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GENETICS Gene Expression Profiles of Two B-Complex Disparate

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GENETICS Gene Expression Profiles of Two B-Complex Disparate GENETICS Ii Gene expression profiles of two B-complex disparate, genetically inbred Fayoumi chicken lines that differ in susceptibility to Eimeria maxima D. K. Kinl.* C. H. Kiin.t S. .T. Lanont4 C. L. Keeler .Jr.. and H. S. Lillehoj*I AnzTnai Parasitic Disases Laboratory. Animal and i'vaturai Re,soaices 1i,.t,tatc, 115124, l3e1tsi ;,iie. AID 20705: tKorcan Biom formation Center. Korea Research Ins tit etc of Bioscience and Biotechnoloqy. Doe jeoi. 305-806. Republic of Korea: .f Department of Animal Science. iowa State Uiwersity, Arries 50011: ii o.dI)cparfmrrenf of Aiwaai and Food Sciences. (ni ic csitq of Delaware. Newark 19716 ABSTRACT This stud y Was conducted to compare the clown), and 92 (33 up. 59 down) mnRNA at the 3 time gene ixprussioli profiles, after Emmn crma maxima infection. points. Functional anal ysis using gene ontology catego- between 2 B-complex congcmc lines of Favonnui chick- rized the genes exhibiting the different expression pat- (-'115 that display differeiicis in disease resistance and terns between 2 chicken lines into several gene ontology innate immunity against avian coccidiosis using cD\A terms including imniunlity and defense. In summary, inicroarrav. When compared with uninfected controls transcriptional profiles showed that more gene expres- using a cutoff of >2.0-fold alteration (P < 0.05), l\I5.1 sion changes occurred with E. maxima infection in the demonstrated altered expression of I (downregulate(l). M15.2 than the A15.1 line. The roost gene expression 12 (6 up. 6 down). and 18 (5 up. 13 clown) infINA at 3. (liffmeices between the 2 chicken lines were exhibited 4. and 5 (II postiuifection. respectivel y. In the M15.2 line, at (1 4 and 5 after E. maxima infection. These results altered expression was observed iii 6 (3 up. 3 (lo\vn). demonstrate that differential gene expression patterns 29 (11 up. 18 down), and 32 (8 up. 24 clown) tran- associated wit,li the host, genetic clifkrence in coccicli- scripts at the 3 time points, compared with uninfected osis resistance provide insights into the host protective controls. Comparison of the expression levels between immune mechanisms and present a rational basis to [5.1 and N115.2 chickens after K. mo:rTrna infection r(, target specific genes and gene products to bolster host vealed alterations in 32 (10 up, 22 down). 98 (13 up. 55 defenses against avian coccidiosis. Key words: coccidiosis, Favounii. complementary DNA niicroarra y, intraepithelial lymphocyte 2009 Poult rv Science 88:1515-1579 (Ion 10.3382/1)s.2009-000 12 INTRODUCTION about the chicken immune sYstein at the molecular level is very limited. Avian coecidiosis is caused 1w infection uvif h pro- lii recent, years, t he chicken EST database has tozoa belonging to the genus Eimecw, amid presents a reached such a. level that anal ysis of the sequence data significant concern to the poultry industry due to its is feasible. There are now more than 580.000 chicken detrimental influence oil efficienc y affecting EST sequences front a wide variet y of tissues aiid dc- survivabilit y, nutrient absorption, growth rate, and egg velopniental stages publicly available (hmttp://www.tigi'. productioii of poultr y (Lill(,hoj and Li, 2004: Lillehoj ci org/tclh/t.(, i/). Therefore. it is now possible to ascribe al.. 2007). Until now, disease control strategies against provisional identities and functions I o genes on the ba- avian coccidiosis have mostl y depended oil prophylactic sis of sequence comparison. High-throughput gemlomn- chemotherapy and vaccination. but both methods have ic analyses have suggested a path toward increasing serious drawbacks (Alin et al. 2005). Genetic selection ideuitificat.ion of transcriptional regulations involved in for disease resistance and iiiiinune responses call time inimnune response (Degen et. al.. 2006). Large-scale to a reduction of drug use and risk of vaccination ill gene expression profiles of host responses to infection commercial poultry production. Hoivever, information could provide enonuuous information oil the iuuteractiomms bet veemm pathogens and the host imnmunie systeni. Time mnicroarray techmniqume is all tool for char- acterizing the biology of inminmumologic processes amid 20(]9 Poult,jv Scicncv A,sociat,ioii un. inunnie-relat ed diseases (van dee Pouw Kraa.n et al.. Received Ja in mv 9. 2(11)9. 111 Accepted April 1-1. 21109. 2004). chicken, several mnicroarm'ay studies have been (:orr('po1ahiu5 author: Hv till. LiIhlioj ii.iiIa.go\ performed for the infect ioums diseases such as March's 1565 1566 i'INi ET AL disease (Levy et al.. 2005: Sarsoii et al.. 2006: Heidari et RNA Extraction and Aminoallyl-Labeled al.. 2008: Sarson et al., 2008). West, Nile virus (Groves RNA Preparation et al., 2008). Salmonella (van Hemert et al., 2006. 2007). avian influenza virus (Degen et al., 2006: Groves et al.. After ent.iiamzation of time birds, jejunal intestines 2008: Zaffuto et al., 2008). avian infectious bronchitis were taken from 5 birds in each infected or noninfected virus (Dar et al., 2005). and Eimeria species (Niiii et group at O. 3. 4. and 5 (1 postinfection (dpi). Intestines al., 2003). were cut longitudinall y and washed 3 1 inies with ice- The Favoumi breed, which originated in Egypt, was cold Hanks' balanced salt solution coiit aimming 100 U/ imported to the United States in 1954 primarily be- mL of penicillin and 100 nmg/riL of streptomycin (5mg- cause of its reported resistance to the avian leukosis. nma. St. Louis. MO). The mucosal layer was carefully Subsequently, it was shown to develop a robust pro- scraped using a surgical scalpel and TEL were isolated tective response against Eimeria, tenella (Pinard-Van from the jejununi as described previously (Lee et al.. Der Laan et al., 1998). Derived from the original Fay- 2007). Total RNA was isolated from a constant number oumi breed, the M5.1 and M15.2 congenic pair lines are of TEL (5.0 x 10) using Trizol (Invitrogen. Carlsbad. highly inbred and geneticall y distant from broiler and CA) arid purified using the RNeasv Mini RNA Puri- Leghorn lines. They share all genetic back- fication Kit (Qiagen, Valencia, CA: \Vu et al.. 2004). ground but differ in the haplotype on chromosome 16 In preliminary experiments, we determined I hat equal carrying the MHC (Zhou and Lamont. 1999, 2003). In cell numbers and equal anmoimuts of total RNA were a previous study, we compared the typical disease pa- obtained per umut volume of gut mnmncosa. (L. K. Kim, rameters of avian coccidiosis. BW gain and fecal ooevst unpublished data). shedding, and transcriptional expression of cytokine Time airuinoahlyl-labeled RNA front IEL from genes between the Fa, voumi M5.1 and M15.2 lilies af- each group was prepared using the Amino Ahlvl Mes- ter oral infection with Eimeria maxima oocysts. The sage Amp 11 aRNA Amplification Kit (t Hoen et al., results demonstrated that line M5.1 is more resistant 2003) according to time protocol of the manufacturer against E. maxima than M15.2 and showed differential (Ainbion. Austin. TX). Briefl y, first strand eDNA was expression of immune-related cytokinies between the 2 prepared by reverse transcription from 2.0 gg of RNA genetically disparate chicken lines after infection. using a modified oligo-dT primer containing a 17 RNA The present study was conducted to compare gene polymerase binding site on the 5' end. followed b y see- expression profiles between these 2 chicken congenic ond strand eDNA synthesis. The double-stranded cDNA hues, which show a difference in disease resistance to gemmerated from first and second cDNA synthesis were coccidiosis, using our avian intestinal intraepithelial transcribed to arninoallyl-labeled RNA using T7 RNA lymphocyte eDNA nncroarray (AVIELA: Kim et al.. pohymerase with amiuioahl yl-iiridine triphosphate. Two 2008). The AVIELA is specific for mucosal transcrip- 20-gg aliquots of each aminoallvl-R NA sample were flu- tional investigations including imnnune response and oresceutly labeled with Alexa Fluor 555 or Alexa Fluor was constructed using an intraepithelial lymphocyte 647 (Invitrogeii) according to the instructions of time (TEL) eDNA library of Eimeria-infected chickens (Min manufacturer and labeled RNA were colunum-purified et al. 2005). Because TEL are the primarimmune cf- using the RNA Amplification Kit. (Ambion; 't. Hoemm lector cells in the gut and play a critical role in eliciting et al.. 2003). Concentration and labeling efficiencies of protective immunity to enteric pathogens, the results RNA were determined spectrophotonietricallv. contribute to comprehensive understanding of the in- nate immune responses in the chicken gut stimulated Microarray Hybridization by E. maxima infection. l3uthi of I lie RNA, labeled with 2 different fluores- MATERIALS AND METHODS cent d yes, from the mmoiiinfected control birds and the treated birds were hybridized to the AVIELA nnicroar- Birds and Experimental Eimeria Infection ray. Time AVIELA was constructed with 10.162 spot dc- meuits from the previously prepared TEL clones (Min et Chicks were bred and nmaint ainccl in the Poultry Ge- al.. 2005) and the imnuiune-related genes from hipopol- netics Program at Iowa State University (Ames). All saccharide (LPS )-activated macrophage (HD 11) eDNA matings were carried out by artificial insemination to library (Mimi et al.. 2003) as well as time direct PCR ensure pedigree accuracy and fl-complex genotypes clones of several cvtokimies and chmeniokiues (Min et al.. were confirmed by serological testing. Day-old chicks 2005). were air-shipped to the Animal and Natural Resources A total of 12 microarrays were used in this study. Ac- Institute. Chickens either remained uninfected or were cording to the reference design (McShane et al., 2003) orally inoculated at 4 wk of age with 1.0 x 104 sporu- with dye swap, 4 values were obtained for each time lated oocvsts/chicken of E.
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