Although there is a familial tendency, the etiology of ulcerative colitis remains undefined, however, there is considerable evidence pointing towards autoimmunity. Acute and chronic inflammation within the colonic mucosa are known to generate inflammatory mediators which perpetuate the inflammatory process. Current therapy for ulcerative colitis remains empirical and consists of treatment with sulfasalazine, glucocorticosteroids, and immunosuppressants. These agents require continuous administration to prevent recurrent inflammation once an acute episode has subsided. In recent years, 5-ASA compounds have been used with reduction in side effects but without much change in response rate as compared to conventional therapy.

The presence of a 40 KDa (Mr 40K, p40) colonic autoantigen and the circulating antibodies reactive against this protein have been detected in idiopathic ulcerative colitis (Takahasi et al., J. Clin. Invest. 76:311,1985) and in cotton top tamarins with spontaneous colitis (Das et al., Gut 33:48, 1992). Using hybridoma technology, a monoclonal antibody (7E 12 H 12 , IgM isotype) was developed against the epithelial antigen associated with ulcerative colitis (Das et al., J. Immunol. 139:77, 1987). The monoclonal antibody 7E 12 H 12 binds specifically to colonocytes along baso-lateral and brush border areas and it does not react with any other parts of the gastrointestinal tract including the small intestine. This colon epithelial specific protein (CSP) is localized in the cell membrane. Three recent studies demonstrated that 7E 12 H 12 reactive protein (CSP) indeed is recognized by a disease specific (ulcerative colitis) autoantibody of IgG1 subclass (Halstensen et al., Gut 34:650, 1993; Dasgupta et al., Gut 35:1712-1717, 1994; Hassan et al., Clin. Exp. Immunol., 1995, 100:1457-1462).

Using an animal model of colitis, researchers have recently shown that the 7E 12 H 12 monoclonal antibody given by enema provides beneficial effect against the Dextran Sulfate Sodium induced murine colitis (Nandiwada et al., Gastroenterology 104:A754, 1993). The study involved intracolonic administration of 7E 12 H 12 prior to and along with Dextran Sulfate Sodium and the results suggested that the 7E 12 H 12 monoclonal antibody is significantly effective in improving the clinical and histological integrity of the colonic mucosa. Autoimmunity has been implicated in the pathogenesis of ulcerative colitis (UC) since its initial report 36 years ago demonstrating the presence of circulating antibody in ulcerative colitis against colonic antigen (Perlman, P., J. Exp. Med. 1959;110:657-673). Subsequently, other investigators reported the presence of various serum antibodies occurring in up to 70% of patients with ulcerative colitis directed against intestinal goblet cells (Brandtzaeg, P., Gastroenterology 1995;109:307312; Hibi et al., Clinical Exp. Immunol. 1983, 54, 163-168) as well as directed against colonic epithelial brush border, suggesting the multiplicity of antigenic cellular proteins. Tissue bound IgG eluted from ulcerative colitis colon but not from non-ulcerative colitis diseased colon, has been shown to react with an Mr 40K colonic protein (p40). The ulcerative colitis colon eluted IgG (CCA-IgG) also reacted with the autologous p40. Lamina propria lymphocytes from ulcerative colitis also secrete IgG reactive to the mucosal extract enriched in p40. Subsequently, a partial sequence study indicated that p40 belonged to a tropomyosin family.

Using highly enriched p40, a murine monoclonal antibody (mAb), termed 7E 12 H 12 (IgM isotype) was developed (Das, K. M. et al., J. Immunol. 1987;139:77-84). Immunocytochemical studies using the 7E 12 H 12 monoclonal antibody demonstrated specific recognition of the colonic epithelial cells and not with 13 other epithelial organs including other parts of the gastrointestinal tract and small intestinal enterocytes. The reactivity was predominantly localized at the plasma membrane in the apical (brush border area) and basolaceral domains of colonocytes (Das, K. M. et al., J. Immunol. 1987;139:77-84). Using two and three color immunofluorescence assay (Halstensen, T. S. et al., Gut 1993;34:650-657), the 7E 12 H 12 reactive epitope was also localized exclusively in colonic enterocytes, but not in small intestinal enterocytes, with increasing intensity caudally, expanding to intense cytoplasmic expression in the rectum. Furthermore, IgG1 antibody and activated complement products, C3b and terminal complement complex, were co-localized with 7E 12 H 12 epitope on the colonic epithelium in ulcerative colitis but not in Crohn's disease (Halstensen, T. S. et al., Gut 1992;33:902-908), suggesting a specific antibody response against the 7E 12 H 12 reactive protein and perhaps followed by activation of complement system. This in situ observation of a specific IgG1 autoantibody response against the 7E 12 H 12 -reactive protein was confirmed using sera from a large number of patients with ulcerative colitis and other disease controls (Dasgupta et al., Gut 35:1712-1717). Sera from patients with primary sclerosing cholangitis also contain specific autoantibody against the 7E 12 H 12 -reactive protein that is shared by colon and biliary epithelial cells (Mandal, A. et al., Gastroenterology 1994; 106:185-192). Indeed, following systematic screening of 17 various epithelial organs using the 7E 12 H 12 monoclonal antibody, epitope(s) cross-reactive to colonocytes were localized only in the epidermis, biliary epithelium, non-pigmented epithelial cells of the ciliary processes in the eye, and chondrocytes of joints (Das, K. M. et al., Gastroenterology 1990:98;464-469; Bhagat et al., Gastroenterology 1994:107;103-108), the extracolonic organs most commonly involved in ulcerative colitis. These findings from several independent studies provide evidence suggesting that an autoimmune response to the 7E 12 H 12 -reactive protein is an important immunopathological event in ulcerative colitis.
 

The present invention pertains to a method for treating ulcerative colitis in a human which comprises orally or rectally administering to the human a therapeutically effective amount of an antibody which binds to a colonic antigen associated with ulcerative colitis.

In another embodiment, the present invention pertains to a method for treating ulcerative colitis in a human which comprises the steps of:

(a) obtaining from a human a colon epithelial cell extract containing a colonic antigen associated with ulcerative colitis;

(b) purifying the colonic antigen until the antigen is substantially homogeneous;

(c) developing an antibody which binds to the colonic antigen;

(d) orally or rectally administering to a human having ulcerative colitis a therapeutically effective amount of the antibody to bind to the colonic antigen associated with ulcerative colitis.

In yet another embodiment, the present invention pertains to a method for vaccinating a human against ulcerative colitis which comprises orally administering to the human a therapeutically effective amount of a colonic antigen associated with ulcerative colitis. 
 

There are also herbal medicines which can very effectively treat colitis & ulcerative colitis. Boswellia is an Ayurvedic  (Indian traditional medicine) herb, used as a natural alternative to drugs. Many studies have found that the effectiveness of Boswellia is similar and even superior to sulfasalazine based prescription drugs. (Source Wikipedia: http://en.wikipedia.org/wiki/Ulcerative_colitis. 

We recommend taking a 4 months course of our Boswellia Serrata Extract.
 
 

Total of 4 bottles-  of Boswellia - 4 Months course - Taken 2 capusles twice a day.
 
 

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