The etiology of ulcerative colitis is unknown. A number of studies have suggested that components of the immune system may mediate or contribute to injury observed in the colonic mucosa, but it remains unclear what initiates the pathogenic processes. It has been suggested that a primary abnormality of the immune system and its regulation might serve as primary initiating factors, or that the disease process might be initiated by an infectious agent and the injury then perpetuated through immune-mediated or other processes. Although the mucosal injury observed during episodes of acute disease can resemble the effects of any of a number of recognized infectious agents, no transmissible infectious agent has been consistently identified with ulcerative colitis. Alternatively, it has been suggested that aberrant structures in the colonic mucosa might increase susceptibility of the colonic mucosa to a lumenal factor, predisposing the colonic mucosa to injury by causing a defect in the mucosal barrier or initiating inappropriate activation of injurious immune-mediated processes.

Longstanding ulcerative colitis is generally recognized as a precancerous lesion, and a finite percentage of those affected with ulcerative colitis develop colonic adenocarcinoma, usually after a disease course of ten years or more. Thus it can be desirable to be able to detect ulcerative colitis early in the patient's life, and to be able to distinguish ulcerative colitis from other intestinal inflammations, including other inflammatory diseases such as ischemic colitis and Crohn's disease and functional disorders such as irritable bowel syndrome. Early intervention can improve the long range prognosis for the patient having ulcerative colitis. Familial studies have suggested that a genetic factor may be involved in ulcerative colitis, and specific detection of the disease in prospective parents can be useful in genetic counseling. A number of studies, including some employing specialized histochemical staining techniques, lectin probes, or direct characterization of glycoprotein heterogeneity in colonic mucosa, have suggested that glycoconjugates in the colonic mucosa are altered in patients having ulcerative colitis.

SUMMARY OF THE INVENTION

We have discovered that there exist "structural determinants" (i.e., antigenic determinants, or "epitopes") which can be present in tissues and tissue extracts from patients having ulcerative colitis, and which are absent from tissues and tissue extracts from clinically normal persons or from persons having inflammatory disease other than ulcerative colitis; and that monoclonal antibodies recognizing these "structural determinants" can be used in a highly specific assay for diagnosing ulcerative colitis. In patients having active ulcerative colitis, samples of colonic mucosa taken from uninvolved regions of the colon can yield a positive diagnosis, so that accurate diagnosis can be accomplished even using a tissue sample taken from a site other than a site of involved tissue. Moreover, samples of colonic mucosa from patients having ulcerative colitis but lacking active disease at the time of biopsy can yield a positive diagnosis, so that the tissue sample can be taken at a time other than during an episode of active inflammation.

The invention thus features a monoclonal antibody which binds preferentially to colonic glycoproteins of cells of persons having ulcerative colitis, compared to colonic glycoproteins of cells of persons not having ulcerative colitis (e.g., those who have other inflammatory diseases of the colon, such as Crohn's disease, or those who have colon cancer). In preferred embodiments, the monoclonal antibody is coupled to a cytotoxic agent; the monoclonal antibody is labeled with a detectable label; the monoclonal antibody is radiolabeled or fluorescently labeled; the monoclonal antibody is produced by a hybridoma cell deposited in the American Type Culture Collection, Rockville, Md., on Jun. 22, 1988, and given ATCC Accession No. HB 9753; or by a hybridoma cell deposited in the American Type Culture Collection on Jun. 24, 1988, and given ATCC Accession No. HB 9756.

In another aspect, the invention features a hybridoma cell capable of producing a monoclonal antibody having the immunological identifying characteristics of (i.e., the same antigen-binding specificity as) the monoclonal antibody produced by the hybridoma cell given ATCC Accession No. HB 9753 or the monoclonal antibody produced by the hybridoma cell given ATCC Accession No. HB 756. In preferred embodiments, the hybridoma cell is the hybridoma cell given ATCC Accession No. HB 9753 or the hybridoma cell given ATCC Accession No. HB 9756.

In another aspect the invention features a method for detecting the presence of ulcerative colitis in a human patient, which method includes contacting a colonic glycoprotein sample from the patient or a sample derived from the blood of the patient with a monoclonal antibody having the immunological identifying characteristics of the monoclonal antibody produced by the hybridoma cell given ATCC Accession No. HB 9753 or of the monoclonal antibody produced by the hybridoma cell given ATCC Accession No. HB 9756, and detecting immune complexes formed with the monoclonal antibody.

In another aspect, the invention features a method for detecting the presence of ulcerative colitis in a human patient, which method includes contacting a sample derived from the blood of the patient with ulcerative colitis-associated colonic glycoproteins and with a monoclonal antibody having the immunological identifying characteristics of the monoclonal antibody produced by the hybridoma cell given ATCC Accession No. HB 9753 or of the monoclonal antibody produced by the hybridoma cell given ATCC Accession No. HB 9756, and detecting immune complexes formed with the monoclonal antibody. In another aspect the invention features a method for treating ulcerative colitis in a person, including administering to the patient in a pharmaceutically suitable carrier substance, a monoclonal antibody which binds preferentially to colonic glycoproteins of cells of persons having ulcerative colitis. Preferably, the monoclonal antibody to be administered in the pharmaceutically suitable carrier substance is coupled to a cytotoxic agent capable of killing the cells targeted by the monoclonal antibody. Other features and advantages of the invention will be apparent from the following detailed description, and from the claims. 
 
 
 

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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