|Zhang, Shuping - MS STATE UNIV, PEARL,MS|
|Kim, Chul-Hong - VIS SCI ANRI,ARS|
|Keeler, Calvin - UNIV DE NEWARK, DE|
|Babu, U - FDA LAUREL, MD|
|Zhang, M - MS STATE UNIV, PEARL,MS|
Submitted to: Developmental Biology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: July 18, 2008
Publication Date: August 20, 2008
Citation: Zhang, S., Lillehoj, H.S., Kim, C., Keeler, C.L., Babu, U., Zhang, M. 2008. Transcriptional response of chicken macrophages to salmonella enterica serovar enteritidis infection. Developmental Biology. 132:153-160. Interpretive Summary: Salmonella enterica induced enterocolitis is a common cause of bacterial food-borne disease worldwide. Among more than 2,300 serovars, Enteritidis (SE) remains the second etiologic agent of non-typhoidal salmonellosis, accounting for 18.6% of all cases in the US. The organism colonizes the intestine of adult chickens and the oviduct of laying hens without causing overt clinical signs while contributing to carcass and egg contamination. To effectively control SE contamination of poultry products, researches should aim at understanding the immunological and molecular mechanisms underlying SE infection and colonization of chickens. In this paper, Scientists at the Mississippi State University in collaboration with ARS scientists investigate host-pathogen interaction using newly developed avian macrophage microarray. Because Salmonellae have evolved the ability to combat macrophage-mediated killing by surviving and replicating within specialized vacuoles or phagosomes of macrophages, identification of virulence mechanisms are important in the development of novel therapeutics against SE. The organism possesses two virulence associated type three secretion systems (TTSS-1 and TTSS-2) that are responsible for invasion of epithelial cells and survival in macrophages, respectively. In this study, the transcriptional response of chicken macrophages to SE infection was investigated using the AMM system and the results indicate the involvement of multiple innate immunity genes which are associated with SE pathogenesis. The finding will provide new information for developing effective control method against SE..
Technical Abstract: The transcriptional profiles of chicken macrophages (HD11) infected with Salmonella enterica serovar Enteritidis (SE) were analyzed by using avian macrophage microarray and real time RT-PCR. Out of 4,906 array elements interrogated, 269 genes exhibited a 2-fold change (P < 0.001) over a 24-hour time-course. Genes coding for proinflammatory cytokines, CC and CXC chemokines, and chemokine ligand were up-regulated; whereas genes associated with transcription, cell adhesion and proliferation were down-regulated. Most transcriptional changes occurred at 5 hours post inoculation (hpi), with more genes down-regulated than up-regulated. At 5 hpi, the levels of Gallinacin 1, Lymphotactin, RhoA, and MHC I B2M transcripts were significantly decreased. In contrast, the levels of CDC42 and MHC II BLB2 mRNA were elevated. Infection of HD11 cells with mutant SE strains carrying an inactivated type three secretion systems (TTSS-1 or TTSS-2) induced significantly higher levels of CCL4, K203, lymphotactin, and RhoA than wild type SE. In conclusion, chicken macrophage genes belonging to diverse functional classes were transcriptionally modulated by SE and selective modulation of host innate responses involved the effectors of TTSS-1/2.