Akash Gugilla
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Akash Gugilla has a total of 14 co-authors. Here are the top co-authors by number of shared publications:
- Brittany Marie Salter
Respiratory Research Group, Department of Medicine, McMaster University, Hamilton, ON L8S 4L8, Canada
1 shared publication - Gail M. Gauvreau
Division of Respirology, Department of Medicine McMaster University Hamilton Ontario Canada
1 shared publication - Galus
Department of Biology, McMaster University, 1280 Main Street West, Hamilton, ON L8S 4K1, Canada
1 shared publication - Joanna Yvonne Wilson
Department of Biology, McMaster University, 1280 Main St. West, Hamilton, ON L8S 4K1, Canada
1 shared publication - John Paul Oliveria
Clinical Urology Research Enterprise (CURE) Program, McMaster Children's Hospital, Hamilton, Ontario, Canada
1 shared publication - Juan Du
Department of Pulmonary and Critical Care Medicine Ruijin Hospital Shanghai Jiao Tong University School of Medicine Shanghai China
1 shared publication
Latest Publications
- 1 November 2020
- Published by Elsevier in Environmental Toxicology and Pharmacology
- Vol. 80, 103463
Prostaglandins prevent acetaminophen induced embryo toxicity in zebrafish (Danio rerio)
- 1 November 2020
- Published by Elsevier in Environmental Toxicology and Pharmacology
- Vol. 80, 103463
Prostaglandins prevent acetaminophen induced embryo toxicity in zebrafish (Danio rerio)
- Open Access
- 13 February 2018
- Published by Wiley in Clinical and Translational Allergy
- Vol. 8 (1) , 5
Interleukin-25 and eosinophils progenitor cell mobilization in allergic asthma
Eosinophil-lineage committed progenitor cells (EoP) migrate from the bone marrow and differentiate locally to provide an ongoing source of mature eosinophils in asthmatic inflammatory responses in the airways. Sputum levels of EoP are increased in asthmatics compared to normal controls suggesting an exaggerated eosinophilopoietic environment in the airways. Understanding what factors promote EoP traffic to the airways is important to understand the diathesis of asthma pathology. Interleukin (IL)-25, is an epithelial-derived cytokine that promotes type 2 inflammatory responses. We have previously shown that levels of IL-25 and expression of the IL-25 receptor (IL-17RA and IL-17RB) on mature eosinophils are greater in allergic asthmatics compared to atopic non-asthmatics and non-atopic normal controls. In addition, these levels were increased significantly increased following allergen inhalation challenge and physiologically relevant levels of IL-25 stimulated eosinophil degranulation, intracellular IL-5 and IL-13 expression and primed migration to eotaxin. The current study, examined the role of IL-25 on allergen-induced trafficking of EoP in atopic asthmatics. Asthmatics (n = 14) who developed allergen-induced early and late responses were enrolled in the study. Blood was collected at pre- and 24 h post-challenge. At each time point, surface expression of IL-17RA and IL-17RB on EoP was evaluated by flow cytometry. Migration assays examined the effect of IL-25 on EoP chemotactic responses, in vitro. In addition, IL-25 knockout ovalbumin (OVA) sensitized and challenged mice were studied to evaluate in vivo mobilization effects of IL-25 on newly formed EoP and mature eosinophils. There was a significant increase in numbers of blood EoP expressing IL-17RB, 24 h post-allergen inhalation challenge in allergic asthmatics. Pre-exposure to IL-25 primed the migrational responsiveness of EoP to stromal cell-derived factor 1α. In OVA-sensitized mice, knocking out IL-25 significantly alleviated OVA-induced eosinophil infiltration in the airway and newly formed eosinophils were reduced in the lung. The findings of this study indicate a potential role for IL-25 in allergen-induced trafficking of EoP to the airways and local differentiation promoting tissue eosiniophilia in asthmatic responses.
- 13 February 2018
- Published by Wiley in Clinical and Translational Allergy
- Vol. 8 (1) , 5
Open AccessInterleukin-25 and eosinophils progenitor cell mobilization in allergic asthma
Eosinophil-lineage committed progenitor cells (EoP) migrate from the bone marrow and differentiate locally to provide an ongoing source of mature eosinophils in asthmatic inflammatory responses in the airways. Sputum levels of EoP are increased in asthmatics compared to normal controls suggesting an exaggerated eosinophilopoietic environment in the airways. Understanding what factors promote EoP traffic to the airways is important to understand the diathesis of asthma pathology. Interleukin (IL)-25, is an epithelial-derived cytokine that promotes type 2 inflammatory responses. We have previously shown that levels of IL-25 and expression of the IL-25 receptor (IL-17RA and IL-17RB) on mature eosinophils are greater in allergic asthmatics compared to atopic non-asthmatics and non-atopic normal controls. In addition, these levels were increased significantly increased following allergen inhalation challenge and physiologically relevant levels of IL-25 stimulated eosinophil degranulation, intracellular IL-5 and IL-13 expression and primed migration to eotaxin. The current study, examined the role of IL-25 on allergen-induced trafficking of EoP in atopic asthmatics. Asthmatics (n = 14) who developed allergen-induced early and late responses were enrolled in the study. Blood was collected at pre- and 24 h post-challenge. At each time point, surface expression of IL-17RA and IL-17RB on EoP was evaluated by flow cytometry. Migration assays examined the effect of IL-25 on EoP chemotactic responses, in vitro. In addition, IL-25 knockout ovalbumin (OVA) sensitized and challenged mice were studied to evaluate in vivo mobilization effects of IL-25 on newly formed EoP and mature eosinophils. There was a significant increase in numbers of blood EoP expressing IL-17RB, 24 h post-allergen inhalation challenge in allergic asthmatics. Pre-exposure to IL-25 primed the migrational responsiveness of EoP to stromal cell-derived factor 1α. In OVA-sensitized mice, knocking out IL-25 significantly alleviated OVA-induced eosinophil infiltration in the airway and newly formed eosinophils were reduced in the lung. The findings of this study indicate a potential role for IL-25 in allergen-induced trafficking of EoP to the airways and local differentiation promoting tissue eosiniophilia in asthmatic responses.