affects intestinal inflammation by modulating the host response to the intestinal microbiota. This variant has been associated with an increased risk of developing a large number of autoimmune disorders, including rheumatoid arthritis, systemic lupus erythematosus and type 1 diabetes, but protects against the onset of chronic inflammatory bowel disease (1BD). such as Crohn's disease (CD) (in affected patients, the presence of the variant is not related to a milder disease course or fewer complications).
PTPN22 is expressed exclusively in immune cells and serves as an important negative regulator of T and B cell activation, regulates type 1 and type 2 interferon signaling, and is involved in the activation of the inflammasome. Furthermore, PTPN22 influences the muramyl dipeptide (MDP) induced signaling pathways of the bacterial cell wall product. Using both mouse cells isolated from mice lacking the PTPN22 gene (PTPN22 -1), and human cells deprived of PTPN22 gene expression, it was possible to demonstrate that the PTPN22 gene controls the generation and function of a group of regulatory cells called Treg FoxP3 +, transcription factors of the forkhead family expressed by regulatory T lymphocytes.
A loss of function of PTPN22 promotes autophagy, a cellular pathway primarily involved in the removal of damaged proteins and organelles from the cytosol.
Defects in autophagy cause impaired cell function and an increased risk of developing IBD. In addition to changes in the composition of the microbiota, differences in the expression of AMPs: it is possible that PTPN22 influences the release of AMP through the regulation of autophagy.
In a recent study (Spalinger et al., 2019) the breeding of WT mice with PTPN22 - / - mice showed that the phenotype of the PTPN22 - / - mice is transmissible, possibly mediated by the microbiota. In line with this, the researchers found profound differences within the intestinal microbiota, both at baseline and also after the induction of chronic colitis (by DSS, Dextrano Sodium Sulphate): the presence of PTPN22 led to an increase in levels of potentially beneficial bacteria, such as Lactobacillus, and a reduction of potential pathogens, such as Turicibacter sanguinis. In contrast, PTPN22 - / - mice showed a characteristic increase in Akkermansia and Ruminococcus in acute colitis patients,
APOAS- APOLIPOPROTEIN A5
Predisposition to metabolic syndrome
Metabolic Syndrome (MS) represents a combination of cardio-metabolic risk factors including abdominal obesity, insulin resistance, hypertension and dyslipidemia. This set of factors increases the predisposition to the development of type 1 diabetes and cardiovascular diseases.
The APOAS gene, which codes for the apolipoprotein AV (ApoA-V), has been associated with the predisposition to develop MS, related to diet and lifestyle.
This gene is located on chromosome 11 at position 11q23 and is made up of 4 exons and 3 introns. In humans, it is expressed almost exclusively in the liver tissue and, to a lesser extent, in the small intestine.
ApoA-V, the apolipoprotein encoded by APOAS, is a key regulator of plasma triglyceride (TG) levels whose increase represents an important risk factor for the onset of atherosclerosis and cardiovascular diseases.
Several polymorphisms of the APOAS gene encoding this protein have been studied, usually found associated with hypertriglyceridemia, but the mechanism of action, especially in humans, is still unclear. The mechanisms suggested in the literature are different: the first mechanism assumes that APOAS functions as a lipoprotein-lipase activator by increasing the metabolism of TG-rich particles; another mechanism predicts a possible effect of APOAS on the secretion of VLDL particles; finally, the third possibility concerns the acceleration of the uptake by the liver of the remains of lipoproteins.
A study by Zhuet al. (2014) on obese or overweight children, identified an increase in the frequencies of SNPS rs662799 and rs651821 in the APOAS gene compared to controls. This result suggests that genetic variants in the APOAS gene may influence the individual's susceptibility to obesity, correlating with the increase in body mass index (BMI) and with the risk of raising total triglycerides and LDL cholesterol levels. .
Metabolic syndrome arises from a comprehensive series of interactions between genome, diet, lifestyle, and the environment. the intestinal microbiota plays a fundamental role in host metabolism and an altered intestinal microbial flora can predispose to develop MS. Lim et al. (2017) evaluated the association between MS and gut microbiota, in particular by investigating the presence of polymorphisms in the APOAS gene (associated with an increased risk of MS). The results of the study highlighted how subjects with positive polymorphism have a reduction in the Actinobacteriaceae and Bifidobacteriaceae families, a condition predisposing to MS.
In conclusion, the intestinal microbiota can influence the metabolism of the host, but also the genetics of the host can influence the variability of the intestinal microflora: the APOAS gene is now identified as one of the genetic factors associated with alteration
intestinal microbiota and predisposing to MS.
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