The present invention relates to, in part, methods for the treatment of methanogen-associated disorders such as, for example, Irritable Bowel Syndrome (IBS) using at least one anti-methanogenic lovastatin analog or derivative. In addition, modified-release formulations comprising at least one anti-methanogenic lovastatin analog or derivative are provided which release the anti-methanogenic lovastatin analog or derivative in the gastrointestinal tract.

An object of the present invention is to provide a method of assisting diagnosis of inflammatory bowel disease, which can specifically determine inflammatory bowel disease.

The present invention relates to “a method of assisting diagnosis of inflammatory bowel disease, the method including subjecting a subject-derived specimen to a reduction treatment and subsequently measuring a human prohaptoglobin amount in the specimen by using an antibody 1 which is an antibody that specifically binds to an amino acid sequence set forth in SEQ ID NO: 1, and determining that a subject has inflammatory bowel disease by using the human prohaptoglobin amount as an indicator, and relates to an examination kit for assisting diagnosis of inflammatory bowel disease, including the antibody 1 a reducing agent”.

Methods of diagnosing Crohn’s disease and ulcerative colitis in subjects is provided based on the determination of metabolites in urine samples, such as serine, hypoxanthine, kynurenine, threonine, dimethylglycine, tryptophan, indoxylsul-fate, phenylacetylglutamine, sialic acid, 5-hydroxy-6-indolyl-o-sulfate, 5-(Δ-carboxybutyl) homocysteine, and/or an anion having m/ z:RMT:polarity of 345.1553:0.770:n, or determination of metabolites in stool samples, such as ketodeoxycholic acid, cholic acid, choline, tryptophan, trimethyllysine, serine, butyric acid, lactic acid, hypoxanthine and/or guanine.

A highly efficient and non-invasive automated diagnosis method of some inflammatory bowel diseases, such as Ulcerative Colitis (UC) and Crohn's Disease (CD), which always allows to avoid duodenal biopsy. Such a method is based on spectroscopic analysis by Raman technique, which operates directly on a protein extract of feces, and reduces the burden of the diagnosis, simultaneously being preferably useful for the automated distinction between Ulcerative Colitis (UC) and Crohn's Disease (CD).

The invention is in the field of therapy of gut inflammatory diseases such as Inflammatory Bowel Diseases (IBD) or Irritable Bowel Syndrome (IBS) including Gluten hypersensitivity. The inventors showed that ELA2A secreted by epithelial cells in the extracellular space is over-expressed in IBD conditions degrading tight junction proteins and controlling cytokines expression. Overexpression of ELA2A conferred a pro-inflammatory phenotype both in cell expression systems and in vivo in animal model of IBD. The inventors also showed that ELA2 over-expressing intestinal epithelial cells increase the release of CXCL8 protein compared to control cells. The increased CXCL-8 protein release observed in cells overexpressing ELA2A is inhibited by ELAFIN addition to the culture, in a dose-dependent manner. In particular, the invention relates to inhibitors of Elastase ELA2A, for use in the treatment of Inflammatory Bowel Diseases, such as Crohn's Disease, Ulcerative Colitis, Celiac disease, and Pouchitis.

In some embodiments, the invention provides a method for identifying an agent beneficial to treat a patient with inflammatory bowel disease comprising: a) determining a status of an intestinal barrier in the patient; and b) categorizing the status as severe dysfunction or moderate dysfunction, wherein a patient categorized as having severe dysfunction is identified as a patient who will benefit from treatment with an agent selected from the group consisting of an anti-TNF agent and/or an anti-IL-12/23 agent, and a patient categorized as having moderate dysfunction is identified as a patient who will benefit from treatment with an anti-integrin agent, an anti-janus kinase agent, and/or and a sphingosine-1-phosphate receptor agonist agent.

Described herein are methods and systems for detecting and/or distinguishing irritable bowel syndrome (IBS) from inflammatory bowel disease (IBD) and celiac disease. The methods and systems can utilize the detection of anti-CdtB antibodies and/or anti-vinculin antibodies to detect IBS, distinguish IBS from IBD and/or celiac disease. Further described are methods for selecting a therapy to treat IBS, IBD or celiac disease.

The present invention relates to a biomarker composition for diagnosing Johne's disease using the measurement of alpha-2-macrogolublin (A2M) and use thereof.

Since the biomarker of the present invention can provide improved sensitivity to subclinical infections by revealing differences in the expressions of host proteins in the serum of MAP-infected subjects during various stages of JD progression, it can be effectively used to eradicate JD from a population of subjects. In particular, since the biomarker of the present invention is detected using the ELISA method, it is possible to diagnose Johne's disease more efficiently than when other methods such as mass spectrometry are used, and it can be directly applied in the field. In addition, it is possible to provide a more excellent diagnostic effect than the existing ELISA kits for diagnosing Johne's disease that are commercially available.

Provided herein are compositions and methods to that target microbial proteases to ameliorate the intestinal barrier dysfunction and restore mucosal integrity. They are useful to treat and prevent diseases and disorders caused by pathogenic bacteria in the gastrointestinal system of a subject.

The invention features compositions and methods for characterizing inflammatory bowel disease and inflammatory bowel disease subtypes, such as well Crohn's disease and ulcerative colitis. In one aspect, the invention provides a panel for characterizing inflammatory bowel disease, the panel including two or more (e.g., 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 20, 25) capture molecules each bound to a substrate, wherein each capture molecule specifically binds a marker polypeptide selected from one or more of the following: CD3, CD4, CDS, CD24, CD25, CD27, CD38, CD44, CD45RA, CD45RO, CD127, CD161, CTLA-4, CXCR3, CCR4, CCR6, CCR7, FOXP3, HLA-DR, IFNγ, IL-10, IL-17A, IL-21, IL-22, CD11c, IL23p19, CD66b, CD163, CD44, ckit, CD16, NKp46, AHR, and TNFα, or a polynucleotide encoding said marker polypeptide.