Increasing the Yield of Eimeria tenella Oocysts in Primary Chicken Kidney Cells

1996 ◽  
Vol 40 (1) ◽  
pp. 63 ◽  
Author(s):  
Jianfei Zhang ◽  
Eric Wilson ◽  
Shiguang Yang ◽  
Mark C. Healey
Parasitology ◽  
1981 ◽  
Vol 82 (2) ◽  
pp. 189-194 ◽  
Author(s):  
Catriona Urquhart

SUMMARYThe pattern of DNA synthesis in chicken kidney (CK) cells parasitized by Eimeria tenella was altered; a 2-fold increase in the uptake of [3H]-thymidine occurred in these cells compared with that shown by the controls. This difference was significantly different at 16 h post-inoculation (p.i.) and reached a peak at 20 h p.i. Non-parasitized cells in co-culture with parasitized cells showed a level of incorporation intermediate between that of the parasitized and non-parasitized mono- cultures. It was shown that this stimulation was due to a factor released into the medium by the parasite or the parasitized cell. A possible course of events leading to induced and prolonged DNA synthesis by the host cell and the significance of this change in the life-cycle of the parasite is discussed.


1997 ◽  
Vol 41 (1) ◽  
pp. 111 ◽  
Author(s):  
Jianfei Zhang ◽  
Eric Wilson ◽  
Shiguang Yang ◽  
Mark C. Healey

Parasite ◽  
2021 ◽  
Vol 28 ◽  
pp. 11
Author(s):  
Xinlei Yan ◽  
Wenying Han ◽  
Xianyong Liu ◽  
Xun Suo

Egress plays a vital role in the life cycle of apicomplexan parasites including Eimeria tenella, which has been attracting attention from various research groups. Many recent studies have focused on early egress induced by immune molecules to develop a new method of apicomplexan parasite elimination. In this study, we investigated whether nitric oxide (NO), an immune molecule produced by different types of cells in response to cytokine stimulation, could induce early egress of eimerian sporozoites in vitro. Eimeria tenella sporozoites were extracted and cultured in primary chicken kidney cells. The number of sporozoites egressed from infected cells was analyzed by flow cytometry after treatment with NO released by sodium nitroferricyanide (II) dihydrate. The results showed that exogenous NO stimulated the rapid egress of E. tenella sporozoites from primary chicken kidney cells before replication of the parasite. We also found that egress was dependent on intra-parasitic calcium ion (Ca2+) levels and no damage occurred to host cells after egress. The virulence of egressed sporozoites was significantly lower than that of fresh sporozoites. The results of this study contribute to a novel field examining the interactions between apicomplexan parasites and their host cells, as well as that of the clearance of intracellular pathogens by the host immune system.


1979 ◽  
Vol 5 (4) ◽  
pp. 227-230 ◽  
Author(s):  
Thomas Petri ◽  
Herbert Meier-Ewert ◽  
Richard W. Compans

2006 ◽  
Vol 87 (5) ◽  
pp. 1209-1216 ◽  
Author(s):  
Christine Winter ◽  
Christel Schwegmann-Weßels ◽  
Dave Cavanagh ◽  
Ulrich Neumann ◽  
Georg Herrler

The importance of sialic acid for infection by avian Infectious bronchitis virus (IBV) has been analysed. Neuraminidase treatment rendered Vero, baby hamster kidney and primary chicken kidney cells resistant to infection by the IBV-Beaudette strain. Sialic acid-dependent infection was also observed with strain M41 of IBV, which infects primary chicken kidney cells but not cells from other species. In comparison with Influenza A virus and Sendai virus, IBV was most sensitive to pre-treatment of cells with neuraminidase. This finding suggests that IBV requires a greater amount of sialic acid on the cell surface to initiate an infection compared with the other two viruses. In previous studies, with respect to the haemagglutinating activity of IBV, it has been shown that the virus preferentially recognizes α2,3-linked sialic acid. In agreement with this finding, susceptibility to infection by IBV was connected to the expression of α2,3-linked sialic acid as indicated by the reactivity with the lectin Maackia amurensis agglutinin. Here, it is discussed that binding to sialic acid may be used by IBV for primary attachment to the cell surface; tighter binding and subsequent fusion between the viral and the cellular membrane may require interaction with a second receptor.


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