In:
PLOS ONE, Public Library of Science (PLoS), Vol. 18, No. 5 ( 2023-5-5), p. e0285415-
Abstract:
Precursor-targeted immune-mediated anemia (PIMA) in dogs is characterized by persistent non-regenerative anemia and ineffective erythropoiesis, and it is suspected to be an immune-mediated disease. Most affected dogs respond to immunosuppressive therapies; however, some are resistant. In this study, we carried out splenectomy as an alternative therapy for refractory PIMA in dogs, and analyzed gene expression levels in the spleen of dogs with or without PIMA and in serum before and after splenectomy. A total of 1,385 genes were found to express differentially in the spleens from dogs with PIMA compared with healthy dogs by transcriptome analysis, of which 707 genes were up-regulated, including S100A12 , S100A8 , and S100A9 that are linked directly to the innate immune system and have been characterized as endogenous damage-associated molecular patterns. Furthermore, immunohistochemistry confirmed that S100A8/A9 protein expression levels were significantly higher in dogs with PIMA compared with those in healthy dogs. A total of 22 proteins were found to express differentially between the serum samples collected before and after splenectomy by proteome analysis, of which 12 proteins were up-regulated in the samples before. The lectin pathway of complement activation was identified by pathway analysis in pre-splenectomy samples. We speculated that S100A8/9 expression may be increased in the spleen of dogs with PIMA, resulting in activation of the lectin pathway before splenectomy. These findings further our understanding of the pathology and mechanisms of splenectomy for PIMA.
Type of Medium:
Online Resource
ISSN:
1932-6203
DOI:
10.1371/journal.pone.0285415
DOI:
10.1371/journal.pone.0285415.g001
DOI:
10.1371/journal.pone.0285415.g002
DOI:
10.1371/journal.pone.0285415.g003
DOI:
10.1371/journal.pone.0285415.g004
DOI:
10.1371/journal.pone.0285415.g005
DOI:
10.1371/journal.pone.0285415.t001
DOI:
10.1371/journal.pone.0285415.t002
DOI:
10.1371/journal.pone.0285415.t003
DOI:
10.1371/journal.pone.0285415.s001
DOI:
10.1371/journal.pone.0285415.s002
DOI:
10.1371/journal.pone.0285415.s003
DOI:
10.1371/journal.pone.0285415.s004
DOI:
10.1371/journal.pone.0285415.s005
Language:
English
Publisher:
Public Library of Science (PLoS)
Publication Date:
2023
detail.hit.zdb_id:
2267670-3
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