Analysis of chicken cytokine and chemokine gene expression following Eimeria acervulina and Eimeria tenella infections.

Abstract

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.

• Authors: Yeong Ho Hong, Hyun S Lillehoj, Sung Hyen Lee, Rami A Dalloul, Erik P Lillehoj
• Journal: Veterinary immunology and immunopathology (Vet Immunol Immunopathol) Vol. 114 Issue 3-4 Pg. 209-23 (Dec 15 2006) ISSN: 0165-2427 [Print] Netherlands
• PMID: 16996141 (Publication Type: Journal Article, Research Support, U.S. Gov't, Non-P.H.S.)

Chemical References

• Chemokines
• Cytokines
• RNA, Messenger

Topics

• Animals
• Cecum (immunology, parasitology)
• Chemokines (biosynthesis, genetics, immunology)
• Chickens
• Coccidiosis (genetics, immunology, parasitology, veterinary)
• Cytokines (biosynthesis, genetics, immunology)
• Duodenum (immunology, parasitology)
• Eimeria tenella (immunology)
• Flow Cytometry (veterinary)
• Gene Expression
• Intestinal Diseases, Parasitic (genetics, immunology, parasitology, veterinary)
• Intestinal Mucosa (immunology, parasitology)
• Lymphocytes (parasitology)
• Poultry Diseases (genetics, immunology, parasitology)
• RNA, Messenger (biosynthesis, genetics)
• Reverse Transcriptase Polymerase Chain Reaction (veterinary)
• Specific Pathogen-Free Organisms