Inflammatory Bowel Disease - Science topic
In medicine, inflammatory bowel disease (IBD) is a group of inflammatory conditions of the colon and small intestine. The major types of IBD are Crohn's disease and ulcerative colitis.
Questions related to Inflammatory Bowel Disease
In our traditional medicine some plants are used to cure Gastrointestinal disease. do some one know about some plants or phytochemical to cure IBD?
I am currently searching for a suitable agent to mimic IBD-like inflammatory condition in HT29 cells. I have found publications where researchers used DSS, TNBS etc. However, I am still in search of some articles about IFN gamma. In some papers, IFN gamma was used to disrupt intestinal barrier function but they did not mention if the condition was similar to IBD or not. I would like suggestions, protocol or related papers on whether I can use IFN gamma to induce IBD or not.
Hi all, I wounld like to know how do you collect the stools from TNBS colitis mice. I found it's hard for C57BL/6 and Balb/c to discharge feces after 2.5%(wt/vol) TNBS enema. 50% mice refuse to discharge their feces. Some mice can only excrete a little brown liquid. I collect their stools by placing them to the empty box with some white tissues and I post a image below about my stool collecting setups. Besides, the body weight of those mice decline rapidly after enema ,therefore I guess the mice may refuse to eat after enema, and which cause it lost weight and have no stools to discharge. But, the stool is important in TNBS colits scoring system. Could anyone please help me on that?
I am trying all the protocol to extract the clean phospholipase A2 from the inflammatory bowel disease patient's stool samples. All the time I am heading to the dead-end.
I have tried Chroloform-methanol extraction and then used the BCA assay to detect the concentration of the proteins. Then that sample used in gel electrophoresis to see the protein bands and could not see any protein bands. Can anyone help what went wrong, please?
Hi every one.
I'm looking for any one who has successfully isolated and grown F.prausnitzii
This year is our first step in our move towards targeted treatment of Inflammatory Bowel Disease in Children.
If you would like to discuss bacterial isolation from stool, share successful methods or ask more questions for your own work I would love to hear from you.
Our first hurdle is finding a replacement for Rumen fluid in our culture methods for isolation.
Before starting, I apologize in advance in case any obvious link eluded me.
By the way, I've recently compared anti-s IgG levels in two people and I couldn’t help but notice a curious fact: IgG levels detected in a young female person with IBD a year after the infection were three times higher (despite treatment with azathioprine) than those detected in another woman who received her second Pfizer vaccine shot.
I’m undoubtedly aware that this comparison isn’t statistically significant nor sufficiently accurate, but I was wondering whether there might be other similar data suggesting a possible explanation.
Thanks in advance to everybody who will indulge my curiosity.
I am trying to differentiate HT-29 cell line using Methotrexate (MTX). I came across an old article that suggested treating cells for 3 months in order to reach their confluence state, leading for mucus secretion.
I was wondering if anyone here could suggest a protocol for differentiating the cells with MTX, so they could be more morphologically similar to goblet cells and secret mucus.
Hello everyone! I am researching the molecular mechanisms which drive depression in the context of gut microbiota. From what I know, depression's pathogenesis primarily relies on Tryptophan metabolism. On one hand, the pathway is perturbed to the kynurenic pathway which leads to the formation of kynurenic metabolites (KYNA, QA, XA, etc). These kynurenic metabolites exert neurotoxic effects which ultimately drive depression phenotypes. They are also able to affect the enteric nervous system, the gut millieu, and immune system which contribute to depression.
On the other hand, Tryptophan metabolism can also be driven towards serotonin synthesis. Inflammatory bowel disease and its likes (Crohn's disease, colitis) have been shown to have increased serotonin (evidenced by increased TPH expression) and decreased SERT expression. Serotonin has been shown to be pro-inflammatory and this supports the inflammatory theory of depression.
While these explanations do not completely contradict each other and that they may simultaneously contribute to depression, an "irony" still exist that one says a perturbation towards kynurenine while the other is towards serotonin. Either way, Tryptophan is consumed and surely leads towards an increased bias to one pathway (ie. increased serotogenic or increased kynurenic). Hence, do you know of any articles which settle this apparent contradiction? Or perhaps there is something I incorrectly understand?
I am investigating the genetic diversity of a few species over geographic distance via IBD. I have my input file in txt format, however, I have troubles specifying populations.
I am writing a proposal for a project concerning IBD research and substitution according to the 3R principle. Therefore I would like to know the actual numbers of animals (mouse, rat, etc.) used for TNBS, DNBS and DSS induded colitis in the years 2017-2019.
I tried the official announcments (e.g. European statistic report on the use of animals), but I only find general information ( e.g. # animals in gastrointestinal research).
Do you have a suggestion how to easily address that matter in short time?
I started now by looking at each publication of each year and manually collecting the numbers, however this is really time consuming. Maybe there is a automated approach.
I am looking forward to any suggestion, thank you very much in advance.
For patients with GI issues with the large intestine (IBS, spastic colon, ulcerative colitis), I have seen a pattern that foods with carageenan and xanathan gum, both polysaccharides used as emulsifiers, worsen GI issues and pain. However, the supplement Inulin seems to helpful for patients. Is there something about the molecular structure of carageenan and xanathan gum that results in more harm than other polysaccharides? Are carageenan and xanathan gum more prone to causing oxidative damage in the large intestine?
please , anyone send me the articles on Bcl-2, Bax, and other apoptosis-associated proteins, focused on inflammatory bowel diseases.
Are there any specific recommendations for management of bisacodyl abuse? Is the approach of stopping bisacodyl immediately ( or tapering it down) + adding lactulose throughout ? Are there any guidelines regarding dosing/regimens/period of tapering bisacodyl and adding lactulose?
How would I go about investigating state of the intestinal epithelium of someone with IBD and colon cancer?what would I observe f I use immunostaining
I am looking to profile the microbiome from stool samples collected from 17 Ulcerative colitis paitents by qPCR. eventually we plan to do 16s sequencing, but it is taking a long time to get samples and I have a student that needs a manageable project.
Does anyone have a good reference or protocol for a panel of qPCR primers that I could use to look at the relative abundance of major groups associated with IBD or energy metabolism?
Also, if I was to do absolute quantification where could I buy positive control DNA to match for each primer set?
I would like to know how do you optimize colitis model in mice/rats. It is known that females are more resistant than males itself but I have some issues on ulceration between male animals too. What is the best amount of TNBS and the ratio of TNBS/Ethanol in practice?
Thanks in advance
In a recent experimentation where we tested an agent's effect on the oxidative stress status on mice (inflammatory model of IBD), we found that livers and colons present a similar response plot.
In the aim to dig deeper, we tried to test our agent on mitochondrial swelling (in vitro). We were surprised to find that low doses induced a significant decrease in Liver mitochondrial activity compared to colons, which were not affected.
any speculation regarding this phenomena is deeply appreciated.
PS: The agent used has a metalloid characteristics.
Patient was diagnosed with acute refractory Ulcerative Colitis 4 years ago. Medications have not helped and thus patient is looking to alternative treatments. Patient reported, upon taking 3 grams of pharmaceutical grade Glycine supplement, number of daily bowel movements immediately reduced from 8 to 2 and bleeding reduced significantly. Has anyone else seen of or heard of such an impact with Glycine? What could be the therapeutic mechanism?
Can anybody suugest some primary cells or cell lines for IBD/Cronh's diseases? What is the common protocol to induce inflammation in the healthy cells in vitro? Is there any diseased/transgenic cell lines?
Is the number of neutrophils and monocytes in "normal" blood high enough to make the fecal calprotectin test become positive even in the case of a non-inflammatory source of bleeding (e.g., bleeding from hemorrhoids)?
Interleukin 17 (IL-17) is a class of closely related molecules known to be increased in the human body by exposure to Fluoride by ingestion from water and food, or metabolism of Fluorocarbon anaesthetics and propellants. IL-17 causes Autoimmune Diseases including Psoriasis, Rheumatoid Arthritis, Asthma, Lupus, Multiple Sclerosis, Inflammatory Bowel Disease, Transplant rejection, and destruction of Liver and Heart Cells. IL-17 is also implicated in Skin Cancer.
Other Interleukins are known to be elevated by Fluoride, leading to attacks on other critical cellular and organ systems. Australia's National Health and Medical Research Council actively suppresses this Interleukin science while promoting Water Fluoridation using industrial waste. Can the science community influence this behaviour?
There are many kinds of IBD models.If I wanna do some research about UC ,which model should I use(to push a drug into clinical research)
Is there any study out there where the genetic risk for IBD has been addressed in the context of a certain microbiota composition, say enterotype, or according to presence/absence of indicator species or metabolic pathways?
We have recently published that for colitis induced by T cells transferred into Rag-deficient recipients, the expression of T-bet by the T cells matters only in the context of a certain microbiota. In one type of recipients, T-bet was critical for disease and T-bet-deficient T cells were unable to induce inflammation whereas in another set of recipients T-bet-deficient T cells induced inflammation just as potently as WT T cells did.
Has anything comparable been shown for humans, e.g. that gene XYZ confers an increased risk for IBD only in the context of a Genus abc-dominated microbiota. Or the other way around, say some kind of dysbiosis predisposes an individual for IBD only in combination with a certain genetic risk factor?
Is laparoscopy the gold standard for inflammatory bowel diseases, such as ulcerative colitis and Crohn's disease?
The pathogenesis of celiac disease involves interplay of genetic, host microbiome and environmental factors like IBD. These include dynamic changes and exposure times starting from neonatal period. Recently there is rise in incidence of both celiac disease and IBD in India. Can anybody say whether this is result of similar changes in microbiome and environmental factors like diet, use of antibiotics?
I have been looking more closely at the reduction of defensin 5 alpha reported by Wu et al in the ALS mouse model as to me, the leaky gut is the first notable symptom for ALS and it occurs ahead of neurological symptoms. My self selecting question about whether or not people had gut issues ahead of ALS found that 60% of respondents said they had gut issues ahead, and for years by some of them. So, given that the lack of defensin 5 alpha is causing a shift away from butyrate forming microbiota to a more harmful one and a reduced protection from intestinal barrier which causes a huge range of other problems, figuring out how to help the body make defensin 5 alpha seems like a good strategy for fighting back.
So, what can help the body make defensin 5 alpha? Anyone have any sources for doing that?
Wu, Shaoping, et al. "Leaky intestine and impaired microbiome in an amyotrophic lateral sclerosis mouse model." Physiological reports 3.4 (2015): e12356.
Ghosh, Dipankar, et al. "Paneth cell trypsin is the processing enzyme for human defensin-5." Nature immunology 3.6 (2002): 583-590.
Wang, Wei, et al. "Effect of bifidobacterium on defensin-5 expression in intestinal injury of preweaning rats." World journal of gastroenterology: WJG 21.9 (2015): 2638.
Hetz, Claudio, et al. "XBP-1 deficiency in the nervous system protects against amyotrophic lateral sclerosis by increasing autophagy." Genes & development 23.19 (2009): 2294-2306. (my note - helps the paneth cells, I think)
Courth, Lioba F., et al. "Crohn's disease-derived monocytes fail to induce Paneth cell defensins." Proceedings of the National Academy of Sciences 112.45 (2015): 14000-14005.
Kaser, Arthur, et al. "XBP1 links ER stress to intestinal inflammation and confers genetic risk for human inflammatory bowel disease." Cell 134.5 (2008): 743-756.
I have trouble inducing T cell transfer colitis in mice. I have been strugling for many years and tried several troubleshooting without any luck. It doesn't seem mice are responding to transferred T cells. Here are my protocol.
Recipient: BALB/c Rag1 KO mouse 8-10wk
Donor: BALB/c Foxp3-eGFP, WT and gene KO I crossed.
I am trying to match gender between recipient and donor.
T cell sorting: CD4+ GFP- CD25- CD45RBhi CD44low
We don't have sorting facility, so I have to take 1 hour travel to nearby university.
injection: 4 x 10^5 sorted T cell via retro orbital sinus injection in 200ul PBS
The problem is that I cannot see weight loss in WT-transferred recipients in next 5-6 weeks. Threre are sometimes visible loss in one or two mice, but I need to see clear weight loss in all WTmice so that I cen tell whether KO of a gene makes any difference.
I tried several troubleshooting such as,
Changing fluorescent Abs: It turned out I was using depleting clones. I switched to non-depleting ones.
Raising recipients in non-SPF condition: colitis is dependent on gut microbiota so I breed Rag1 KO in non-SPF condition. I also use non-autoclaved water and non-irradiated chow.
T cell viability: since FACS facility is far, I keep cells on ice and count viable cells with trypan blue right before the injection. Also I coat harvesting tube for sorting with FBS as I heard that it helps with cell viability.
It would be a great help if somebody can tell what I am doing wrong. Thanks.
β casomorphin-7, a bioactive peptide present in A1 milk can increase the production of gastric and intestinal mucin. It is hypothesised that the production of such mucin may protect the intestinal endothelium in inflammatory bowel disease.
We want to estimate gut inflammation and oxidative stress. For certain reasons, we can't use gut tissue in human disease model. Can we use stool samples to estimate inflammation cytokines and oxidative stress? Alternatively, I read somewhere that there are few cytokines, which are only associated with gut inflammation and can act as indicator of gut inflammation only. They can be studied in plasma. Are there existing similar oxidative stress indicator for gut as well?
Here I did microarrary analysis of the mice colon mucosa, the results shwed that Immunoglobulin heavy chain (gamma polypeptide) and immunoglobulin kappa joining 1 expression increased 11 fold in gene KO mice, so here I want to ask, this Immunoglobulin heavy chain (gamma polypeptide) is IgA or IgG? how to explain this increased fold change.
53.5 588.9 3.46 11.02 0.1139 " Mus musculus mRNA for immunoglobulin gamma-2a heavy chain, complete cds, anti-malathion monoclonal antibody MLT2-23. " AB097847 Ighg Immunoglobulin heavy chain (gamma polypeptide) 12 F2|12 380794.
237.4 1011.4 2.09 4.26 0.1544 " Mus musculus cDNA clone MGC:36290 IMAGE:4224032, complete cds. " BC027418 Igkj1 immunoglobulin kappa joining 1 6 C|6 30.0 cM 110759
I have some question about Peyer's patches in mice ileum:
1. What is the number of Peyer's patches in mice ileum?
2. What is the length of ileum? 10 cm?
3. I want to compare the size of Peyer's patches between WT and KO mice, do I need to measure all the Peyer's patches in mice ileum, and then compare the average size between WT and KO?
i need help for solution of this case really?what is the best treatment with a case of 45 years old male patient with 1.5*2 cm large superfacial oral ulcers affecting unilateral buccal mucosa and lateral tongue surfaces with burrning pain with a history of recurrence every 3 months for 2 years peroid.The patient took topical and systemic steroids with out benefit, systemically he had drugs for colitis for the past 7months??
I am trying to treat the 21 days differentiated Caco2 monolayer with LPS at the concentration of 5µg/ml.
During the differentiate stage (21 days), I feed the cells with DMEM 10%FBS, 1% NEAA, 1% Glutamax, 2.5% HEPES, 4.5g/L D-Glucose and 110mg/L sodium pyruvate.
After that, I use the HBSS media with 2.5% HEPES for LPS treating.
I add the LPS with HBSS media to the apical side of the trans well at the total of 450µl, and 750µl HBSS media alone in the basolateral side.
After 24hrs, the LPS did not show any effect on the TEER of the monolayer, but the cells is dying at this time due the serum free media HBSS.
Normally LPS take long time to have some effect (More than 48hrs I think) but I cannot change the media in the middle of experiment.
Should I wait more for the LPS to take effect or I should change it back to the growth media (DMEM) ? Because if the monolayer is damaged, it's definitely affect the TEER value.
Many trials were done for treatment of many diseases using stem cell therapy including chronic inflammatory bowel diseases
I am looking for a panel of immune cell subtypes that in your opinion are fundamenatl to understand the possible immune imbalance in the intestine and mesenteric lymph node of DSS-induced colitis mice.
Which markers for which cells?
I am planning to do in vivo neutralization of IL-6 cytokine in DSS-induced colitis mouse model. I am wondering if anyone has used anti IL-6 monoclonal antibody to do that in a colitis model before. The majority of papers out there are using anti IL-6R monoclonal antibody and mainly in adoptive T-cell transfer models. I found one paper that used anti IL-6 antibody to neutralize the cytokine itself (link below) in a mouse model of DSS-induced intestinal inflammation and wanted to know if other groups have used that clone to neutralize IL-6 in vivo?
Link to the paper of IL-6 neutralization in DSS-induced colitis mouse model:
Thanks in advance!
I am debating with pharmacology colleagues whether ampicillin and amoxicillin, which possess an NH2 group and, the latter, also an OH group more than penicillin G are more hydrophilic or more lipophilic than penicillin G. I always explain to students that aminopenicillins are more hydrophilic, and, therefore, pass more easily through Gram negative bacteria LPS, via the porins. My colleagues instead think that amoxicillin and ampicillin are more lipophilic and diffuse better through lipids of Gram negative lipid outer layer. Who is right?
I want to test the implications of a potentially pro inflammatory substance provided through diet, that affects the epithelium integrity, on developing chronic inflammation of the GI tract, I need a mouse model that develops inflammatory phenotype once the epithelium is disrupted. I'd like to know if anyone has experienced using this model? Are there any other mouse models that are more suitable?
Chronic diarrhea (started at 4 months of age - anamnesis); colonoscopy shows non-specific aspect - friability of the mucosa, hyperemia, edematous in the recto-sigmoid area, other segments are not explored!).
Rectal mucosa shows no architectural disturbance, no pathologic inflammation, no other significant pathologic changes but evident pseudomelanosis coli.
Interferon Gamma Release Assay is a test done to detect Interferon-gamma release by lymphocytes sensitised to mycobacterium tuberculosis. Its a test often done to detect latent TB. Crohn's disease is an IBD, in which Interferon-gamma plays an important role. So since this cytokine is common to both, is it possible to have a false postive IGRA in a patient with active Crohn's disease? Especially in countries like India, where almost everyone has been either vaccinated (with BCG), or exposed to the tubercle bacillus at some point of time; but not everybody develops the disease.
Please do give your inputs, with any references if possible.
Thanks in advance !
IL-22 was suggested to play a protective role in the pathogenesis of IBD. For example, IL-22 induces the expression of mucus-associated molecules and the restitution of mucus-producing goblet cells, hence probably enhancing the innate defence mechanisms. however, Previous studies demonstrated that either the expression of IL-22 or the numbers of IL-22+ cells was higher in IBD patients as well as the murine models of colitis. these findings seems to be paradoxical. That is why? thank you!
I'm looking for a significative dosage to evaluate intestinal permeability in chronic disease but not in inflammatory bowel diseases
I was trying to do the TNBS model in C57BL/6 mouse. I was following the paper
Wirtz S, Neufert C, Weigmann B, et al. Chemically induced mouse models of intestinal inflammation[J]. Nature protocols, 2007, 2(3): 541-546.
However, I found out drug reflex is a big problem which made the result very inconsistent. Wondering anyone has experience on this.
I heard some people suggest fast mouse for 24h. But I found the colon lumen still have poop after this. When the stool is in the colon, the drug can't distribute evenly in the colon.
Some suggest wash the colon with saline before TNBS induction, if this is helpful, I'd like to know more details.
Or, any other suggestions?
I want to know that which passage of CaCO-2 can i use as IBD model and method for its differentiation?
BDP and budesonide are locally acting steroid drugs with very low systemic availability and toxicity. Commercially used in the treatment of colitis. Most reasearchers used budesonide for colon delivery, Please comments
A 19 year old who was operated for Heirshprung's disease (Ileoanl anstamosis) 2years ago elsewhere presented with subacute small bowel obstruction. Abdomen is distended and small bowel loops are seen. It is not tender. Digital rectal examination is normal. CT scan showed distended small bowel loops up to the anus and Anus is collapsed.
My current protocol suggests mice aged 8-12 weeks infected on day 0 with a single 5exp9 dose of Citrobacter rodentium. I have tried a few variations of this based on literature searches (younger mice etc) and failed to induce colitis each time. Prior to infection I have check the viability of the bacteria using a luminescent imager and post infection plated dilutions of the innouculum to confirm the dose. I am happy that my gavage is reaching the GI tract and plating of faecal pellet suspensions seems to confirm bacterial attachment and shedding. Any suggestions?
I would like to do a TNBS experiment in mice on 129SvEv background. Are these mice susceptible to the TNBS ? what dose do you typically use for the enema and do you sensitize the mice a week before that ?
Finally, did anyone try to induce TNBS colitis in Rag2-/- mice a couple of weeks after transfer of CD4 cells. Does this work ?
Thank you, appreciate your help !
I am going to evaluate the effect of Herbal medicine extract and Probiotic in TNBS-induced mice colitis by modulating the gut microbiota structure .In order to find out the most influenced or changed species by high-throughput sequencing. The fecal sample is important .
I tend to A plan. Because the drug and probiotic have Sufficient time to adjust the mice gut mirobiota before TNBS administration.But I confused about the collecting time point . Most colitis gut microbiome study just have two time point like B Plan ,before and after treatment . In A plan.it has three time point.From day -21to day 0, it is easy to find the microbiota change in nnormal circumstances.but under the environment of TNBS, should I compared day-21,day3 or day-21,day3?
If I choose the B plan,I wonder whether the short-term treatment of in the acute colitis models might have a significant change in the microbial distribution. So,Can anyone give me some suggestions?
The duration and depth of anesthesia is variable widely .A prolonged anesthesia may increase contact time of the TNBS solution with the colon. I did it by Ether ,but it is hard to control .So which is the ideally anesthesia ?intraperitoneal anesthesia or inhalation anesthesia? I know it may be Continuous Inhalation Anesthesia.because the anesthesia machine is not access to use for me.in addtion,if the mice can not be anesthesiaed ,how to avoid the mice quickly excrete the TNBS solution?
the average weight of BALB/c mice is about 20g, but in some groups the weight is not homogeneous，for example the mini is 18g ,the max is 23g.in order to reduce that disparity.Should I match the mice by body weight ? if I put the 18g or 23g around in each group? I wonder whether it will have a influence on the colitis model ?
i want to perform a genetic association study on inflammatory bowel disease, which is suggested to be not common in China. for example, i attempt to do four Single nucleotide polymorphisms in a special gene, what is the perfect ratio of the case to control? 1:1.5 or 1:2 ? i am really troubled. thanks.
What is the consensus on the morbidity, if any, and treatments recommended.
Treating refractory IBD a-UC with anti TNF alpha AB seems not to be the right answer for most of the developing countries specially in Latin American populations, due to the high pharmacoeconomic impact that this therapeutic strategy implied. Therefore, more pragmatical approach is needed and there is growing evidence that microbiota and some helminths (i.e. T.suis and/or N. americanus) help with down regulating the IL-17/IL-22 relationship.
a colleague of mine was recently baffled when looking at liver tissue coming from IL10 knockout mice which spontaneously develop a chronic inflammatory bowel disease.
Can anyone with experience in histo(patho)logy tell me what the brighter structures in the attached picture are? Is this some kind of fibrosis or what are these cells?
Thank you alot in advance!
On mice colon mucosal mirobiome study, treat mice with DSS to induce colitis, then collect the mucosal microorganism to analyze mirobiome change, but colon has four different parts, so which part of colon I should use to collect the mucosal microorganism and can reflect the mirobiome change under colitis?
Through comparative proteome and immunohistochemistry, we found some molecules showed higher expression in IBS than the normal controls. Those molecules are very new for intestine or IBS, at first, we wish to understand their roles in IBS or functional gastrointestinal disorders based on the clinical data, then, to explore their basic mechanisms and the therapeutic potential with experiments.
If anyone have interest in this research please join us, especially, welcome the clinical researchers who can provide the samples and data of IBS patients.
Local factors contributing to the certain clinico-morphologic form of the acute calculous cholecystitis to develop remain obscure. What is your opinion, may some histological alterations including the pseudopylorization or the intestinal metaplasia take part in the pathogenesis of this disease being more prominent in the case comparing to the pattern of the mucosal lining in the chronic cholecystitis?
In a prospective study on patients with pelvic malignancies undergoing pelvic radiotherapy, we found an association between vitamin D deficiency and severity of radiation induced proctitis. This association was independent from age, gender, cancer type, and BMI. What could be the mechanisms behind this association?
We are going to evaluate the immunomodulatory effects of vitamin D in an intestinal mucosal injury model. What are the Pros and Cons of measuring 1,25(OH)2D in contrast to 25(OH)D for this investigation?
Total number of genome regions known to be associated with inflammatory bowel disease is up to 99.
There is a 5 year old child who developed UC at 2 years and subsequently sclerosing cholangitis. Steroids / Immuran and Ramicade x 1 year are unable to induce remission. Is there a possibility of it being a IL10R involvement though he does not meet the criteria of being an EO/VEO UC? Has anyone faced a similar issue?
In the literature it is either unclear or not mentioned what people do and if there is a consensus of how to do this.
From what I have seen, when you prime with LPS, you are in complete media but then you change media for without FBS before adding ATP. Is that correct?
My second question is: once you're done priming with LPS do you change media before pulsing with ATP (if you are using complete media all the way through)?
32years with nearly 5 years history of confirmed ulcerative colitis(pan colitis) who is on pentosa,mesalamine ,steroids and other supportive measures presented with daily rectal bleeding ,loss of weight of over 20kgs,feverish feeling but no fever.His quality of life is getting affected.Azathiaprine has not yet tried.Seeks a remedy for this.would you suggest pursuing medical management or Total colectomy with Ileo-Anal pouch?
Citrobacter rodentium were grown overnight in LB broth ,after centrifugation ,the pellet were resuspended with PBS.BABL/C mice were inoculated by oral gavage (approximately 2X10^8 CFU).
But after one week ,the mice show no significant body weight loss,however, in some article the authors reported that Cr-infected mice demonstrated significant weight loss by day2-day3 postinfection.So I would like to know whether the rapid loss of body weight is a overt clinical sign of infection? and is 2X10^8 CFU enough to induced the colitis ?should I increase the concentration?
Two studies up to now have shown an association between adenosine deaminase activity and disease activity in patients with Crohn’s disease and ulcerative colitis. We conducted a similar study in Crohn’s disease and in addition evaluated fecal calprotectin which is a known accurate disease activity marker for IBDs. But, we found no association between ADA activity and disease activity (evaluated by CDAI). Also no association was between ADA activity and FC, CRP, or ESR. But, ESR, CRP, and FC were all associated with disease activity.
What could be the reason for this difference between the study results?