Powell, M. D.3; Yousaf, M. N.3; Rasmussen, Karina Juhl4; Kollner, B.3; Zou, J.3; Secombes, C.3; Speare, D. J.3
1 Department of Cancer and Inflammation Research, Department of Molecular Medicine, Det Sundhedsvidenskabelige Fakultet, SDU2 Det Sundhedsvidenskabelige Fakultet, SDU3 unknown4 Department of Cancer and Inflammation Research, Department of Molecular Medicine, Det Sundhedsvidenskabelige Fakultet, SDU
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 TNF alpha 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. (c) 2014 Elsevier Ltd. All rights reserved.
Fish and Shellfish Immunology, 2014, Vol 40, Issue 1, p. 91-98