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Differential protein expression in chicken macrophages and heterophils in vivo following infection with Salmonella Enteritidis
Z. Sekelova, H. Stepanova, O. Polansky, K. Varmuzova, M. Faldynova, R. Fedr, I. Rychlik, L. Vlasatikova,
Language English Country Great Britain
Document type Journal Article, Research Support, Non-U.S. Gov't
NLK
BioMedCentral
from 2011-12-01
BioMedCentral Open Access
from 2011
Directory of Open Access Journals
from 2011
Free Medical Journals
from 2011
PubMed Central
from 2009
Europe PubMed Central
from 2009
ProQuest Central
from 2015-01-01
Open Access Digital Library
from 2009-01-01
Open Access Digital Library
from 2011-01-01
Medline Complete (EBSCOhost)
from 2015-01-13
Health & Medicine (ProQuest)
from 2015-01-01
ROAD: Directory of Open Access Scholarly Resources
from 1993
Springer Nature OA/Free Journals
from 2011-12-01
- MeSH
- Chickens metabolism microbiology MeSH
- Real-Time Polymerase Chain Reaction veterinary MeSH
- Macrophages metabolism MeSH
- Poultry Diseases metabolism microbiology MeSH
- Proteome MeSH
- Antibodies, Heterophile metabolism MeSH
- Flow Cytometry veterinary MeSH
- Gene Expression Regulation MeSH
- Salmonella enteritidis * MeSH
- Salmonella Infections, Animal metabolism microbiology MeSH
- Animals MeSH
- Check Tag
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
In this study we compared the proteomes of macrophages and heterophils isolated from the spleen 4 days after intravenous infection of chickens with Salmonella Enteritidis. Heterophils were characterized by expression of MMP9, MRP126, LECT2, CATHL1, CATHL2, CATHL3, LYG2, LYZ and RSFR. Macrophages specifically expressed receptor proteins, e.g. MRC1L, LRP1, LGALS1, LRPAP1 and a DMBT1L. Following infection, heterophils decreased ALB and FN1, and released MMP9 to enable their translocation to the site of infection. In addition, the endoplasmic reticulum proteins increased in heterophils which resulted in the release of granular proteins. Since transcription of genes encoding granular proteins did not decrease, these genes remained continuously transcribed and translated even after initial degranulation. Macrophages increased amounts of fatty acid elongation pathway proteins, lysosomal and phagosomal proteins. Macrophages were less responsive to acute infection than heterophils and an increase in proteins like CATHL1, CATHL2, RSFR, LECT2 and GAL1 in the absence of any change in their expression at RNA level could even be explained by capturing these proteins from the external environment into which these could have been released by heterophils.
References provided by Crossref.org
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- $a In this study we compared the proteomes of macrophages and heterophils isolated from the spleen 4 days after intravenous infection of chickens with Salmonella Enteritidis. Heterophils were characterized by expression of MMP9, MRP126, LECT2, CATHL1, CATHL2, CATHL3, LYG2, LYZ and RSFR. Macrophages specifically expressed receptor proteins, e.g. MRC1L, LRP1, LGALS1, LRPAP1 and a DMBT1L. Following infection, heterophils decreased ALB and FN1, and released MMP9 to enable their translocation to the site of infection. In addition, the endoplasmic reticulum proteins increased in heterophils which resulted in the release of granular proteins. Since transcription of genes encoding granular proteins did not decrease, these genes remained continuously transcribed and translated even after initial degranulation. Macrophages increased amounts of fatty acid elongation pathway proteins, lysosomal and phagosomal proteins. Macrophages were less responsive to acute infection than heterophils and an increase in proteins like CATHL1, CATHL2, RSFR, LECT2 and GAL1 in the absence of any change in their expression at RNA level could even be explained by capturing these proteins from the external environment into which these could have been released by heterophils.
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- $a Fedr, Radek $u Department of Cytokinetics, Institute of Biophysics of the CAS, Kralovopolska 135, 612 65, Brno, Czech Republic. Center of Biomolecular and Cellular Engineering, International, Clinical Research Center, St. Anne's University Hospital Brno, Pekarska 53, 656 91, Brno, Czech Republic.
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