Quantitative analysis of pro-inflammatory cytokine mRNA expression in Theileria annulata-infected cell lines derived from resistant and susceptible cattle
The pathogenic mechanisms involved in tropical theileriosis, caused by the tick-borne protozoan parasite Theileria annulata, are unclear. Pathology is associated with the schizont stage of the parasite, which resides within bovine macrophages. Breed-specific differences in pathology have been observ...
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Veröffentlicht in: | Veterinary immunology and immunopathology 2004-05, Vol.99 (1), p.87-98 |
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Sprache: | eng |
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Zusammenfassung: | The pathogenic mechanisms involved in tropical theileriosis, caused by the tick-borne protozoan parasite
Theileria annulata, are unclear. Pathology is associated with the schizont stage of the parasite, which resides within bovine macrophages. Breed-specific differences in pathology have been observed in cattle, several
Bos indicus breeds are relatively resistant to tropical theileriosis whilst
Bos taurus cattle are highly susceptible. Infected cells express pro-inflammatory cytokines and it has been hypothesized that these cytokines play a major role in the pathology of the disease. Therefore, using quantitative RT–PCR we investigated the expression of the key candidates, interleukin 1 beta (IL-1β), IL-6 and tumour necrosis factor alpha (TNF-α), in
T. annulata low passage infected cell lines derived ex vivo from experimental infection of resistant and susceptible cattle. mRNA for each cytokine was detected in all cell lines investigated at levels higher than those observed in resting monocytes. However, the analyses did not identify any breed-specific differences. Therefore, these results are not consistent with the hypothesis that differential regulation of infected cell derived pro-inflammatory cytokines (IL-1β, IL-6 and TNF-α) accounts for the breed-related differences in resistance and susceptibility to
T. annulata infection. Other, currently unknown mechanisms may be of greater importance. |
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ISSN: | 0165-2427 1873-2534 |
DOI: | 10.1016/j.vetimm.2004.01.003 |