The present invention is directed to methods of using biomarkers to assess treatment of gastrointestinal inflammatory disorders with beta7 antagonists. More particularly, the present invention relates to methods of using the level of gut-homing lymphocytes in peripheral blood, the level of drug occupancy on gut-homing lymphocytes, and/or the level of beta7 integrin receptors on gut-homing lymphocytes as indicators (or biomarkers) of the effect, efficacy, safety, prognosis, and/or dosing of therapeutic agents, such as beta7 integrin antagonists, for the treatment of gastrointestinal inflammatory disorders.

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

The invention relates to methods of treating fibrosis and inflammatory bowel disease. In one embodiment, the present invention treats gut inflammation by administering a therapeutically effective dosage of TL1A inhibitors and/or DR3 inhibitors to an individual. In another embodiment, the present invention provides a method of reversing tissue fibrosis in an individual by inhibiting TL1A-DR3 signaling function.

The present invention generally pertains to methods of characterizing at least one protein of interest in a biological sample. In particular, the present invention pertains to the use of automated iterative tandem mass spectrometry (AIMS) to identify, quantify and characterize at least one protein of interest and/or biomarker from a biological sample such as plasma.

In some aspects, the present invention provides methods for predicting whether a subject will develop autoantibodies to an anti-TNFα drug during the course of anti-TNFα drug therapy. In other aspects, the present invention provides methods for predicting the level of an anti-TNFα drug in a subject during the course of anti-TNFα drug therapy. Systems for predicting anti-TNFα drug levels and the likelihood of autoantibody formation during the course of anti-TNFα drug therapy are also provided herein. The present invention further provides methods for predicting a clinical outcome (e.g., endoscopic response) of a subject on anti-TNFα drug therapy.

Mucosal healing is an indication to the disease activity level in patients affected by inflammatory bowel diseases, and it is thus far mainly monitored by endoscopy. Instead or in addition to endoscopy, the invention provides blood test using biomarkers and an index that allows a practitioner to assess the status of mucosal healing, to change or adapt dosage of treatment and to predict which patient will become responder versus non-responder to treatment as assessed by endoscopy. While none of neutrophils cell count, c-reactive protein (CRP), Human type of Cathelicidin (LL-37), or Chitinase 3-like 1 (CHI3L1) alone is able to provide an assessment means of mucosal healing, the invention provides a novel combination of the levels of these biomarkers to assess the level of mucosal healing in relation to endoscopic healing.

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.

Mucosal healing is an indication to the disease activity level in patients affected by inflammatory bowel diseases, and it is thus far mainly monitored by endoscopy. Instead or in addition to endoscopy, the invention provides blood test using biomarkers and an index that allows a practitioner to assess the status of mucosal healing, to change or adapt dosage of treatment and to predict which patient will become responder versus non-responder to treatment as assessed by endoscopy. While none of neutrophils cell count, c-reactive protein (CRP), Human type of Cathelicidin (LL-37), or Chitinase 3-like 1 (CHI3L1) alone is able to provide an assessment means of mucosal healing, the invention provides a novel combination of the levels of these biomarkers to assess the level of mucosal healing in relation to endoscopic healing.

The present disclosure relates to methods of diagnosing a dysbiosis in a subject, methods of determining a suitable treatment, and methods of treating a dysbiosis. In some aspects, the present disclosure relates to diagnosing or determining a subtype of irritable bowel syndrome (IBS).

Provided herein is a method of treating an individual afflicted with an inflammatory bowel disease utilizing Candida abundance as a biomarker of responsiveness. The method comprises determining levels of Candida in a sample from the gastrointestinal tract of an individual, and if the level of Candida is higher than a reference level, identifying the individual as suitable for microbiota transplantation therapy (MTT), and optionally, administering to such an individual the MTT, and in individuals having gastrointestinal tract Candida levels lower than a reference level, increasing the Candida levels prior to prior to administration of MTT.