In various embodiments methods of distinguishing Crohn's disease from ulcerative colitis are provided. In certain embodiments the methods comprise determining, or causing to be determined, the level of IgG antibodies that bind a malondialdehyde-acetaldehyde adduct (MAA adduct) in a biological sample from a mammal, where an elevated level of said antibodies as compared to the average level found in a mammal with Crohn's disease is an indicator that the mammal has ulcerative colitis rather than Crohn's disease.

Provided herein are materials and methods for isolation of eukaryotic nucleic acid from a human or non-human animal stool sample. Also provided are methods of analysis of eukaryotic biomarkers present in a human or non-human animal stool sample.

The present invention relates to a method for determining the distinctive nutritional requirements of a patient with specific nutritional needs and providing a composition meeting the distinctive nutritional requirements of said patient.

The invention relates to methods and products for the identification of a clinically significant immune response in subjects treated with a therapeutic protein. Aspects of the invention relate to methods and compositions for identifying a clinically significant immune response in patients treated with therapeutic amounts of a VLA4 binding antibody (e.g., natalizumab).

With the aim of proving an antibacterial composition against oral bacteria and the like capable of inducing Th1 cell proliferation or activation in an intestinal tract, the present inventors have found out that bacteria that suppress colonization and the like of the oral bacteria and the like in the intestinal tract are present in an intestinal microbiota. Moreover, the present inventors have succeeded in isolating intestinal bacteria that suppress intestinal colonization and the like of oral bacteria and the like.

The invention relates to markers for Crohn's disease and to specific compounds for detecting said markers. The invention also relates to methods for detecting, diagnosing and monitoring the progression of Crohn's disease as well as to methods for evaluating the efficacy of a treatment for said disease, and to compositions and kits that can be used for implementing said methods.

Methods and materials are disclosed for testing biomarkers in a subject suffering from inflammatory bowel disease (IBD) are described herein. Such detection can be useful for diagnosing and treating ulcerative colitis (UC) and Crohn's disease (CD), two forms of IBD that are otherwise difficult to distinguish. The method includes measuring the level of one or more of several biomarkers, including HD5 or MMP-7, which are expressed differentially in patents with UC and CD. A treatment may be based on the determination of whether the subject has ulcerative colitis or Crohn's disease.

This invention is directed to compositions and methods to detect and treat gastrointestinal diseases.

Described herein are sets of metabolite and lipid (e.g., fatty acid) markers that can be used in the detection of early stage colorectal cancer and/or early development of adenomatous polyps. Presented herein are illustrative pathology-linked panels. In certain embodiments, the markers presented herein (or subsets thereof) are used as a panel for detecting either colorectal cancer or adenomatous polyps at the same time. The markers presented herein include metabolites and lipids (e.g., fatty acid) freely detectable and accurately quantifiable in human serum. In certain embodiments, the sample may be plasma, urine, saliva, whole blood, dried blood spot or dried serum spot.

The present invention relates to the finding that TL1A enhances differentiation of TH17 cells, and enhance IL17 secretion from TH17 cells. In one embodiment, the present invention provides a method of treating an inflammatory disease comprising determining the presence of a TL1A signaling profile, and treating the disease by administering a composition comprising a therapeutically effective dosage of one or more inhibitors of TL1A or TH17 cell differentiation. In another embodiment, the disease is characterized by TH17 differentiation.