Abstract: Disclosed are methods of diagnosing and treating a subject with active or inactive eosinophilic esophagitis (EoE). The methods may include the steps of detecting whether a level of eosinophil lineage-committed progenitor (EoP) is elevated in a blood sample obtained from a subject, diagnosing the subject with active EoE when an EoP level in the sample is elevated above a pre-determined cut-off value and diagnosing the subject with inactive EoE when the EoP level in the sample is below a pre-determined cut-off value; and treating the subject diagnosed with active EoE. Kits related to same are also disclosed.

Abstract: Disclosed are methods of diagnosing and treating a subject with active or inactive eosinophilic esophagitis (EoE). The methods may include the steps of detecting whether a level of eosinophil lineage-committed progenitor (EoP) is elevated in a blood sample obtained from a subject, diagnosing the subject with active EoE when an EoP level in the sample is elevated above a pre-determined cut-off value and diagnosing the subject with inactive EoE when the EoP level in the sample is below a pre-determined cut-off value; and treating the subject diagnosed with active EoE. Kits related to same are also disclosed.

Abstract: Disclosed are methods of diagnosing and treating a subject with active or inactive eosinophilic esophagitis (EoE). The methods may include the steps of detecting whether a level of eosinophil lineage-committed progenitor (EoP) is elevated in a blood sample obtained from a subject, diagnosing the subject with active EoE when an EoP level in the sample is elevated above a pre-determined cut-off value and diagnosing the subject with inactive EoE when the EoP level in the sample is below a pre-determined cut-off value; and treating the subject diagnosed with active EoE. Kits related to same are also disclosed.

Abstract: Disclosed are methods of diagnosing and treating a subject with active or inactive eosinophilic esophagitis (EoE). The methods may include the steps of detecting whether a level of eosinophil lineage-committed progenitor (EoP) is elevated in a blood sample obtained from a subject, diagnosing the subject with active EoE when an EoP level in the sample is elevated above a pre-determined cut-off value and diagnosing the subject with inactive EoE when the EoP level in the sample is below a pre-determined cut-off value; and treating the subject diagnosed with active EoE. Kits related to same are also disclosed.

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.