Unique responses of the avian macrophage to different species of Eimeria

Dalloul, Rami A.; Bliss, Travis W.; Hong, Yeong Ho; Ben-Chouikha, Imed; Park, Dong Woon; Keeler, Calvin L.; Lillehoj, Hyun S.

doi:10.1016/j.molimm.2006.02.004

Cited by 60 publications

(36 citation statements)

References 25 publications

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“…6B and C). Eimeria species are intracellular protozoan parasites that typically invade intestinal epithelial cells and induce increased levels of cytokine genes (e.g., IL-1␤ and IFN-␥) (25,38,39). Therefore, IL-1␤ and IFN-␥ transcript levels were monitored postinfection.…”

Section: Resultsmentioning

confidence: 99%

Downregulation of Chicken Interleukin-17 Receptor A during Eimeria Infection

et al. 2014

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e Both interleukin-17A (IL-17A) and IL-17F are proinflammatory cytokines that have an important role in intestinal homeostasis via receptor signaling. These cytokines have been characterized in chickens, but very little is known about their receptors and their functional activity. We provide here the first description of the sequence analysis, bioactivity, and comparative expression analysis of chicken IL-17RA (chIL-17RA) in chickens infected with Salmonella and Eimeria, two major infectious agents of gastrointestinal diseases of poultry of economic importance. A full-length chIL-17RA cDNA with a 2,568-bp coding region was identified from chicken thymus cDNA. chIL-17RA shares ca. 46% identity with mammalian homologues and 29.2 to 31.5% identity with its piscine counterparts. chIL-17RA transcript expression was relatively high in the thymus and in the chicken macrophage cell line HD11. The chIL-17RA-specific small interfering RNA inhibits interleukin-6 (IL-6), IL-8, and IL-1␤ mRNA expression in chicken embryo fibroblast cells (but not in DF-1 cells) stimulated with chIL-17A or chIL-17F. Interaction between chIL-17RA and chIL-17A was confirmed by coimmunoprecipitation. Downregulation of chIL-17RA occurred in concanavalin A-or lipopolysaccharide-activated splenic lymphocytes but not in poly(I·C)-activated splenic lymphocytes. In Salmonella-and Eimeria-infected chickens, the expression levels of the chIL-17RA transcript were downregulated in intestinal tissues from chickens infected with two Eimeria species, E. tenella or E. maxima, that preferentially infect the cecum and jejunum, respectively. However, chIL-17RA expression was generally unchanged in Salmonella infection. These results suggest that chIL-17RA has an important role in mucosal immunity to intestinal intracellular parasite infections such as Eimeria infection.

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Section: Resultsmentioning

confidence: 99%

Downregulation of Chicken Interleukin-17 Receptor A during Eimeria Infection

et al. 2014

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“…Damage to the intestinal barrier also increases the mortality of the birds. Eimeria infection is responsible for losses of $3 billion annually in the poultry industry (Dalloul et al, 2007). The 3 species of Eimeria that mainly impact the poultry industry in the United States are E. acervulina, E. maxima, and E. tenella.…”

Section: Introductionmentioning

confidence: 99%

“…Cell-mediated immune responses are the major host immune response during Eimeria infection, and they also can provide protection against reinfection (Lillehoj and Trout, 1996;Lillehoj and Lillehoj, 2000;Lillehoj et al, 2004). T-lymphocytes, natural killer cells, and macrophages are involved in the avian cellular immune response to Eimeria infection (Lillehoj and Trout, 1996;Dalloul et al, 2007). Host defense peptides not only show direct antimicrobial activity by disrupting membrane integrity but also enhance mucosal barrier 2421 function by inducing expression of mucins and tight junction proteins (Robinson et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

Expression of host defense peptides in the intestine of Eimeria-challenged chickens

Dwyer

Miska³

et al. 2017

Poultry Science

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Avian coccidiosis is caused by the intracellular protozoan Eimeria, which produces intestinal lesions leading to weight gain depression. Current control methods include vaccination and anticoccidial drugs. An alternative approach involves modulating the immune system. The objective of this study was to profile the expression of host defense peptides such as avian beta-defensins (AvBDs) and liver expressed antimicrobial peptide 2 (LEAP2), which are part of the innate immune system. The mRNA expression of AvBD family members 1, 6, 8, 10, 11, 12, and 13 and LEAP2 was examined in chickens challenged with either E. acervulina, E. maxima, or E. tenella. The duodenum, jejunum, ileum, and ceca were collected 7 d post challenge. In study 1, E. acervulina challenge resulted in down-regulation of AvBD1, AvBD6, AvBD10, AvBD11, AvBD12, and AvBD13 in the duodenum. E. maxima challenge caused down-regulation of AvBD6, AvBD10, and AvBD11 in the duodenum, down-regulation of AvBD10 in the jejunum, but upregulation of AvBD8 and AvBD13 in the ceca. E. tenella challenge showed no change in AvBD expression in any tissue. In study 2, which involved challenge with only E. maxima, there was down-regulation of AvBD1 in the ileum, AvBD11 in the jejunum and ileum, and LEAP2 in all 3 segments of the small intestine. The expression of LEAP2 was further examined by in situ hybridization in the jejunum of chickens from study 2. LEAP2 mRNA was expressed similarly in the enterocytes lining the villi, but not in the crypts of control and Eimeria challenged chickens. The lengths of the villi in the Eimeria challenged chickens were less than those in the control chickens, which may in part account for the observed down-regulation of LEAP2 mRNA quantified by PCR. Overall, the AvBD response to Eimeria challenge was not consistent; whereas LEAP2 was consistently down-regulated, which suggests that LEAP2 plays an important role in modulating an Eimeria infection.

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“…Taking into account these observations, significantly increased iNOS mRNA in the caecum and the liver can be related to the up-regulation of IFN- mRNA in these tissues of infected animals. In caecal coccidiosis, iNOS mRNA induction is related to the haemorrhage that is frequently observed after E. tenella challenge (Laurent et al, 2001;Dalloul et al, 2007). Similar changes in iNOS mRNA were observed in the duodenum although IFN- mRNA was not affected and this tissue was not a target for E. tenella.…”

Section: Discussionmentioning

confidence: 70%

Influence of experimentally induced Eimeria tenella infection on gene expression of some host response factors in chickens

Milanova¹,

Santos²,

Lashev³

et al. 2016

BJVM

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Coccidiosis in poultry is associated with significant damage of intestinal integrity and involvement of innate immunity. Therefore, the aim of this study was to evaluate genes, encoding the innate immune response in broiler chickens, such as LEAP, IFN-, iNOS and IL-8 together with PepT1 and ABCG2 transporters after E. tenella challenge. E. tenella infection provoked up-regulation of iNOS mRNA in the duodenum and of IFN- and iNOS mRNAs in the caecum and the liver. IL-8 mRNA expression in the liver was increased and LEAP mRNA was decreased. On the sixth day after the challenge with E. tenella, ABCG2 mRNA was increased in the duodenum and the liver while PepT1 mRNA was upregulated in the duodenum. The expression of these genes in the caecum was not changed. In conclusion, several factors of the host immune response can be affected by E. tenella infection not only in the target caecal tissue but also in the liver and to a lesser degree in the duodenum. The caecal coccidiosis can provoke significant changes in the integrity of the intestines by affecting of ABCG2 and PepT1 mRNA levels.

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Unique responses of the avian macrophage to different species of Eimeria

Cited by 60 publications

References 25 publications

Downregulation of Chicken Interleukin-17 Receptor A during Eimeria Infection

Downregulation of Chicken Interleukin-17 Receptor A during Eimeria Infection

Expression of host defense peptides in the intestine of Eimeria-challenged chickens

Influence of experimentally induced Eimeria tenella infection on gene expression of some host response factors in chickens

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