Browsing by Author "Peebles, R. Stokes, Jr."

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    Bovine Serum Albumin Elicits IL-33–Dependent Adipose Tissue Eosinophilia: Potential Relevance to Ovalbumin-induced Models of Allergic Disease
    (American Association of Immunologists, 2023) Caslin, Heather L.; Bolus, W. Reid; Thomas, Christopher; Toki, Shinji; Norlander, Allison E.; Peebles, R. Stokes, Jr.; Hasty, Alyssa H.; Anatomy, Cell Biology and Physiology, School of Medicine
    All cells of the immune system reside in adipose tissue (AT), and increasing type 2 immune cells may be a therapeutic strategy to improve metabolic health. In our previous study using i.p. IL-5 injections to increase eosinophils, we observed that a standard vehicle control of 0.1% BSA also elicited profound AT eosinophilia. In this study, we aimed to determine whether BSA-induced AT eosinophilia results in metabolic benefits in murine models of diet-induced obesity. I.p. 0.1% BSA injections increased AT eosinophils after 4 wk. Despite elevating eosinophils to >50% of immune cells in the AT, body weight and glucose tolerance were not different between groups. Interestingly, BSA elicited epithelial IL-33 production, as well as gene expression for type 2 cytokines and IgE production that were dependent on IL-33. Moreover, multiple models of OVA sensitization also drove AT eosinophilia. Following transplantation of a donor fat pad with BSA-induced eosinophilia, OVA-sensitized recipient mice had higher numbers of bronchoalveolar lavage eosinophils that were recipient derived. Interestingly, lungs of recipient mice contained eosinophils, macrophages, and CD8 T cells from the donor AT. These trafficked similarly from BSA- and non-BSA-treated AT, suggesting even otherwise healthy AT serves as a reservoir of immune cells capable of migrating to the lungs. In conclusion, our studies suggest that i.p. injections of BSA and OVA induce an allergic response in the AT that elicits eosinophil recruitment, which may be an important consideration for those using OVA in animal models of allergic disease.
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    IL-33 promotes the egress of group 2 innate lymphoid cells from the bone marrow
    (Rockefeller University Press, 2018-01-02) Stier, Matthew T.; Zhang, Jian; Goleniewska, Kasia; Cephus, Jacqueline Y.; Rusznak, Mark; Wu, Lan; Kaer, Luc Van; Zhou, Baohua; Newcomb, Dawn C.; Peebles, R. Stokes, Jr.; Pediatrics, School of Medicine
    Group 2 innate lymphoid cells (ILC2s) are effector cells within the mucosa and key participants in type 2 immune responses in the context of allergic inflammation and infection. ILC2s develop in the bone marrow from common lymphoid progenitor cells, but little is known about how ILC2s egress from the bone marrow for hematogenous trafficking. In this study, we identified a critical role for IL-33, a hallmark peripheral ILC2-activating cytokine, in promoting the egress of ILC2 lineage cells from the bone marrow. Mice lacking IL-33 signaling had normal development of ILC2s but retained significantly more ILC2 progenitors in the bone marrow via augmented expression of CXCR4. Intravenous injection of IL-33 or pulmonary fungal allergen challenge mobilized ILC2 progenitors to exit the bone marrow. Finally, IL-33 enhanced ILC2 trafficking to the lungs in a parabiosis mouse model of tissue disruption and repopulation. Collectively, these data demonstrate that IL-33 plays a critical role in promoting ILC2 egress from the bone marrow.
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    Prostaglandin I2 and T Regulatory Cell Function: Broader Impacts
    (Mary Ann Liebert, 2021) Norlander, Allison E.; Peebles, R. Stokes, Jr.; Anatomy, Cell Biology and Physiology, School of Medicine
    Tregulatory cells (Tregs) are an important member of the adaptive immune system and function to reduce and resolve inflammation. Prostaglandin I2 (PGI2) is a lipid mediator that has potent anti-inflammatory effects on immune cells. Several studies have investigated the interplay between PGI2 and Tregs. Together, the data from these studies demonstrate that PGI2 promotes the formation and function of Tregs. This suggests that therapeutic supplementation of PGI2 may be a treatment for various autoimmune or inflammatory diseases through enhancement of Treg function.
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    Prostaglandin I2 Therapy Promotes Regulatory T Cell Generation in Patients with Pulmonary Arterial Hypertension
    (American Thoracic Society, 2023) Norlander, Allison E.; Abney, Masako; Cephus, Jacqueline-Yvonne; Roe, Caroline E.; Irish, Jonathan M.; Shelburne, Nicholas J.; Newcomb, Dawn C.; Hemnes, Anna R.; Peebles, R. Stokes, Jr.; Anatomy, Cell Biology and Physiology, School of Medicine
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    Reply to Yasuma et al.
    (American Thoracic Society, 2023) Norlander, Allison E.; Abney, Masako; Cephus, Jacqueline-Yvonne; Roe, Caroline E.; Irish, Jonathan M.; Shelburne, Nicholas J.; Newcomb, Dawn C.; Hemnes, Anna R.; Peebles, R. Stokes, Jr.; Medicine, School of Medicine