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PubMed abstracts for UC distal/proctitis digest 002

Saved 20 records from NCBI E-utilities on 2026-06-17.

PMID 22914296 — Ulcerative colitis.

Ulcerative colitis is an idiopathic, chronic inflammatory disorder of the colonic mucosa, which starts in the rectum and generally extends proximally in a continuous manner through part of, or the entire, colon; however, some patients with proctitis or left-sided colitis might have a caecal patch of inflammation. Bloody diarrhoea is the characteristic symptom of the disease. The clinical course is unpredictable, marked by alternating periods of exacerbation and remission. In this Seminar we discuss the epidemiology, pathophysiology, diagnostic approach, natural history, medical and surgical management, and main disease-related complications of ulcerative colitis, and briefly outline novel treatment options. Enhanced understanding of how the interaction between environmental factors, genetics, and the immune system results in mucosal inflammation has increased knowledge of disease pathophysiology. We provide practical therapeutic algorithms that are easily applicable in daily clinical practice, emphasising present controversies in treatment management and novel therapies.

PMID 30837080 — A comprehensive review and update on ulcerative colitis.

Ulcerative colitis (UC) is a chronic idiopathic inflammatory bowel disorder of the colon that causes continuous mucosal inflammation extending from the rectum to the more proximal colon, with variable extents. UC is characterized by a relapsing and remitting course. UC was first described by Samuel Wilks in 1859 and it is more common than Crohn’s disease worldwide. The overall incidence and prevalence of UC is reported to be 1.2-20.3 and 7.6-245 cases per 100,000 persons/year respectively. UC has a bimodal age distribution with an incidence peak in the 2nd or 3rd decades and followed by second peak between 50 and 80 years of age. The key risk factors for UC include genetics, environmental factors, autoimmunity and gut microbiota. The classic presentation of UC include bloody diarrhea with or without mucus, rectal urgency, tenesmus, and variable degrees of abdominal pain that is often relieved by defecation. UC is diagnosed based on the combination of clinical presentation, endoscopic findings, histology, and the absence of alternative diagnoses. In addition to confirming the diagnosis of UC, it is also important to define the extent and severity of inflammation, which aids in the selection of appropriate treatment and for predicting the patient’s prognosis. Ileocolonoscopy with biopsy is the only way to make a definitive diagnosis of UC. A pathognomonic finding of UC is the presence of continuous colonic inflammation characterized by erythema, loss of normal vascular pattern, granularity, erosions, friability, bleeding, and ulcerations, with distinct demarcation between inflamed and non-inflamed bowel. Histopathology is the definitive tool in diagnosing UC, assessing the disease severity and identifying intraepithelial neoplasia (dysplasia) or cancer. The classical histological changes in UC include decreased crypt density, crypt architectural distortion, irregular mucosal surface and heavy diffuse transmucosal inflammation, in the absence of genuine granulomas. Abdominal computed tomographic (CT) scanning is the preferred initial radiographic imaging study in UC patients with acute abdominal symptoms. The hallmark CT finding of UC is mural thickening with a mean wall thickness of 8 mm, as opposed to a 2-3 mm mean wall thickness of the normal colon. The Mayo scoring system is a commonly used index to assess disease severity and monitor patients during therapy. The goals of treatment in UC are three fold-improve quality of life, achieve steroid free remission and minimize the risk of cancer. The choice of treatment depends on disease extent, severity and the course of the disease. For proctitis, topical 5-aminosalicylic acid (5-ASA) drugs are used as the first line agents. UC patients with more extensive or severe disease should be treated with a combination of oral and topical 5-ASA drugs +/- corticosteroids to induce remission. Patients with severe UC need to be hospitalized for treatment. The options in these patients include intravenous steroids and if refractory, calcineurin inhibitors (cyclosporine, tacrolimus) or tumor necrosis factor-α antibodies (infliximab) are utilized. Once remission is induced, patients are then continued on appropriate medications to maintain remission. Indications for emergency surgery include refractory toxic megacolon, colonic perforation, or severe colorectal bleeding.

PMID 25687266 — Pathogenesis, diagnosis, and management of ulcerative proctitis, chronic radiation proctopathy, and diversion proctitis.

Chronic proctitis refers to persistent or relapsing inflammation of the rectum, which results from a wide range of etiologies with various pathogenic mechanisms. The patients may share similar clinical presentations. Ulcerative proctitis, chronic radiation proctitis or proctopathy, and diversion proctitis are the 3 most common forms of chronic proctitis. Although the diagnosis of these disease entities may be straightforward in the most instances based on the clinical history, endoscopic, and histologic features, differential diagnosis may sometimes become problematic, especially when their etiologies and the disease processes overlap. The treatment for the 3 forms of chronic proctitis is different, which may shed some lights on their pathogenetic pathway. This article provides an overview of the latest data on the clinical features, etiologies, diagnosis, and management of ulcerative proctitis, chronic radiation proctopathy, and diversion proctitis.

PMID 15365396 — Diagnosis and treatment of ulcerative proctitis.

Proctitis refers to inflammation of the rectum, a diagnosis made by endoscopic evaluation. Symptoms of proctitis include rectal bleeding, urgency, tenesmus, diarrhea or constipation, and occasionally rectal pain. The causes of proctitis include infection, medication, ischemia, radiation, and ulcerative proctitis. Ulcerative proctitis is an important and increasingly common subcategory of ulcerative colitis (UC) in which inflammation is limited to the rectum. Historically, oral aminosalicylates have been the mainstay of acute and maintenance therapy. A growing body of data, however, indicates that topical aminosalicylates are effective first line agents in ulcerative proctitis and distal UC. Topical aminosalicylates act more effectively and rapidly to induce and maintain remission compared with their oral counterparts or topical steroids. Rarely ulcerative proctitis is refractory to topical therapy and in these instances systemic corticosteroids, antibiotics, immunomodulators, or surgery is required. This review highlights the pathogenesis, diagnosis, and treatment of ulcerative proctitis.

PMID 19897972 — Medical management of ulcerative colitis.

Ulcerative colitis (UC) is a chronic and relapsing inflammation limited to the colonic mucosa and always involving the rectum with variable extension towards the cecum. The aim of medical treatment is to induce and maintain clinical remission. In contrast to Crohn’s disease for which a ‘top-down’ or ‘early aggressive’ therapy is discussed, in UC the concept of a step-up treatment is still valid. This step-up approach includes local or systemic administration of 5-aminosalicylic acid as first-line therapy followed by topical or systemic steroid administration as well as azathioprine, 6-mercaptopurine, cyclosporine, and more recently anti-tumor necrosis factor monoclonal antibodies as options in refractory or chronic active disease. Colectomy may be necessary if medical treatments are unsuccessful or if complications develop. The decision about the individual therapy of UC is dependent on both disease activity and on disease location. Different therapy strategies are applied in ulcerative proctitis, left-sided colitis, pancolitis and fulminant colitis as well as in chronic active disease and maintenance of remission. This overview presents important concepts in the treatment of UC based on the published guidelines.

PMID 24424198 — Diagnosis and classification of ulcerative colitis.

Ulcerative colitis (UC) is a chronic relapsing inflammatory bowel disease (IBD) characterised by superficial mucosal ulceration, rectal bleeding, diarrhoea, and abdominal pain. In contrast to Crohn’s disease (CrD), UC is restricted to the colon and the inflammation is limited to the mucosal layer. Classic UC affects the colon in a retrograde and continuous fashion starting from the rectum and extending proximally. Dependent on the anatomic extent of involvement, UC can be classified as proctitis, left-sided colitis, or pancolitis. Inflammatory arthropathies and primary sclerosing cholangitis (PSC) are the most common and clinically most important extraintestinal manifestations of UC. The aetiopathogenesis of UC is incompletely understood, but immune-mediated mechanisms are responsible for dysregulated immune responses against intraluminal antigens in genetically predisposed individuals. The diagnosis is based on the history, as well as clinical, radiological, endoscopic and histological features. Autoantibodies, mainly antineutrophil cytoplasmic antibodies (ANCA) and anti-goblet cell antibodies (GAB) may be helpful in the early diagnosis of UC and in differentiating it from CrD.

PMID 7450438 — Proctitis and colitis following diversion of the fecal stream.

Inflammation limited to excluded segments of the colon was observed in 10 patients without prior inflammatory bowel disease who had undergone colostomy or ileostomy for various indications. With the exception of 1 patient who complained of mucoid rectal discharge, the patients were asymptomatic when the lesion was discovered; 2 others subsequently developed mild symptoms. The proctoscopic findings were similar in appearance to those of mild ulcerative colitis. In 8 of 10 patients the inflammatory changes were confined to the distal few centimeters of the rectum, while in the remaining 2 patients the entire excluded segment was affected. Microscopic alterations were focal and included crypt abscesses, epithelial cell degeneration, acute and chronic inflammation in the lamina propria, and regenerative changes in the crypts. The inflammation persisted for as long as 8 yr in the 5 patients who did not have restoration of intestinal continuity, but subsided in the 5 patients whose colostomies were closed. The prior as subsequent clinical courses of these patients, together with the focal, nonspecific microscopic features, strongly suggest that the inflammation in these patients resulted from diversion of the fecal stream and was not a recognized form of specific or idiopathic colitis. Diversion-related colitis must not be confused with other forms of inflammation since this may result in improper therapy and/or delay in treatment of the condition for which the fecal diversion was performed.

PMID 1916483 — Diversion colitis: histological features in the colon and rectum after defunctioning colostomy.

Diversion of the faecal stream by ileostomy or colostomy leads to inflammation in the defunctioned segment, known as diversion colitis. The affected bowel is rapidly restored to normality by reanastomosis. Diversion colitis should not be mistaken for inflammatory bowel disease, for which reanastomosis would be inappropriate. Studies of biopsy material from patients with diversion colitis have shown a variety of histological features, but no consistent pattern. The histology in resection specimens of defunctioned large bowel from 15 patients with no pre-existing inflammatory bowel disease was studied. Nine patients had symptoms of abdominal pain or rectal discharge of blood or mucus that developed between 9 months and 17 years after diversion procedure. The histology was abnormal in all. Findings were similar in 14 patients, regardless of the duration of faecal diversion, and comprised diffuse mild chronic inflammation with or without mild crypt architectural abnormalities, crypt abscesses, or follicular lymphoid hyperplasia. One patient had more severe changes, resembling active ulcerative colitis. These features in biopsy specimens are unlikely to be diagnostic but should provide useful information in avoiding a mistaken diagnosis of inflammatory bowel disease in these patients.

PMID 2909876 — Treatment of diversion colitis with short-chain-fatty acid irrigation.

A condition known as diversion colitis frequently develops in segments of the colorectum after surgical diversion of the fecal stream; it persists indefinitely unless the excluded segment is reanastomosed. The disease is characterized by bleeding from inflamed colonic mucosa that mimics the bleeding of idiopathic inflammatory bowel disease, and it may culminate in stricture formation. We hypothesized that this condition is caused by the absence of luminal short-chain fatty acids, the preferred metabolic substrates of colonic epithelium. We studied four patients with diversion colitis, none of whom had evidence of Crohn’s, idiopathic ulcerative, or infectious colitis. The excluded segment of the rectosigmoid contained negligible concentrations of short-chain fatty acids. When D-glucose was instilled, it did not undergo appreciable anaerobic fermentation. Instillation of a solution containing short-chain fatty acids twice daily resulted in the disappearance of symptoms and the inflammatory changes observed at endoscopy, over a period of four to six weeks. Remission has been maintained for up to 14 months (in one patient) by instillation daily to twice weekly. Administering enemas containing isotonic saline, or omitting treatment for periods of two to four weeks during the regimen, by contrast, did not produce any improvement or rapid relapse of the colitis. Histologic observation revealed a distinctive type of mucosal inflammation that resolved more slowly and less completely than the gross appearance of the inflamed mucosa. From these preliminary studies we infer that diversion colitis may represent an inflammatory state resulting from a nutritional deficiency in the lumen of the colonic epithelium, which is effectively treated by local application of short-chain fatty acids, the missing nutrients.

PMID 9145448 — Effects of short-chain fatty acids on the inflamed colonic mucosa.

Selected inflammatory conditions of the distal alimentary tract may respond to topical SCFA treatment. The rationale for using SCFA enemas is based on Roediger’s (1980) observation that butyrate is the preferred fuel of colonocytes and that SCFA deficiency could lead, in the short term, to mucosal hypoplasia and, in the long term, to colitis. The absence of luminal nutrients is especially evident in the excluded rectum after complete diversion of the faecal stream. Harig et al. (1989) were the first to treat successfully diversion colitis with SCFA irrigation (acetate 60 mM, propionate 30 mM, n-butyrate 40 mM). However, subsequent studies could not reproduce the initial positive data. In distal ulcerative colitis an impaired mucosal oxidation of SCFAs has been described despite their luminal abundance. Pilot studies using either the SCFA mixture or butyrate monotherapy have yielded promising results. However, extended confirmatory studies with a larger sample size have not yet been performed. Preliminary data are also available for the use of SCFA in pouchitis and radiation proctitis. In summary, SCFA topical therapy seems to be a promising option in distinct forms of inflammatory bowel disease; however, the routine use of SCFAs cannot be recommended until their efficacy has been confirmed in larger trials.

PMID 11768558 — The bacterial flora in inflammatory bowel disease: current insights in pathogenesis and the influence of antibiotics and probiotics.

The pathogenesis of inflammatory bowel disease (IBD) remains unknown, although in recent years more data have become available. The contribution of genetic and environmental factors is evident, and the luminal bacterial flora plays a major role in the initiation and perpetuation of chronic IBD. Animal models of IBD have shown that colitis does not occur in a germ-free environment. In human IBD, inflammation is present in parts of the gut containing the highest bacterial concentrations. Moreover, the terminal ileum, caecum and rectum are areas of relative stasis, providing prolonged mucosal contact with luminal contents. Enhanced mucosal permeability may play a pivotal role in maintaining a chronic inflammatory state, due to a genetic predisposition or as a result of direct contact with bacteria or their products. A detective epithelial barrier may cause a loss of tolerance to the normal enteric flora. Furthermore, an increased mucosal absorption of viable bacteria and bacterial products is found in IBD. Serum and secreted antibodies are increased and mucosal T-lymphocytes that recognize luminal bacteria are present. However, there is evidence that the immune system reacts over aggressively towards the normal luminal flora rather than the flora being altered in IBD. Several approaches have been used in attempts to discover a specific microbial agent in the cause of IBD. These include demonstration of the presence of organisms or specific antigens in affected tissues, culture of microbes firm the affected tissues, demonstration of serological responses to several agents, and localization and detection of individual pathogen-specific nucleic acid sequences in affected tissue by in situ hybridization and polymerase chain reaction. So far, no specific micro-organism has been directly associated with the pathogenesis of IBD. Analysis of the luminal enteric flora, however, has revealed differences in the composition of this flora compared to healthy controls. In Crohn disease, concentrations of Bacteroides, Eubacteria and Peptostreptococcus are increased, whereas Bifidobacteria numbers are significantly reduced. Furthermore, in ulcerative colitis, concentrations of facultative anaerobic bacteria are increased. The arrival of new molecular techniques qualifying and quantifying the complex intestinal flora has induced a revival of interest in this microflora. Therapeutic approaches geared towards changing the environment at the mucosal border have been attempted by the use of elemental diets, total parenteral nutrition, surgical diversion of the faecal stream and antibiotics. Over the past few years, the use of probiotics in IBD and other intestinal disorders has gained attention. Strengthened by promising experimental data and commercial interests, research in this field is rapidly expanding. Manipulation of the colonic bacteria with antibiotic drugs and probiotic agents may prove to be more effective and better tolerated than immunosuppressants in the future.

PMID 34966763 — Nicotine Oral Administration Attenuates DSS-Induced Colitis Through Upregulation of Indole in the Distal Colon and Rectum in Mice.

Nicotine affects the gastrointestinal environment and modulates ulcerative colitis (UC). However, the associations among nicotine, gut metabolites, and UC are still largely unknown. We investigated whether orally administered nicotine affected gut metabolites and dextran sodium sulfate (DSS)-induced colitis. C57BL/6 male mice were orally administered nicotine solution in drinking water prior to inducing DSS-induced colitis. Short-chain fatty acids (SCFAs) and indole in gut contents and fecal samples were measured by GC-MS and hydroxylamine-based indole assays, respectively. Oral administration of nicotine increased indole concentration in feces, but, in contrast, SCFA values did not differ with nicotine administration. Indole levels were increased in the distal colon and rectum but not in the cecum and proximal colon. DSS-induced colitis was less severe clinically and histological changes were minimal in the rectum of orally nicotine-administered mice compared to mice drinking only water. 16S rRNA microbiome on the feces revealed an increasing in Clostridium and Porphyromonas in nicotine-administered mice. In conclusion, nicotine administration was associated with increased indole levels in the distal colon and rectum and attenuated DSS-induced colitis. Oral administration of nicotine may play a potential role in indole upregulation and prevention of UC.

PMID 20805871 — Bacteria penetrate the inner mucus layer before inflammation in the dextran sulfate colitis model.

Protection of the large intestine with its enormous amount of commensal bacteria is a challenge that became easier to understand when we recently could describe that colon has an inner attached mucus layer devoid of bacteria (Johansson et al. (2008) Proc. Natl. Acad. Sci. USA 105, 15064-15069). The bacteria are thus kept at a distance from the epithelial cells and lack of this layer, as in Muc2-null mice, allow bacteria to contact the epithelium. This causes colitis and later on colon cancer, similar to the human disease Ulcerative Colitis, a disease that still lacks a pathogenetic explanation. Dextran Sulfate (DSS) in the drinking water is the most widely used animal model for experimental colitis. In this model, the inflammation is observed after 3-5 days, but early events explaining why DSS causes this has not been described. When mucus formed on top of colon explant cultures were exposed to 3% DSS, the thickness of the inner mucus layer decreased and became permeable to 2 microm fluorescent beads after 15 min. Both DSS and Dextran readily penetrated the mucus, but Dextran had no effect on thickness or permeability. When DSS was given in the drinking water to mice and the colon was stained for bacteria and the Muc2 mucin, bacteria were shown to penetrate the inner mucus layer and reach the epithelial cells already within 12 hours, long before any infiltration of inflammatory cells. DSS thus causes quick alterations in the inner colon mucus layer that makes it permeable to bacteria. The bacteria that reach the epithelial cells probably trigger an inflammatory reaction. These observations suggest that altered properties or lack of the inner colon mucus layer may be an initial event in the development of colitis.

PMID 23426893 — Bacteria penetrate the normally impenetrable inner colon mucus layer in both murine colitis models and patients with ulcerative colitis.

The inner mucus layer in mouse colon normally separates bacteria from the epithelium. Do humans have a similar inner mucus layer and are defects in this mucus layer a common denominator for spontaneous colitis in mice models and ulcerative colitis (UC)? The colon mucus layer from mice deficient in Muc2 mucin, Core 1 O-glycans, Tlr5, interleukin 10 (IL-10) and Slc9a3 (Nhe3) together with that from dextran sodium sulfate-treated mice was immunostained for Muc2, and bacterial localisation in the mucus was analysed. All murine colitis models revealed bacteria in contact with the epithelium. Additional analysis of the less inflamed IL-10(-/-) mice revealed a thicker mucus layer than wild-type, but the properties were different, as the inner mucus layer could be penetrated both by bacteria in vivo and by fluorescent beads the size of bacteria ex vivo. Clear separation between bacteria or fluorescent beads and the epithelium mediated by the inner mucus layer was also evident in normal human sigmoid colon biopsy samples. In contrast, mucus on colon biopsy specimens from patients with UC with acute inflammation was highly penetrable. Most patients with UC in remission had an impenetrable mucus layer similar to that of controls. Normal human sigmoid colon has an inner mucus layer that is impenetrable to bacteria. The colon mucus in animal models that spontaneously develop colitis and in patients with active UC allows bacteria to penetrate and reach the epithelium. Thus colon mucus properties can be modulated, and this suggests a novel model of UC pathophysiology.

PMID 24945909 — Spontaneous colitis in Muc2-deficient mice reflects clinical and cellular features of active ulcerative colitis.

The colonic mucus layer plays a critical role in intestinal homeostasis by limiting contact between luminal bacteria and the mucosal immune system. A defective mucus barrier in animal models allows bacterial contact with the intestinal epithelium and results in spontaneous colitis. A defective mucus barrier is also a key feature of active ulcerative colitis (UC). Alterations in the immune compartment due to intestinal bacterial breach in mice lacking the colon mucus barrier have not been characterized and correlated to active UC. To characterize alterations in the immune compartment due to intestinal bacterial breach in Muc2-/- mice, which lack the colon mucus barrier, and correlate the findings to active UC. Bacterial contact with colon epithelium and penetration into colon tissue was examined in Muc2-/- mice and colon biopsies from patients with active UC using fluorescence microscopy and qPCR. Neutrophils, lymphocytes, CD103+ dendritic cell subsets and macrophages in colon from Muc2-/- mice and biopsies from UC patients were quantitated by flow cytometry. Inflamed UC patients and Muc2-/- mice had bacteria in contact with the colon epithelium. Bacterial rRNA was present in colonic mucosa in humans and Muc2-/- mice and in the draining lymph nodes of mice. Inflamed Muc2-/- mice and UC patients had elevated colon neutrophils, T cells and macrophages while a reduced frequency of CD103+ DCs was present in the inflamed colon of both mice and humans. The parallel features of the colon immune cell compartment in Muc2-/- mice and UC patients supports the usefulness of this model to understand the early phase of spontaneous colitis and will provide insight into novel strategies to treat UC.

PMID 32385500 — Muc5ac Expression Protects the Colonic Barrier in Experimental Colitis.

The mucus gel layer (MGL) lining the colon is integral to exclusion of bacteria and maintaining intestinal homeostasis in health and disease. Some MGL defects allowing bacteria to directly contact the colonic surface are commonly observed in ulcerative colitis (UC). The major macromolecular component of the colonic MGL is the secreted gel-forming mucin MUC2, whose expression is essential for homeostasis in health. In UC, another gel-forming mucin, MUC5AC, is induced. In mice, Muc5ac is protective during intestinal helminth infection. Here we tested the expression and functional role of MUC5AC/Muc5ac in UC biopsies and murine colitis. We measured MUC5AC/Muc5ac expression in UC biopsies and in dextran sulfate sodium (DSS) colitis. We performed DSS colitis in mice deficient in Muc5ac (Muc5ac-/-) to model the potential functional role of Muc5ac in colitis. To assess MGL integrity, we quantified bacterial-epithelial interaction and translocation to mesenteric lymph nodes. Antibiotic treatment and 16S rRNA gene sequencing were performed to directly investigate the role of bacteria in murine colitis. Colonic MUC5AC/Muc5ac mRNA expression increased significantly in active UC and murine colitis. Muc5ac-/- mice experienced worsened injury and inflammation in DSS colitis compared with control mice. This result was associated with increased bacterial-epithelial contact and translocation to the mesenteric lymph nodes. However, no change in microbial abundance or community composition was noted. Antibiotic treatment normalized colitis severity in Muc5ac-/- mice to that of antibiotic-treated control mice. MUC5AC/Muc5ac induction in the acutely inflamed colon controls injury by reducing bacterial breach of the MGL.

PMID 24246979 — Mucus and the goblet cell.

The discovery of an inner mucus layer normally impervious to bacteria has changed our way of understanding the interaction between commensal bacteria and the host epithelial cells. This inner colon mucus layer is rapidly renewed and converted into the outer mucus layer by host controlled endogenous proteolytic processing. The mucus characteristics esteem from the properties of the main protein component of these layers, the MUC2 mucin. This forms an enormously large net-like structure that builds the laminated inner mucus layer that largely acts as a size exclusion filter excluding bacteria. In the absence of MUC2 mucin, there is no inner mucus layer and bacteria reach the epithelial cell surface, penetrate the crypts and are also found inside epithelial cells, something that leads to severe inflammation. Other mouse models that spontaneously develop colitis due to different defects, like an absent ion channel (Nhe3) or immunological mediators (Tlr5, IL-10), all also have a defective inner colon mucus layer. Human patients with active ulcerative colitis have this layer penetrable to bacteria and beads the size of bacteria. Some of the ulcerative colitis patients in remission have a normal mucus layer whereas others have a penetrable inner mucus layer. Together, this suggests that the inner mucus layer and its integrity is important for the protection of the colon epithelium and inhibiting activation of the immune system as in ulcerative colitis.

PMID 25025717 — Mucus layers in inflammatory bowel disease.

The intestinal epithelium is covered with mucus with the main structural building block being the densely O-glycosylated MUC2 mucin. The intestinal epithelium is exposed to ingested material, our digestive machinery, and large amounts of microorganisms. Mucus is the first line of defense and aids to limit exposure to all these threats to the epithelium. In the small intestine, mucus acts as a matrix, which contains antimicrobial products, such as defensins and immunoglobulin A that limit epithelial exposure to the luminal bacteria. In the colon, the stratified inner mucus layer acts as a physical barrier excluding bacteria from the epithelium. Bacterial penetration of this normally restricted zone is observed in many colitis models and also in patients with ulcerative colitis. Mucus defects that allow bacteria to reach the epithelium and to stimulate an immune system response can lead to the development of intestinal inflammation. The current state of our knowledge concerning the function of the mucus layers and the main mucin component, MUC2, in inflammatory bowel disease is described in this review.

PMID 35602503 — The Role and Function of Mucins and Its Relationship to Inflammatory Bowel Disease.

Mucus is present throughout the gastrointestinal tract and is essential for regulating gut microbiota homeostasis and preventing disease by protecting the gastrointestinal barrier from microorganisms, pathogens and toxins or other irritants. Mucin (MUC)-2 is a secreted protein produced by epithelial goblet cells as the main component of mucus. Defects in the gastrointestinal tract, such as inflammation and ulcers, cause damage to the mucus barrier, which can worsen mucus quality and reduce mucus production. Therefore, we would like to review the characteristics of MUC2 and its role in intestinal disorders and highlight the importance of further studies. We also investigated whether the role of MUC2 differs between children and adults, ulcerative colitis (UC) and Crohn’s disease (CD).

PMID 23585269 — [Mucosal protection by phosphatidylcholine as new therapeutic concept in ulcerative colitis].

The colonic mucus serves a first barrier towards invasion of commensal bacteria in stool. One essential component of intestinal mucus is phosphatidylcholine (PC) which represents more than 90 % of the phospholipids in mucus indicative for a selective transport of PC into this compartment. It is arranged in lamellar structures as surfactant-like particles which provide a hydrophobic surface on top of the hydrated mucus gel to prevent invasion of bacteria from the intestinal lumen. In ulcerative colitis (UC) the mucus PC content is reduced by 70 % irrespective of the state of inflammation. Thus, it could represent an intrinsic primary pathogenetic condition predisposing to bacterial invasion and precipitation of inflammation. Since PC was shown to be mainly secreted by the ileal mucosa from where it is assumed to move distally to the colon, the PC content along the colonic wall towards the rectum gradually thins out with lowest PC content in the rectum. It explains the start of the clinical manifestation of UC in the rectum and expansion from there to the upper parts of the colon. When the lacking mucus PC in the UC was supplemented by an oral, delayed released PC preparation, it was shown in three clinical trials that the inflammation improved and even resolved. The data indicate the essential role of the mucus phosphatidylcholine content for protection against inflammation in colon. This can be the basis for the development of an innovative therapy for ulcerative colitis using orally available delayed released phosphatidylcholine.

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