Disclosed are compositions and methods to detect proteins associated with diseases associated with exposure to inhaled carcinogens. Such markers may be useful to allow individuals susceptible to diseases associated with exposure to inhaled carcinogens to manage their lifestyle and reduce further progression of disease.

Provided herein are, inter alia, methods, compositions, and systems, for detecting and treating dysbiosis such as nasal and sinus dysbiosis. In aspects, included herein are methods, compositions, and systems for detecting asthma, chronic rhinosinusitis, and infections (such as rhinovirus infections), and methods of treating such disorders. Also provided are methods, compositions, and systems for detecting whether a subject has an increased risk of asthma, an infection, asthma exacerbation, chronic rhinosinusitis, or nasal polyposis, as well as methods of treating at-risk subjects. Methods, compositions, and systems for monitoring subjects diagnosted as having a disease or risk as disclosed herein are also included.

Described are methods and uses employing metabolomic data to diagnose an asthma disease state or a Chronic Obstructive Pulmonary Disease (COPD) state. Further described are methods of uses of employing metabolomic data to distinguish between asthma and COPD. In particular, urinary metabolomic profiles are employed to enable differential diagnosis of asthma and COPD.

Provided herein are methods for diagnosing the COPD inflammatory phenotype of an individual, and methods for selecting individuals with COPD for treatment based on their COPD inflammatory phenotype. In particular embodiments the methods comprise determining the level of expression of one or more genes selected from CLC, CPA3, DNASE1L3, IL1B, ALPL and CXCR2, or determining the expression profile CLC, CPA3, DNASE1L3, IL1B, ALPL and CXCR2, in one or more biological samples from an individual, wherein the expression levels or expression profile are indicative of the COPD inflammatory phenotype.

Described herein are monoclonal antibodies, assay kits and immumoassay methods for quantifying elastin fragments with a C-terminus amino acid sequence LPGGYGLPYT (SEQ ID NO: 1) in a patient biofluid sample, and uses thereof for detecting or quantifying fibrotic diseases such as chronic obstructive lung disease (COPD).

The present invention provides a method of reducing the quantity of mucus in the respiratory tract of a subject with elevated levels of mucus in said respiratory tract. The method includes administering to the subject a compound or composition containing a therapeutically effective amount of a fusion protein comprising a sialidase or an active portion thereof and an anchoring domain. The therapeutically effective amount comprises an amount of the fusion protein that results in a reduction of the quantity of mucus in the respiratory tract after administration of the compound or composition when compared to the quantity of mucus present prior to administration of the compound or composition.

This disclosure provides a robust, sensitive, and specific assay for the detection and measurement of periostin levels in samples obtained from human patients having, or suspected of having an IL-13-mediated disease or disorder. The disclosure further provides novel antiperiostin monoclonal antibodies that recognize at least isoforms 1, 2, 3, 4, 7, and 8 of human periostin, and assay kits comprising one or more of these antibodies.

The present invention refers to an antibody able to recognize and bind to an epitope comprised in a sequence of human Migration Stimulating Factor (MSF), and that doesn't recognize and bind human Fibronectin 1 (hFn1) and to uses in diagnostic methods and therapy.

The present invention provides a method for identifying epithelial cells circulating in peripheral blood, which allows individuals who suffer from a disease that presents with epithelial cell destruction to be discriminated from those who do not. The invention also relates to a kit or device for carrying out the methods of the invention.

This disclosure relates to devices, assays, and methods related to airway inflammation caused by polymorphonuclear neutrophils (PMNs). In certain embodiments, the disclosure relates to a model device that emulates the changes in airway cell physiology due to transmigration of PMNs from blood to the cells at the air-liquid interface. In certain embodiments, the airway cells are supported on a collagen layer wherein the collagen layer is further supported by a porous polymer from which PMNs can migrate. In certain embodiments, the disclosure contemplates adding bacteria, fungi and/or viruses to the device to emulate disease states. In certain embodiments, the disclosure relates to the use of the model system to test compounds to identify drug candidates and diagnose subjects with airway-related diseases and conditions.