Analysis of chicken cytokine and chemokine gene expression following Eimeria acervulina and Eimeria tenella infections.
The expression levels of mRNA encoding a panel of 28 chicken cytokines and chemokines were quantified in intestinal lymphocytes following Eimeria acervulina and Eimeria tenella primary and secondary infections. Compared with uninfected controls, transcripts of the pro-inflammatory cytokines IFN-alpha, IL-1beta, IL-6, and IL-17 were increased up to 2020-fold following primary infection. By contrast, following secondary infection by either microorganism, pro-inflammatory mRNAs levels were relatively unchanged (< or = 20-fold). Transcripts encoding the Th1 and Th1 regulatory cytokines IFN-gamma, IL-2, IL-10, IL-12, IL-15, IL-16, and IL-18 were uniformly increased 14-2471-fold after E. acervulina primary infection, but either unchanged (IL-15, IL-16, IL-18), increased (IFN-gamma, IL-10, IL-12), or decreased (IL-2) following E. tenella primary infection. Following secondary infections, Th1 cytokine mRNA levels were relatively unchanged, with the exception of IL-12 which was increased 1.5 x 10(5)-fold after E. acervulina and decreased 5.1 x 10(4)-fold after E. tenella infection. Transcripts for the Th2 or Th2 regulatory cytokines IL-3 and GM-CSF were increased up to 327-fold following primary or secondary infection with both parasites, while IL-4 and IL-13 mRNAs were decreased 25- to 2 x 10(5)-fold after primary or secondary infection. The dynamics of chicken chemokine expression revealed modest changes (<100-fold) following primary or secondary infection except for lymphotactin. When lymphocyte subpopulations were similarly analyzed, IFN-gamma, IL-2, IL-3, IL-15, and MIF were most highly increased in TCR2(+) cells following E. acervulina infection, while TCR1(+) cells only expressed high levels of IL-16 following E. tenella infection. In contrast, CD4(+) cells only expressed highest levels of IL-10 after E. acervulina infection, whereas these cells produced abundant transcripts for IFN-gamma, IL-3, IL-15, and MIF after E. tenella infection. We conclude that coccidiosis induces a diverse and robust primary cytokine/chemokine response, but a more subdued secondary response.
Hong
Yeong Ho
YH
Animal Parasitic Diseases Laboratory, Animal and Natural Resources Institute, United States Department of Agriculture, Building 1040, BARC-East, Beltsville, MD 20705, USA.
Lillehoj
Hyun S
HS
Lee
Sung Hyen
SH
Dalloul
Rami A
RA
Lillehoj
Erik P
EP
D000818:Animals; D002432:Cecum / Q000276:immunology / Q000469:parasitology; D018925:Chemokines / Q000096:biosynthesis* / Q000235:genetics / Q000276:immunology; D002645:Chickens; D003048:Coccidiosis / Q000235:genetics / Q000276:immunology / Q000469:parasitology / Q000662:veterinary*; D016207:Cytokines / Q000096:biosynthesis* / Q000235:genetics / Q000276:immunology; D004386:Duodenum / Q000276:immunology / Q000469:parasitology; D016786:Eimeria tenella / Q000276:immunology*; D005434:Flow Cytometry / Q000662:veterinary; D015870:Gene Expression; D007411:Intestinal Diseases, Parasitic / Q000235:genetics / Q000276:immunology / Q000469:parasitology / Q000662:veterinary*; D007413:Intestinal Mucosa / Q000276:immunology / Q000469:parasitology; D008214:Lymphocytes / Q000469:parasitology; D011201:Poultry Diseases / Q000235:genetics / Q000276:immunology* / Q000469:parasitology*; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000662:veterinary; D013047:Specific Pathogen-Free Organisms
D018925:Chemokines; D016207:Cytokines; D012333:RNA, Messenger