Waverunner
Senior Member
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How sinus infections can contribute to/cause ulcerative colitis
A very interesting study. The basic principle behind it, is, that during chronic and normal sinus infections we swallow down mucus/bacteria/toxins/antigens. When these reach our intestines they cause inflammation, increased intestinal permeability and damage over time. Therefor they can highly contribute to ulcerative colitis.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC555745/
A murine model of ulcerative colitis: induced with sinusitis-derived superantigen and food allergen
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) V? 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 V? 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.
A very interesting study. The basic principle behind it, is, that during chronic and normal sinus infections we swallow down mucus/bacteria/toxins/antigens. When these reach our intestines they cause inflammation, increased intestinal permeability and damage over time. Therefor they can highly contribute to ulcerative colitis.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC555745/
A murine model of ulcerative colitis: induced with sinusitis-derived superantigen and food allergen
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) V? 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 V? 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.
