Project description:We took a global approach to identify the genome-wide transcriptome in native murine eosinophils sorted from the bone marrow of C57BL6J mice at homeostasis.
Project description:This study aimed to investigate the effect of IL-33 in eosinophil in the context of arthritis. To address this, bone marrow derived eosinophils were generated and treated with or without IL-33 for 3 hours. Then total RNAs were subjected to the study.
Project description:The eosinophil transcriptome analysis indicated a robust transcription change in eosinophils following allergen challenge in the lung. Eosinophils were FACS-sorted from Saline or OVA challenged lung with high purity and then subjected to genome-wide RNA microarray
Project description:Chemokine receptors control cell migration within the body. Here we reveal interactions between eosinophils and monocytes in the bone marrow, indirectly controlled by the atypical chemokine receptor ACKR2. In the absence of ACKR2, there are decreased numbers of eosinophils in the bone marrow. As a result, eosinophil and monocyte interactions are reduced within the bone marrow niche, and are associated with changes in monocyte gene expression. Monocytes from ACKR2-/- mice are recruited to the tissues but are fundamentally altered in their ability to differentiate into macrophages, in the lung, peritoneal cavity and cavity wall. Bacterial elimination is impaired in ACKR2-/- mice during peritoneal infection. ACKR2 is therefore a key regulator of eosinophil-driven monocyte education in the bone marrow, required for full monocyte differentiation and macrophage function within the tissues.
Project description:Aim of the experiment was to assess differences in expression of coding RNA between bone marrow eosinophils arising in IL-5 knock-out mice (C57BL/6-Il5tm1Kopf/J) or wild-type littermates and their response to cytokine stimulation. Bone marrow eosinophils were sorted by FACS submitted to RNA-seq immediately or after 4 hours of stimulation with IL-5 and IL-33 in culture plates.
Project description:Mature eosinophils were differentiated from mouse bone marrow progenitors We performed transcriptome sequencing on Listeria monocytogenes infected eosinophils and resting eosinophils to shed light on the transcriptional changes of cytokines and chemokines.
Project description:Microbial exposure at barrier interfaces drives development and balance of the immune system, but the consequences of local infections for systemic immunity and secondary inflammation are unclear. Here, we show that dermal exposure to the bacterium Staphylococcus aureus persistently shapes the immune system of mice with specific impact on progenitor and mature bone marrow neutrophil and eosinophil populations. The infection-imposed changes in eosinophils were long-lasting with functional changes associated with epigenetic and metabolic reprogramming, indicative of trained immunity. Bacterial exposure enhanced dermal allergic sensitization and resulted in exacerbated allergen-induced lung inflammation. S. aureus-mediated reprogramming of bone marrow eosinophils was driven by the alarmin interleukin 33 and the complement cleavage fragment C5a. Our study highlights the systemic impact of skin inflammation and reveals eosinophil progenitor training and organ-crosstalk mechanisms that modulate systemic responses to allergens.