Immunohistochemical localization of inflammatory cells and cell cycle proteins in the gills of Loma salmonae infected rainbow trout (Oncorhynchus mykiss)

Microsporidial gill diseases particularly those caused by Loma salmonae incur significant economic losses to the salmonid aquaculture industry. The gill responses to infection include the formation of xenomas and the acute hyperplastic inflammatory responses once the xenomas rupture releasing infect...

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Published inFish & shellfish immunology Vol. 40; no. 1; pp. 91 - 98
Main Authors Powell, Mark D., Yousaf, M. Naveed, Rasmussen, Karina Juhl, Köllner, Berndt, Zou, Jun, Secombes, Chris, Speare, David J.
Format Journal Article
LanguageEnglish
Published England Elsevier Ltd 01.09.2014
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Abstract Microsporidial gill diseases particularly those caused by Loma salmonae incur significant economic losses to the salmonid aquaculture industry. The gill responses to infection include the formation of xenomas and the acute hyperplastic inflammatory responses once the xenomas rupture releasing infective spores. The aim of this work was to characterize the inflammatory responses of the gill to both the presence of the xenomas as well as the hyperplasia associated with L. salmonae infection in the rainbow trout gill following an experimental infection using immunohistochemistry. Hyperplastic lesions demonstrated numerous cells expressing PCNA as well as an apparent increased expression of caspase-3 and number of apoptotic cells (TUNEL positive cells). There was an expression of TNFα in individual cells within the gill and increased expression of a myeloid cell line antigen indicating the presence of granulocyte infiltration of both the hyperplastic lesions as well as the xenomas. Similar immune-reactivity was seen in gill EGCs. Hyperplastic gill lesions showed a marked infiltration of CD8+ cells and expression of MHC class I antigens. These findings suggest that L. salmonae xenomas may be subject to infiltration by the host immune cells as well as the mounting or a marked cellular cytotoxic immunoreaction in the resultant hyperplasia following xenoma rupture and spore release. •Increased PCNA, caspase 3 and TUNEL staining in L. salmonae infected gills.•Weak TNFα and HIF1α staining was marginally enhanced in L. salmonae infected gills.•Positive reaction to granulocyte markers and strong staining in EGCs.•Increased expression of CD8 and MHCI in lesions indicated a cytotoxic cell reaction.
AbstractList Microsporidial gill diseases particularly those caused by Loma salmonae incur significant economic losses to the salmonid aquaculture industry. The gill responses to infection include the formation of xenomas and the acute hyperplastic inflammatory responses once the xenomas rupture releasing infective spores. The aim of this work was to characterize the inflammatory responses of the gill to both the presence of the xenomas as well as the hyperplasia associated with L. salmonae infection in the rainbow trout gill following an experimental infection using immunohistochemistry. Hyperplastic lesions demonstrated numerous cells expressing PCNA as well as an apparent increased expression of caspase-3 and number of apoptotic cells (TUNEL positive cells). There was an expression of TNFα in individual cells within the gill and increased expression of a myeloid cell line antigen indicating the presence of granulocyte infiltration of both the hyperplastic lesions as well as the xenomas. Similar immune-reactivity was seen in gill EGCs. Hyperplastic gill lesions showed a marked infiltration of CD8+ cells and expression of MHC class I antigens. These findings suggest that L. salmonae xenomas may be subject to infiltration by the host immune cells as well as the mounting or a marked cellular cytotoxic immunoreaction in the resultant hyperplasia following xenoma rupture and spore release. •Increased PCNA, caspase 3 and TUNEL staining in L. salmonae infected gills.•Weak TNFα and HIF1α staining was marginally enhanced in L. salmonae infected gills.•Positive reaction to granulocyte markers and strong staining in EGCs.•Increased expression of CD8 and MHCI in lesions indicated a cytotoxic cell reaction.
Microsporidial gill diseases particularly those caused by Loma salmonae incur significant economic losses to the salmonid aquaculture industry. The gill responses to infection include the formation of xenomas and the acute hyperplastic inflammatory responses once the xenomas rupture releasing infective spores. The aim of this work was to characterize the inflammatory responses of the gill to both the presence of the xenomas as well as the hyperplasia associated with L. salmonae infection in the rainbow trout gill following an experimental infection using immunohistochemistry. Hyperplastic lesions demonstrated numerous cells expressing PCNA as well as an apparent increased expression of caspase-3 and number of apoptotic cells (TUNEL positive cells). There was an expression of TNFα in individual cells within the gill and increased expression of a myeloid cell line antigen indicating the presence of granulocyte infiltration of both the hyperplastic lesions as well as the xenomas. Similar immune-reactivity was seen in gill EGCs. Hyperplastic gill lesions showed a marked infiltration of CD8+ cells and expression of MHC class I antigens. These findings suggest that L. salmonae xenomas may be subject to infiltration by the host immune cells as well as the mounting or a marked cellular cytotoxic immunoreaction in the resultant hyperplasia following xenoma rupture and spore release.Microsporidial gill diseases particularly those caused by Loma salmonae incur significant economic losses to the salmonid aquaculture industry. The gill responses to infection include the formation of xenomas and the acute hyperplastic inflammatory responses once the xenomas rupture releasing infective spores. The aim of this work was to characterize the inflammatory responses of the gill to both the presence of the xenomas as well as the hyperplasia associated with L. salmonae infection in the rainbow trout gill following an experimental infection using immunohistochemistry. Hyperplastic lesions demonstrated numerous cells expressing PCNA as well as an apparent increased expression of caspase-3 and number of apoptotic cells (TUNEL positive cells). There was an expression of TNFα in individual cells within the gill and increased expression of a myeloid cell line antigen indicating the presence of granulocyte infiltration of both the hyperplastic lesions as well as the xenomas. Similar immune-reactivity was seen in gill EGCs. Hyperplastic gill lesions showed a marked infiltration of CD8+ cells and expression of MHC class I antigens. These findings suggest that L. salmonae xenomas may be subject to infiltration by the host immune cells as well as the mounting or a marked cellular cytotoxic immunoreaction in the resultant hyperplasia following xenoma rupture and spore release.
Microsporidial gill diseases particularly those caused by Loma salmonae incur significant economic losses to the salmonid aquaculture industry. The gill responses to infection include the formation of xenomas and the acute hyperplastic inflammatory responses once the xenomas rupture releasing infective spores. The aim of this work was to characterize the inflammatory responses of the gill to both the presence of the xenomas as well as the hyperplasia associated with L. salmonae infection in the rainbow trout gill following an experimental infection using immunohistochemistry. Hyperplastic lesions demonstrated numerous cells expressing PCNA as well as an apparent increased expression of caspase-3 and number of apoptotic cells (TUNEL positive cells). There was an expression of TNFα in individual cells within the gill and increased expression of a myeloid cell line antigen indicating the presence of granulocyte infiltration of both the hyperplastic lesions as well as the xenomas. Similar immune-reactivity was seen in gill EGCs. Hyperplastic gill lesions showed a marked infiltration of CD8+ cells and expression of MHC class I antigens. These findings suggest that L. salmonae xenomas may be subject to infiltration by the host immune cells as well as the mounting or a marked cellular cytotoxic immunoreaction in the resultant hyperplasia following xenoma rupture and spore release.
Author Speare, David J.
Rasmussen, Karina Juhl
Köllner, Berndt
Yousaf, M. Naveed
Secombes, Chris
Powell, Mark D.
Zou, Jun
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Keywords PCNA
CD8
Granulocyte
Microsporidial gill disease
Xenoma
Apoptosis
MHC I
Language English
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Snippet Microsporidial gill diseases particularly those caused by Loma salmonae incur significant economic losses to the salmonid aquaculture industry. The gill...
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SubjectTerms Animals
Apoptosis
aquaculture industry
caspase-3
CD8
cell cycle
Cell Cycle Proteins - genetics
Cell Cycle Proteins - metabolism
cytotoxicity
financial economics
Fish Diseases - immunology
Fish Diseases - parasitology
gills
Gills - immunology
Gills - parasitology
Granulocyte
hyperplasia
Hyperplasia - immunology
Hyperplasia - parasitology
Hyperplasia - veterinary
immunohistochemistry
Immunohistochemistry - veterinary
In Situ Nick-End Labeling - veterinary
Inflammation
Loma - physiology
MHC I
Microsporidial gill disease
Microsporidiosis - immunology
Microsporidiosis - parasitology
Microsporidiosis - veterinary
Oncorhynchus mykiss
PCNA
proliferating cell nuclear antigen
spores
tumor necrosis factor-alpha
Xenoma
Title Immunohistochemical localization of inflammatory cells and cell cycle proteins in the gills of Loma salmonae infected rainbow trout (Oncorhynchus mykiss)
URI https://dx.doi.org/10.1016/j.fsi.2014.06.004
https://www.ncbi.nlm.nih.gov/pubmed/24979224
https://www.proquest.com/docview/1552808346
https://www.proquest.com/docview/2000299151
Volume 40
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