|Pan, Deng -|
|Ebner, Paul -|
Submitted to: Research Workers in Animal Diseases Conference Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: October 1, 2011
Publication Date: December 4, 2011
Citation: Pan, D., Rostagno, M.H., Ebner, P., Eicher, S.D. 2011. Salmonella serovars differentially stimulate bovine leukocyte responses in vitro. Research Workers in Animal Diseases Conference Proceedings. 74P. Technical Abstract: The majority of Salmonella serovars cause no clinical signs in cattle, while some serovars, such as Salmonella enterica serovar Typhimurium (ST) and Dublin (SD), may cause severe disease. Mechanisms underlying the difference in pathogenesis between different serovars are not clear. The objective of this study was to determine innate immune responses of bovine leukocytes against in vitro infection with SD, ST, and Salmonella enterica serovar Enteritidis (SE), and their role in development of pathogenesis and host specificity. Jugular blood was collected from 10 Holstein calves at approximately 3 week of age and infected in vitro with non-opsonized or serum-opsonized SD, ST, and SE for 2 hours. Leukocyte phagocytosis and oxidative burst, cell surface expression of cluster of differentiation (CD) 14 and CD18 were analyzed using flow cytometry. Leukocyte mRNA expression of interleukin-8 (IL-8), IL-12, tumor necrosis factor (TNF)-a, and toll-like receptor 4 (TLR4) were determined using qRT-PCR. Results indicated that SD infection, not ST or SE infection, increased cell surface CD14 (P = 0.006). Opsonized SD failed to increase cell surface CD14 (P > 0.05). Only SE infection increased oxidative burst (P = 0.025). In addition, opsonized SD and ST increased oxidative burst in blood leukocytes (P < 0.001 and P = 0.002, respectively). All 3 serovars increased cell surface CD18 and mRNA expression of TNF-a, IL-8, and IL-12. However, none of these serovars affected mRNA expression of TLR4. Our results suggested that, compared to ST and SE, bovine-host-adapted SD enhanced its uptake by bovine phagocytic immune cells by upregulating CD14 expression on host cell surfaces. Additionally, SD as well as ST, suppressed the oxidative burst in phagocytes, which benefit its survival, replication, and dissemination within host cells. In contrast, SE did not induce uptake by phagocytes and showed no oxidative burst suppressing effect. Thus, SE infection in cattle is likely to be restrained within the gastrointestinal tract, and to be eliminated at the early stage of infection. Results also indicated that antibodies in serum control SD infection through downregulation of CD14 and upregulation of oxidative burst.