Do you have reoccuring sinus infections or constant nasal drip?

That *could be* Staph or Strep species seeding your intestines and causing all kind of havoc.

www.ncbi.nlm.nih.gov/pmc/articles/PMC555745/

Discussion

Our knowledge about the etiology of ulcerative colitis is still limited. Although some theories about its origins have been advanced, such as genetic predisposition, autoimmune disorders, infection, and so on [23,24], the precise pathogenesis needs to be further understood. In clinical practice, we noted a close association between CS and UC in some patients and their UC was significantly improved after having removed sinus pathology (data not shown). The results of animal experiments verified our speculation: superantigen SEB from sinusitis cooperated with ingested antigen to induce intestinal sensitization. Challenge with the obligate antigen initiated colonic mucosal inflammation as well as the clinical symptom diarrhea. Book DT et al [25] also noted the same phenomenon and suggested that IBD was more prevalent in those people with chronic sinusitis than in other populations.

Rhinosinuses are empty cavities lined with mucosa. The anatomic feature, only having a small ostium, makes them very easily to be blocked and subsequently infected. Infection with S. aureus in sinuses is frequently encountered [4,5]. Thus, chronically infected sinuses may be a source of SEB that is released to nasal cavity frequently. A mucus blanket on the surface of nasal mucosa naturally traps small particles from air and the secretions from sinuses and removes them subsequently. Since the direction of the locomotion of the mucus blanket is backward, people sometimes swallow the secretions into the gastrointestinal tract (e.g., during sleep).

There are many toxic substances in the secretions from chronic sinusitis. SEB is one that has been well characterized. The unique feature of SEB is that it can down regulate intestinal barrier function [6,13], activate T lymphocytes without the help from antigen presenting cells to activate T cells. Superantigens bind directly to MHC class II molecules and to a subset of T-cell receptor (TCR) Vβ chains [26,27]. Unlike conventional antigens, superantigens do not require processing by antigen-presenting cells to activate immune cells [31]. Administration of superantigen results in initial selective expansion of T cells that bear specific Vβ chains that recognize the superantigen, followed by their deletion [29]. Another unique feature of superantigen is that it mutes T suppression cell function and promotes Th1/Th2 skewing [30]. It primes an environment to develop sensitization in local tissue. The results in the present animal experiments are consistent with previous studies. Mice treated with SEB-containing SWF and OVA developed intestinal sensitization, but not in those mice treated with only OVA, or SEB-depleted SWF plus OVA. This finding demonstrates that SEB plays a crucial role in the sensitization of the intestinal mucosa to luminal antigen in these mice. Louini D et al [31] reported that SEB also directly sensitized skin and caused Th2 pattern inflammation in the local skin.

Intestinal epithelial cells form a barrier between the luminal contents and the subepithelial region. The barrier restricts substances to be absorbed. It only allows some small molecules such as water to pass it freely. Antigens are macromolecular proteins that are not allowed to be absorbed before being digested to small peptides or amino acids under normal physiological conditions. But in reality, intact antigens do pass the intestinal barrier to reach lamina propria to induce inappropriate immune reactions under certain circumstance. How antigens cross the intestinal epithelial barrier is still a mystery. By introducing both SWF and HRP to mouse gastrointestinal tract, intact HRP in the colonic tissue was increased nearly 11 times compared to control. The results implicate that superantigen SEB is one of the factors that facilitate antigens to be absorbed without destroying their antigenicity. Lu et al also reported that SEB significantly increased colonic mucosal permeability in a mouse study [13].

We have begun to appreciate that food allergy plays a role in the inflammation of intestinal mucosa [32]. The results of this animal model support that inappropriate immune reactions initiate intestinal inflammation. Simply delivering OVA to gastrointestinal tract did not show sensitization in the mice while the combination of SEB-containing SWF and OVA induced sensitization in the colonic mucosa. Based on these data, we suggest that SEB facilitate sensitization of the intestinal mucosa to OVA. The mechanism behind this phenomenon might be that SEB increases permeability of the intestinal mucosa [6,13]. Thus OVA in the intestinal lumen can be transported to deep region of the mucosa. This exogenous protein then contacts the local immune cells to initiate inappropriate immune reactions and sensitizes the mucosa subsequently. The results of challenge with OVA show extensive inflammation in the colonic mucosa in this study. The inflammatory changes may be a result of local mast cell degranulation in response to OVA challenge. Mast cells release chemical mediators such as histamine that is able to increase vascular permeability and to induce edema in the tissue that was noted in the present study and also reported elsewhere [33].

In chronic allergic diseases such as asthma, during continuous antigen exposure, eosinophils are primed by IL-5 and attracted by chemokines, infiltrating the local tissue [34]. We also observed extensive eosinophil infiltration in the colonic tissue after three challenges with specific antigen OVA in the present study. These eosinophils are believed to be responsible for the late phase of the allergic reaction, producing the major basic protein which is toxic to the epithelium [34]. The micro-ulcers on the surface of colonic mucosa may be caused by eosinophil activation. Supportive evidence acquired from EM observation demonstrates that most eosinophils have been activated by showing extensive degranulation. We also noted this phenomenon in the jejunal mucosa in the late phase reaction in a rat model of food allergy [32].

Marked mast cell hyperplasia in the colonic tissue was observed in this study. In general, mast cell numbers in tissues are relatively constant, even though mast cell hyperplasia is observed in both the inflammatory and in repair/remodeling stage of various inflammatory disorders [35]. The functional significance of the accumulation of mast cells in these processes is largely unknown. In allergy, apart from their classical role in eliciting the early phase, mast cells also have an important role in late and chronic stages as we observed in a previous study [32]. In these stages they may interact with and be activated by infiltrated inflammatory cells and by resident structural cells such as epithelial cells, smooth muscle cells and fibroblasts. In the case of allergic reaction, mast cells are mainly activated by the mechanism of IgE mediated FcεRI bridging that accounts for the mast cell activation in the present study. The roles of mast cells in the late phase reactions may be amplified by eosinophils, platelets and neutrophils [36]. If a sensitized patient frequently ingests an obligate antigen unconsciously whereas the allergic reaction only reaches subclinical level, an early inflammation may progress without being noticed until reaching the advanced stage. The data also show that the degranulation type of mast cells and eosinophils in this study is mainly piecemeal. It indicates that the nature of the degranulation type belongs to a chronic process [37]. The local inflammation may progress to chronic status in the tissue without any further medical intervention.

Striking epithelial damage of colonic mucosa of the sensitized mice after challenge with OVA was observed in this study. This phenomenon has been well-documented in airway allergy [38]. Although ulcers are one of the main clinical signs in inflammatory bowel diseases, the etiology is not clear. There have not been many studies considering an association between the ulcers and allergic reactions in the gastrointestinal tract. Eosinophil released major basic protein is suggested to be the major offender to cause epithelial cell exfoliation in the airway mucosa [38]. The erosion and prominent damage to the epithelial barrier can explain the phenomenon of bacterial adhering to and penetrating to colonic mucosa in this study. These bacteria are commensal bacteria. They usually are not considered pathogenic. The damaged epithelium may provide an entry port for the colonizing bacteria to invade the colonic mucosa and to establish an infection.
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Conclusion

In summary, we reported a murine model of ulcerative colitis in this paper that was induced with sinusitis-derived SEB and OVA sensitization followed by repeat challenges with specific antigen OVA. The histopathology of the colonic mucosa included inflammatory cell infiltration, activation of mast cell/eosinophil, epithelial barrier damage, micro-ulcer formation on the surface of colonic mucosa, bacteria translocation and abscesses formation in the subepithelial region.

Post Edited (PathogenKiller) : 5/21/2013 1:15:33 PM (GMT-6)

Hmmm my bro has uc and chronic sinusitis. I'll pass this on to him though he likely won't do much about it since neither bother him too much. IMA, i know people use pure essential oils for this but I'm not sure how. Pretty sure I've seen it come up when looking at DoTerra oils - there may be something on their site?

Plague oil (I think doterra's version is called onguard) taken internally can help with this, you drop 5 drops in a gel cap and take it before food. HOWEVER, that may be way too harsh for someone with very active UC..There is a company that sells a plague oil tooth suds that Ive heard positive things about too. Various other oils like cinnamon likely have an effect.. Ill post more on this. The things I take arent necessarily things I feel comfortable guinea pigging others with ;)

The test for strep in the gut is elusive. Sometimes you will get it on a Comprehensive Stool analysis. But most times not. The test to let you know if you have a systemic strep issue (and if you do and you have UC, it's effecting your gut) is the Anti-Streptolysin O test

en.wikipedia.org/wiki/Anti-streptolysin_O

As for coagulase negative staph, Im not positive how one gets tested for that these days. I know there were a couple labs that did testing but dont remember who, Ill try to figure that out.

Strep and staph are hard to get clear from the system, but its good to start at your sinuses and mouth.

Things that help get the numbers down
Netipot of distilled water and xylitol

xylitol nasal spray

If you have clogged or inflamed ears, drops of xylitol water in your ears

Do not swallow post nasal drip, spit it out

Multiple times daily, preferably after you brush following every meal, mouthwash and gargle with xylitol water.

Reseed the oral cavity with Blis K12 probiotic.

Triphala is effective against both staph and strep. I need to cross reference the other things I know of for safety and Ill post more later. Im curious about the use of xylitol in enemas.. Ive never researched that.

I'm not really sure about this paper. They used healthy individuals as a control, which was good, but 1) they didn't indicate that they used the healthy SWF anywhere except to measure levels of SEB (i.e. they didn't use the healthy SWF in the mice), and 2) they're missing two additional controls: people with CS but no UC, and people with UC but no CS.

Regarding #1: It's important that they measured the SEB levels in the SWF from healthy individuals. Since their diagnosis of CS was based on criteria that didn't involve testing for the presence of bacteria, they needed to show somewhere that bacteria had involvement with the CS in the patients they tested. So far so good.

However, I would have liked to see that used in the experiment. The controls they used later on were all appropriate (OVA, OVA+SWF, SWF, OVA+SWF+anti-SEB, saline). However, because they didn't use the health SWF, they can't say for sure that it wouldn't have had the same effect as the CS/UC-SWF. Do I think it would have had the same effect? I doubt it, but they have to show it.

Regarding #2: Along the same lines, they're missing two other important controls. There are two differences between the SWF they're using: CS and UC. Any first-year biology student who paid any attention in intro bio lab would be able to tell you that if you change two variables, you can't determine which variable is responsible for a difference.

They should have used two more control groups. Specifically, they should have collected SWF from a group of patients with CS but not UC, and from a group of patients with UC but not CS.

I also want to emphasize that, regardless of the discussion section of the paper, the only conclusions the authors make (and, really, the only conclusion they CAN make from their results) is that they've established a murine model of ulcerative colitis. This isn't "no big deal;" there are already models of murine UC, but more is better. It's great to be able to use multiple models of disease in the same animal and compare the histopathology.

But there's a reason they only conclude that they've created a murine model of UC: because that's all they showed definitively. They didn't show that chronic sinusitis causes UC, or that it even contributes to it.

I know that it's frustrating to not know what's caused your UC, but please make sure you look at papers critically (and also this paper is from 8 years ago).

I'm just saying, a paper published 8 years ago and I haven't heard anything about this since ... probably not a ground-breaking paper. And I'm not saying, "This paper is bad, ergo staph is unrelated to UC." I'm saying, "This paper has some major flaws, and it does not conclude what you're suggesting it concludes."

You don't have to tell me that no paper is perfect. I just read through a paper today published in Molecular Cell that had some pretty badly constructed figures. But you do have to read through the paper--this paper does not demonstrate a definitive link between CS and UC.

I'm happy to read through more of these papers you're mentioning, but I'm not really in the mood to lit search for UC papers, given that I am working on a qualifying exam and am a little lit-search-maxed out.

Scientific literacy is important--it's important to recognize what the actual conclusions of the paper are, and how the authors arrived at those conclusions. People are working very hard to figure out what causes UC and how to treat it more effectively, and I think it does them a disservice to ignore missing controls and to jump to conclusions about the implications of results.

Post Edited (ScienceGirl) : 5/20/2013 9:14:31 PM (GMT-6)

Mouse models are important. Putting pieces of the puzzle together is important. But this study does not conclude that staph and strep from chronic sinusitis might cause UC. So I don't think it's appropriate for you to say, as you do with the topic title and the first line of your post, that people with recurring sinusitis should be aware of all the staph and strep that's hurting their colons, based on this paper that does not show that.

I work in biomedical research, and I think it's inappropriate to cite a paper while misrepresenting its conclusions.

Please don't call me "hun."

For the record, I have CD (though it's affecting my colon, if that makes any difference) and since I was a kid I had issues with stuffy nose at night and kinda runny during the day...I do have chronic sinusitis as well, and I was actually addicted to nasal spray on 2 different occasions, once when I was around 9-10 yrs old then again in my teens until it started working against me then I had to spend nights sleeping sitting up because I was totally blocked up in my nose...I still get somewhat of a nasal drip and stuffy at times but it's not near what it was (or at least doesn't bother me as much) compared to when I was younger...I got my IBD in my early/mid 20's with the exception of my perianal crohn's skin tags starting in my teens but no other CD symptoms until my 20's....after having first baby.

i think from now on, in the interest of peacefulness and harmoniousness, we should ALL refer to each other as " hun "

it just sounds right to me

thanks for the post hun (pk)

i myself have had antibiotic treated sinus infections since my late 20's !

I think that it's fairly common to have more than one autoimmune issue and chronic sinusitis is an immune disorder according to research....clearly my immune system has always been fighting me with my CD being the worst....before I started to notice major issues with my chronic sinusitis, at a younger age I had severe eczema that was so bad it literally looked like flesh eating disease and I suffered for a very long time with it being severe before my mom finally took me to a doctor for it...which it still wasn't treated properly, I had difficulty as a 9 yr old swallowing those big (to me) caps of antibiotics to treat the severity of my eczema so I'm sure that compounded the issue and may have brought on my other immune issues as well, possibly, who knows, all I know is I've been suffering one way or another since I was a kid.

Thanks for your post Sciencegirl and, from once scientist to another, thanks also for highlighting a very important point. Some of the messages which quote "research" are not of a scienctific basis on here. No citing, isolated cases when it is, misquoting the nature of the article. I'm reminded of a quote from Star Trek where Kirk turns to Spock and says "that's the trouble with logic Mr. Spock, you can use it to prove anything". It's interesting that most of these misquotes come from the more established members.

"There is no statistiscal evidence to support" does not imply that the assertion is true nor false. It implies that at the statistical level assumed for the experiment designed there is not enough evidence to support the hypothesis.

It took science 45 years or so to find the Higgs Boson. I'm glad during that time everybody didn't revaluate their opinion on its existence.

D

I'm in a pretty long remission. Credit to the 5-ASAs, a gluten free diet and the moderating effects of menopause.

I was actually under the impression that the mechanism of action for 5-asas isn't known, but that it might work through PPAR or COX-2. I can't find anything at the moment, but the thunderstorm is slowing my internet.

PathogenKiller, these drugs have all undergone clinical trials. It's not necessary for the mechanism of action to be known or understood in order for drugs to 1) be effective, 2) be safe, and 3) pass clinical trials. Knowing the mechanism is helpful, though, which is why it often helps to know it prior to clinical trials, and why people don't stop trying to discern the mechanism AFTER the drug has passed trials.

And again, being critical of papers is part of publishing and conducting science. As I stated already, the study you linked to did not conclude that staph/strep from chronic sinusitis causes UC; it concluded (as the authors state very clearly) that they had demonstrated a mouse model of UC. This isn't, "They let out a control, so they're wrong!" It's, "The paper doesn't conclude what you're suggesting it concludes. Also, I wish they had included these additional controls." Had I been a reviewer, I would have requested that the authors add in the controls I mentioned in my earlier post.

I do care about determining what causes UC, and how to treat it better. To do those things, we need scientific literacy.

damo123, I know what you mean! I've seen some papers where their conclusions are almost entirely hypothesis + super weak evidence from their results. Like, "Yep, we were right, this causes that!" when their data was not statistically significant. Or showing a statistical significance ... but not a biological one. I appreciate that the paper linked at the top actually had a very reasonable and clearly stated conclusion, but their intro/discussion text keeps veering into hypothesizing about topics outside the scope of their experiment. And again, so frustrating that they're missing those controls!