4 results on '"Puttur, F"'
Search Results
2. Inception of early-life allergen-induced airway hyperresponsiveness is reliant on IL-13+CD4+ T cells.
- Author
-
Saglani, Sejal, Gregory, Lisa G., Manghera, Avneet K., Branchett, William J., Uwadiae, Faith, Entwistle, Lewis J., Oliver, R. A., Vasiliou, Jessica E., Sherburn, Rebekah, Lui, Stephen, Puttur, F., Vöhringer, David, Walker, Simone A., Buckley, James, Grychtol, Ruth, Fainardi, Valentina, Denney, Laura, Byrne, Adam, von Mutius, Erika, and Bush, Andrew more...
- Subjects
ALLERGENS ,INTERLEUKIN-13 ,CD4 antigen ,T cells ,INTERLEUKIN-33 ,INNATE lymphoid cells - Abstract
Airway hyperresponsiveness (AHR) is a critical feature of wheezing and asthma in children, but the initiating immune mechanisms remain unconfirmed. We demonstrate that both recombinant interleukin-33 (rIL-33) and allergen [house dust mite (HDM) or Alternaria alternata] exposure from day 3 of life resulted in significantly increased pulmonary IL-13
+ CD4+ T cells, which were indispensable for the development of AHR. In contrast, adult mice had a predominance of pulmonary LinnegCD45+CD90+IL-13+ type 2 innate lymphoid cells (ILC2s) after administration of rIL-33. HDM exposure of neonatal IL-33 knockout (KO) mice still resulted in AHR. However, neonatal CD4creIL-13 KO mice (lacking IL-13+ CD4+ T cells) exposed to allergen from day 3 of life were protected from AHR despite persistent pulmonary eosinophilia, elevated IL-33 levels, and IL-13+ ILCs. Moreover, neonatal mice were protected from AHR when inhaled Acinetobacter lwoffii (an environmental bacterial isolate found in cattle farms, which is known to protect from childhood asthma) was administered concurrent with HDM. A. lwoffii blocked the expansion of pulmonary IL-13+ CD4+ T cells, whereas IL-13+ ILCs and IL-33 remained elevated. Administration of A. lwoffii mirrored the findings from the CD4creIL-13 KO mice, providing a translational approach for disease protection in early life. These data demonstrate that IL-13+ CD4+ T cells, rather than IL-13+ ILCs or IL-33, are critical for inception of allergic AHR in early life. [ABSTRACT FROM AUTHOR] more...- Published
- 2018
- Full Text
- View/download PDF
Catalog
3. Neutrophils restrain allergic airway inflammation by limiting ILC2 function and monocyte-dendritic cell antigen presentation.
- Author
-
Patel DF, Peiró T, Bruno N, Vuononvirta J, Akthar S, Puttur F, Pyle CJ, Suveizdytė K, Walker SA, Singanayagam A, Carlin LM, Gregory LG, Lloyd CM, and Snelgrove RJ
- Subjects
- Animals, Female, Humans, Mice, Mice, Inbred BALB C, Antigen Presentation immunology, Dendritic Cells immunology, Hypersensitivity immunology, Immunity, Innate immunology, Inflammation immunology, Lymphocytes immunology, Monocytes immunology, Neutrophils immunology
- Abstract
Neutrophil mobilization, recruitment, and clearance must be tightly regulated as overexuberant neutrophilic inflammation is implicated in the pathology of chronic diseases, including asthma. Efforts to target neutrophils therapeutically have failed to consider their pleiotropic functions and the implications of disrupting fundamental regulatory pathways that govern their turnover during homeostasis and inflammation. Using the house dust mite (HDM) model of allergic airway disease, we demonstrate that neutrophil depletion unexpectedly resulted in exacerbated T helper 2 (T
H 2) inflammation, epithelial remodeling, and airway resistance. Mechanistically, this was attributable to a marked increase in systemic granulocyte colony-stimulating factor (G-CSF) concentrations, which are ordinarily negatively regulated in the periphery by transmigrated lung neutrophils. Intriguingly, we found that increased G-CSF augmented allergic sensitization in HDM-exposed animals by directly acting on airway type 2 innate lymphoid cells (ILC2s) to elicit cytokine production. Moreover, increased systemic G-CSF promoted expansion of bone marrow monocyte progenitor populations, which resulted in enhanced antigen presentation by an augmented peripheral monocyte-derived dendritic cell pool. By modeling the effects of neutrophil depletion, our studies have uncovered previously unappreciated roles for G-CSF in modulating ILC2 function and antigen presentation. More broadly, they highlight an unexpected regulatory role for neutrophils in limiting TH 2 allergic airway inflammation., (Copyright © 2019 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.) more...- Published
- 2019
- Full Text
- View/download PDF
4. Pulmonary environmental cues drive group 2 innate lymphoid cell dynamics in mice and humans.
- Author
-
Puttur F, Denney L, Gregory LG, Vuononvirta J, Oliver R, Entwistle LJ, Walker SA, Headley MB, McGhee EJ, Pease JE, Krummel MF, Carlin LM, and Lloyd CM
- Subjects
- Animals, Cell Movement drug effects, Collagen immunology, Eosinophils immunology, Extracellular Matrix immunology, Female, Fibronectins immunology, Humans, Immunity, Innate, Inflammation immunology, Interleukin-33 pharmacology, Lymphocytes drug effects, Mice, Inbred BALB C, Mice, Transgenic, Recombinant Proteins pharmacology, Lung immunology, Lymphocytes immunology
- Abstract
Group 2 innate lymphoid cells (ILC2s) are enriched in mucosal tissues (e.g., lung) and respond to epithelial cell-derived cytokines initiating type 2 inflammation. During inflammation, ILC2 numbers are increased in the lung. However, the mechanisms controlling ILC2 trafficking and motility within inflamed lungs remain unclear and are crucial for understanding ILC2 function in pulmonary immunity. Using several approaches, including lung intravital microscopy, we demonstrate that pulmonary ILC2s are highly dynamic, exhibit amoeboid-like movement, and aggregate in the lung peribronchial and perivascular spaces. They express distinct chemokine receptors, including CCR8, and actively home to CCL8 deposits located around the airway epithelium. Within lung tissue, ILC2s were particularly motile in extracellular matrix-enriched regions. We show that collagen-I drives ILC2 to markedly change their morphology by remodeling their actin cytoskeleton to promote environmental exploration critical for regulating eosinophilic inflammation. Our study provides previously unappreciated insights into ILC2 migratory patterns during inflammation and highlights the importance of environmental guidance cues in the lung in controlling ILC2 dynamics., (Copyright © 2019 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.) more...
- Published
- 2019
- Full Text
- View/download PDF
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.