There is provided a method of identifying pro-inflammatory dendritic cells, the method comprising: determining an expression of CD5, CD14 and/or CD163 in cells, wherein CD5.sup.−, CD14.sup.+ and/or GD163.sup.+ cells are identified as pro-inflammatory dendritic cells. Also disclosed is a method of characterising inflammation and/or inflammatory disease in a subject, the method comprising: determining a proportion of CD5.sup.−, CD14.sup.+ and/or GD163.sup.+ dendritic cells in the subject's sample, wherein the proportion positively correlates with the level of inflammation and/or the severity of inflammatory disease in the subject.

Disclosed herein are immunoassay methods for detecting and quantifying human neutrophil elastase (HNE) generated fragments of calprotectin in a biofluid sample; and monoclonal antibodies and assay kits for use in such methods. The methods may be used for detecting, monitoring and/or determining the status or severity of a disease characterized by or exhibiting inflammation in a patient.

Provided herein are, in various embodiments, methods of detecting an acute inflammatory response associated with a viral infection in a patient, methods of predicting a likelihood of developing an acute inflammatory response (e.g., an acute respiratory distress syndrome) in a patient having a viral infection, such as a SARS-CoV2 infection, and methods of preparing a bodily fluid sample that is useful for performing the disclosed methods. The present invention also provides methods of treating a patient having a viral infection with a therapy that inhibits acute inflammation, such as acute inflammation mediated by the kinin-kallikrein system and/or the renin-angiotensin system (RAS).

A method for modulating the adrenomedullin (ADM) activity of a patient by administering to the patient an anti-adrenomedullin (ADM) antibody or an anti-adrenomedullin antibody fragment. The method may be used, for example, in therapy of a chronical or acute disease or acute condition of a patient for prevention or reduction of organ dysfunction or organ failure. In a preferred embodiment the method is for use in therapy of a chronical or acute disease or acute condition of a patient for prevention or reduction of kidney dysfunction or kidney failure or liver dysfunction or liver failure.

The invention provides a method for detection of allergic inflammation in a subject that comprises assaying a test sample of peripheral blood from the subject for a marker of DNA damage. An elevated amount of marker present in the test sample compared to control sample is indicative of inflammation. The method can be adapted for quantitatively monitoring the efficacy of treatment of allergic inflammation in a subject. Markers of DNA damage include single- and/or double-stranded breaks in leukocytes, oxidative DNA damage in leukocytes, or a marker of nitric oxide oxidative activity (protein nitrosylation in leukocytes). This unexpected discovery of markers of systemic genotoxicity present in circulating leukocytes enables detection of allergic inflammation with a relatively simple and minimally invasive assay using peripheral blood.

A kit for detecting an inflammation level of an oral cavity based on a biomarker indicative of inflammation, the kit comprising at least one rinsing substance; a cup sized to contain a predetermined amount of at least one rinsing substance; a colourimetric reference corresponding to a predetermined inflammation level, and a colourimetric indicator reactive to the biomarker in the at least one rinsing substance consistently with the colourimetric reference.

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.

Provided herein are methods and kits for analyzing a biological sample obtained from a subject having, suspected of having, or being at risk for a disease associated with the contact activation system.

The present application provides quinoline-3-carboxamide compounds covalently linked to a label for use in the diagnosis of an inflammatory disease at local site. The above mentioned compounds can be used to detect or image accumulation of S100A9 in the body of a subject at sites of inflammation, using in vivo non-invasive molecular imaging techniques for the detection of said compounds. Accordingly, labeled quinoline-3-carboxamide compounds can be applied to evaluate the risk of a subject of developing an inflammatory disease and to follow the progress of the disease.

Provided are methods and systems for determining functional relationships between ex vivo skin models and an inflammatory skin condition. Also provided are methods and systems for identifying modulators of inflammation of skin, as well as the use of modulators identified by such methods or systems for the preparation of cosmetic compositions, personal care products, or both.