Effect of the Salmonella Pathogenicity Island 2 Type III Secretion System on Salmonella Survival in Activated Chicken Macrophage-Like HD11 Cells

Abstract

In order to better identify the role of the Salmonella pathogenicity island 2 (SPI-2) type III secretion system (T3SS) in chickens, we used the well-known gentamicin protection assay with activated HD11 cells. HD11 cells are a macrophage-like chicken cell line that can be stimulated with phorbol 12-myristate 13-acetate (PMA) to exhibit more macrophage-like morphology and greater production of reactive oxygen species (ROS). Activated HD11 cells were infected with a wild-type Salmonella enterica subspecies enterica serovar Typhimurium (S. Typhimurium) strain, a SPI-2 mutant S. Typhimurium strain, a wild-type Salmonella enterica subspecies enterica serovar Enteritidis (S. Enteritidis) strain, a SPI-2 mutant S. Enteritidis strain, or a non-pathogenic Escherichia coli (E. coli) strain. SPI-2 mutant strains were found to survive as well as their parent strain at all time points post-uptake (PU) by the HD11 cells, up to 24 h PU, while the E. coli strain was no longer recoverable by 3 h PU. We can conclude from these observations that the SPI-2 T3SS of S. Typhimurium and S. Enteritidis is not important for survival of Salmonella in the activated macrophage-like HD11 cell line, and that Salmonella must employ other mechanisms for survival in this environment, as E. coli is effectively eliminated.

A Comparative Study on Invasion, Survival, Modulation of Oxidative Burst, and Nitric Oxide Responses of Macrophages (HD11), and Systemic Infection in Chickens by Prevalent Poultry Salmonella Serovars

“…Colonization by Salmonella in poultry has been extensively studied and well documented (Foley et al, 2011); however, most are epidemiological investigations focused on prevalence. Information regarding Salmonella invasion and colonization mechanisms and interactions with host cells in chickens is limited and poorly defined (Boyd et al, 2007;Lillehoj et al, 2007;Chappell et al, 2009;Wisner et al, 2010Wisner et al, , 2011.…”

Salmonella enterica Serovar Enteritidis Antimicrobial Peptide Resistance Genes Aid in Defense against Chicken Innate Immunity, Fecal Shedding, and Egg Deposition

“…Many experiments performed with S. Enteritidis focus on the mechanisms of the T3SS-1 and T3SS-2 during invasion and intracellular replication within various chicken tissues (10,(41)(42)(43). Recent studies have focused on survival strategies of S. Enteritidis under the stressful conditions encountered by pathogens of the chicken such as those present in egg white.…”

“…Each dot represents the average bacterial load of each strain per dpi, and each bar represents the overall average from 5 days. edge of the role AMPR genes virK and ybjX play during S. Enteritidis infection in chickens (10,24,42,43).…”

Genetic Basis of Salmonella Enteritidis Pathogenesis in Chickens

“…In addition, the colonization of the internal organs by SPI-2 mutant of SE was impaired in 1-day-, 5-day-, and 24-week-old chickens after oral, intraperitoneal, and intravenous inoculation (Bohez et al, 2008). Finally, there are also conflicting reports on the intracellular survivability of SPI-2 mutant of SE within chicken macrophages (Bohez et al, 2008;Wisner et al, 2011). Thus more research is needed to clearly define the role of SPI-1 and SPI-2 in the pathogenesis of SE in chickens.…”