ORCiD
Cassio Almeida-da-Silva: 0000-0001-9173-7208
Department
Biomedical Sciences
Document Type
Article
Publication Title
Mediators of Inflammation
ISSN
0962-9351
Volume
2015
DOI
10.1155/2015/495430
First Page
1
Last Page
12
Publication Date
5-4-2015
Abstract
Exogenously administered glucocorticoids enhance eosinophil and neutrophil granulocyte production from murine bone-marrow. A hematological response dependent on endogenous glucocorticoids underlies bone-marrow eosinophilia induced by trauma or allergic sensitization/challenge. We detected a defect in granulopoiesis in nonsensitized, perforin-deficient mice. In steady-state conditions, perforin- (Pfp-) deficient mice showed significantly decreased bone-marrow and blood eosinophil and neutrophil counts, and colony formation in response to GM-CSF, relative to wild-type controls of comparable age and/or weight. By contrast, peripheral blood or spleen total cell and lymphocyte numbers were not affected by perforin deficiency. Dexamethasone enhanced colony formation by GM-CSF-stimulated progenitors from wild-type controls, but not Pfp mice. Dexamethasone injection increased bone-marrow eosinophil and neutrophil counts in wild-type controls, but not Pfp mice. Because perforin is expressed in effector lymphocytes, we examined whether this defect would be corrected by transferring wild-type lymphocytes into perforin-deficient recipients. Short-term reconstitution of the response to dexamethasone was separately achieved for eosinophils and neutrophils by transfer of distinct populations of splenic lymphocytes from nonsensitized wild-type donors. Transfer of the same amount of splenic lymphocytes from perforin-deficient donors was ineffective. This demonstrates that the perforin-dependent, granulopoietic response to dexamethasone can be restored by transfer of innate lymphocyte subpopulations.
Recommended Citation
Xavier-Elsas, P.,
Almeida-Da-Silva, C. L.,
Vieira, B. M.,
&
Masid-de-Brito, D.
(2015).
The In Vivo Granulopoietic Response to Dexamethasone Injection Is Abolished in Perforin-Deficient Mutant Mice and Corrected by Lymphocyte Transfer from Nonsensitized Wild-Type Donors.
Mediators of Inflammation, 2015, 1–12.
DOI: 10.1155/2015/495430
https://scholarlycommons.pacific.edu/dugoni-facarticles/709
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 International License.
