Abstract: Methods and compositions disclosed herein generally relate to methods of treating eosinophilic esophagitis (EE) and eosinophilic disorders by providing or enhancing a diagnosis of EE and eosinophilic disorders. In particular, the invention relates to obtaining a sample from a patient, then quantifying from the sample an amount of one or more microRNAs (miRNAs) associated with EE, wherein an altered level of the miRNA correlates with a positive diagnosis of EE. An EE diagnosis can then be provided or enhanced, based upon the quantifying step, and an appropriate treatment can be administered to the patient. The invention further relates to diagnostic kits, tests, and/or arrays that can be used to quantify the one or more miRNAs associated with EE, as well as treatments developed to up-regulate or down-regulate one or more miRNAs and/or their downstream pathways relevant to EE or asthma. The invention further relates to the use of IGF1 and IGF1R inhibitors for the treatment of EE and eosinophilic disorders.

Abstract: A method to evaluate eosinophilic esophagitis based on information in an eosinophilic esophagitis transcriptome.

Abstract: The invention provides methods of treating allergic inflammatory conditions using an anti-neurotrophin tyrosine kinase receptor 1 (NTRK1)-based therapeutic agent, and related compositions and methods.

Abstract: The disclosure provides compositions and methods related to the diagnosis, prognosis, and treatment of inflammatory diseases and disorders, especially allergic inflammatory diseases and disorders.

Abstract: The disclosure provides methods and compositions for diagnosing a patient eosinophilic esophagitis, the methods based upon the patient's gene expression profile for a panel of genes. The methods can also be used to exclude a diagnosis of chronic esophagitis.

Abstract: Methods and compositions disclosed herein generally relate to methods of treating eosinophilic esophagitis (EE) and eosinophilic disorders by providing or enhancing a diagnosis of EE and eosinophilic disorders. In particular, the invention relates to obtaining a sample from a patient, then quantifying from the sample an amount of one or more microRNAs (miRNAs) associated with EE, wherein an altered level of the miRNA correlates with a positive diagnosis of EE. An EE diagnosis can then be provided or enhanced, based upon the quantifying step, and an appropriate treatment can be administered to the patient. The invention further relates to diagnostic kits, tests, and/or arrays that can be used to quantify the one or more miRNAs associated with EE, as well as treatments developed to up-regulate or down-regulate one or more miRNAs and/or their downstream pathways relevant to EE or asthma. The invention further relates to the use of IGF1 and IGF1R inhibitors for the treatment of EE and eosinophilic disorders.

Abstract: Embodiments of the invention are directed to methods of diagnosing eosinophilic gastritis (EG), or remission therefrom in a subject, wherein the methods include applying a sample from the subject to a diagnostic panel that contains selected markers for EG, analyzing the results thereof, and making a determination as to the EG status of the subject. Embodiments of the invention are also directed to methods of monitoring the pathological development or medical prognosis of EG in a subject. Embodiments of the invention are also directed to use of CDH26 as a marker for EG, eosinophilic esophagitis, or allergic inflammatory conditions. Embodiments of the invention also relate to the use of anti-CDH26-based therapeutics to treat allergic inflammatory conditions.

Abstract: The invention provides methods of treating allergic inflammatory conditions using an anti-neurotrophin tyrosine kinase receptor 1 (NTRK1)-based therapeutic agent, and related compositions and methods.

Abstract: Methods and compositions disclosed herein generally relate to methods of treating eosinophilic esophagitis (EE) and eosinophilic disorders by providing or enhancing a diagnosis of EE and eosinophilic disorders. In particular, the invention relates to obtaining a sample from a patient, then quantifying from the sample an amount of one or more microRNAs (miRNAs) associated with EE, wherein an altered level of the miRNA correlates with a positive diagnosis of EE. An EE diagnosis can then be provided or enhanced, based upon the quantifying step, and an appropriate treatment can be administered to the patient. The invention further relates to diagnostic kits, tests, and/or arrays that can be used to quantify the one or more miRNAs associated with EE, as well as treatments developed to up-regulate or down-regulate one or more miRNAs and/or their downstream pathways relevant to EE or asthma. The invention further relates to the use of IGF1 and IGF1R inhibitors for the treatment of EE and eosinophilic disorders.

Abstract: CD48, a surface-marker molecule present in eosinophils, is disclosed herein as a key molecule in allergic conditions, particularly in allergic airway inflammations like asthma, allergy and nasal polyposis. CD48 is thus presented as a target molecule in the treatment of said conditions. In addition, diagnostic methods, and a kit for the diagnosis of allergic inflammatory conditions are described, based on the detection of CD48 expression.

Abstract: Embodiments of the invention are directed to methods of diagnosing eosinophilic esophagitis (EoE), or remission therefrom in a subject, wherein the methods include applying a sample from the subject to a diagnostic panel that contains selected markers for EoE, analyzing to obtain relatedness information relative to an EoE cohort and making a determination as to the EoE status of the subject, wherein an analysis indicating grouping with an EoE cohort or a quantitative score similar to that of an EoE cohort are indicative of EoE in the subject. Embodiments of the invention are also directed to methods of monitoring the pathological development or medical prognosis of EoE in a subject.

Abstract: Methods and compositions disclosed herein generally relate to methods of treating eosinophilic esophagitis (EE) and eosinophilic disorders by providing or enhancing a diagnosis of EE and eosinophilic disorders. In particular, the invention relates to obtaining a sample from a patient, then quantifying from the sample an amount of one or more microRNAs (miRNAs) associated with EE, wherein an altered level of the miRNA correlates with a positive diagnosis of EE. An EE diagnosis can then be provided or enhanced, based upon the quantifying step, and an appropriate treatment can be administered to the patient. The invention further relates to diagnostic kits, tests, and/or arrays that can be used to quantify the one or more miRNAs associated with EE, as well as treatments developed to up-regulate or down-regulate one or more miRNAs and/or their downstream pathways relevant to EE or asthma. The invention further relates to the use of IGF1 and IGF1R inhibitors for the treatment of EE and eosinophilic disorders.

Abstract: Embodiments of the invention are directed to methods of diagnosing eosinophilic gastritis (EG), or remission therefrom in a subject, wherein the methods include applying a sample from the subject to a diagnostic panel that contains selected markers for EG, analyzing the results thereof, and making a determination as to the EG status of the subject. Embodiments of the invention are also directed to methods of monitoring the pathological development or medical prognosis of EG in a subject. Embodiments of the invention are also directed to use of CDH26 as a marker for EG, eosinophilic esophagitis, or allergic inflammatory conditions. Embodiments of the invention also relate to the use of anti-CDH26-based therapeutics to treat allergic inflammatory conditions.

Abstract: It has long been known that eosinopenia is observed during acute bacterial infection yet the mechanism remains undefined. Herein, we investigated the consequence of exposure to microbial products, specfically bacterial lipopolysaccharide (LPS), on eosinophil production. We demonstrate that developing murine eosinophils transiently express mRNA for six Toll-like receptors (TLR5) with highest expression of TLR2 and TLR4 throughout eosinophil development and nearly undetectable levels on mature eosinophils. LPS stimulation of eosinophil progenitors ex vivo markedly inhibited IL-5- mediated cellular proliferation and expansion Further LPS adrninistratwn in vivo reduced numbers of eosinophil progenitors in the bone marrow and blood in mice. Notably, LPS effectively reduced eosinophilia even in hypereosinophilic mice induced by the IL-S transgene.

Abstract: Methods and compositions disclosed herein generally relate to methods of providing or enhancing a diagnosis of eosinophilic esophagitis (EE). In particular, the invention relates to obtaining a sample from a patient having at least one indication of EE, then quantifying from the sample an amount of one or more cytokines associated with EE or an mRNA corresponding to the cytokine or its receptor, wherein an altered level of the cytokine or mRNA correlates with a positive diagnosis of EE. An EE diagnosis can then be provided or enhanced, based upon the quantifying step. The invention further relates to diagnostic kits, tests, and/or arrays that can be used to quantify the one or more cytokines associated with EE or an mRNA corresponding to the cytokine or its receptor.

Abstract: CD48, a surface-marker molecule present in eosinophils, is disclosed herein as a key molecule in allergic conditions, particularly in allergic airway inflammations like asthma, allergy and nasal polyposis. CD48 is thus presented as a target molecule in the treatment of said conditions. In addition, diagnostic methods, and a kit for the diagnosis of allergic inflammatory conditions are described, based on the detection of CD48 expression.

Abstract: Eosinophilic esophagitis (EE), an emerging disorder with poorly understood pathogenesis, was examined. Esophageal tissue was analyzed by a genome wide microarray expression analysis. EE patients had a transcript signature involving 1% of the genome that was conserved across gender, age, and atopic status, and was distinct from that associated with chronic esophagitis (CE). The eosinophil specific chemokine eotaxin-3 was the top induced gene compared with normal controls. Levels C of eotaxin-3 mRNA and protein correlated with disease severity. A single nucleotide polymorphism in the human eotaxin-3 gene conferred susceptibility to disease. Mice deficient in the eotaxin-3 receptor (CCR-3) were protected from experimental EE. Eotaxin-3 was identified as a specific effector molecule, biomarker, and genetic risk factor for EE, and distinguished EE from CE.

Abstract: The present invention concerns methods useful in diagnosing, identifying and monitoring the progression of eosinophilic esophagitis through measurements of gene products.

Abstract: Several genes are upregulated in the lung of asthma or allergy sufferers. Many of the genes up-regulated in asthma are involved in arginine metabolism in the lung. Moreover, a set of 291 signature genes was found that can be used to indicate a patient's predilection for developing asthma or the patient's degree of suffering. Also, a set of 59 signature genes were found that indicate a patient's predilection for developing allergies. Many of the up-regulated genes relating to asthma were from the arginine metabolic pathway. Other genes, such as ADAM8, SPRR2A and SPRR2B were also strongly up-regulated in asthma. Treatment of asthma may be accomplished by administering compositions which decrease the levels of Arginase I, Arginase II, CAT2, or other arginase pathway members in the lung. Additionally, detection of altered levels of these proteins or the mRNA encoding them may be useful to diagnose the presence of asthma in a patient.

Abstract: A method to evaluate eosinophilic esophagitis based on information in an eosinophilic esophagitis transcriptome.