A comparison of the role of kinins and serotonin in endotoxin induced fever and Trypanosoma vivax infections in the goat

Veenendaal, G.; Miert, A. S. J. P. A. M. van; Ingh, T.S.G.A.M. van den; Schotman, A. J. H.; Zwart, D.

doi:10.1016/s0034-5288(18)33335-6

Cited by 31 publications

(14 citation statements)

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“…example, goats infected with Ehrlichia phagocytophila or Trypanosoma vivax show among other signs high fever, some depression of food intake, and a slight inhibition of rumen contractions, whereas cows suffering from severe Escherichia coli mastitis show fever, anorexia, and ruminal stasis (71,73,147,149,150,158). Similar observations have been made with goats injected with staphylococcal enterotoxins, endotoxins (LPS) from E.coli or Salmonella typhimurium, Newcastle's disease virus, poly I: poly C, sodium nucleinate from yeast, or johnin challenge after vaccination with Mycobacterium johnei (20, 63, 77, 78, 137-139, 149, 159).…”

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Pro‐inflammatory cytokines in a ruminant model: Pathophysiological, pharmacological, and therapeutic aspects

Miert

1995

Veterinary Quarterly

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Infection evokes complex changes which are thought to be caused by production and release of pro-inflammatory cytokines such as tumour necrosis factor (TNF-alpha), interferons (INFs), and interleukins (ILs). They regulate local inflammatory reactions, but may also gain access to the circulation and induce systemic effects collectively known as the Acute Phase Response. To improve our understanding of the pathophysiology of pro-inflammatory cytokines in ruminants, studies have been performed with TNF-alpha, IL1-alpha/beta, and IFN-alpha/ gamma as well as with cytokine-inducers in dwarf goats. In relation to therapy, the following aspects may be of interest: a) Cytokine therapy given before or just after microbial challenge induces in vivo antimicrobial activity. Moreover, cytokines potentiate in vivo the antimicrobial activity of antibiotics, b) Cytokines may act as biological response modifiers for enhancing specific immunity to vaccines, and c) Cytokines may affect drug absorption, disposition, and metabolite formation in disease states. Although studies of the actions of corticosteroids, nonsteroidal anti-inflammatory and antipyretic agents, antibodies to endotoxin, TNF-alpha, or IL-1, synthetic E. coli lipid A precursors, hydrazine, isoniazid, chloroquine, polymyxin B, bicyclic imidazoles, hydroxamates, and tyrosine kinase inhibitors in endotoxaemic animals have shed further light on inflammatory processes, clinical studies in this field are urgently required to evaluate their beneficial effect.

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Pro‐inflammatory cytokines in a ruminant model: Pathophysiological, pharmacological, and therapeutic aspects

Miert

1995

Veterinary Quarterly

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“…This peptide was reported to facilitate T. cruzi cell invasion through B1 receptors since addition of [Leu8]-des-Arg9-BK, a B1 receptor antagonist, is known to reduce the parasite infectivity [27]. In the case of T. brucei , the kallikrein-kinin system was reported to be severely dysregulated in trypanosome-infected hosts [28]. Thus, Tb MCP-1 could be a good candidate to influence the activity of host vasoactive kinins.…”

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confidence: 99%

Characterization of the M32 metallocarboxypeptidase of Trypanosoma brucei: Differences and similarities with its orthologue in Trypanosoma cruzi

Frasch

Carmona

Juliano

et al. 2012

Molecular and Biochemical Parasitology

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Metallocarboxypeptidases (MCP) of the M32 family of peptidases have been identified in a number of prokaryotic organisms but they are absent from eukaryotic genomes with the remarkable exception of those of trypanosomatids. The genome of Trypanosoma brucei, the causative agent of Sleeping Sickness, encodes one such MCP which displays 72% identity to the characterized TcMCP-1 from Trypanosoma cruzi. As its orthologue, TcMCP-1, Trypanosoma brucei MCP is a cytosolic enzyme expressed in both major stages of the parasite. Purified recombinant TbMCP-1 exhibits a significant hydrolytic activity against the carboxypeptidase B substrate FA (furylacryloil)-Ala-Lys at pH 7.0–7.8 resembling the T. cruzi enzyme. S everal divalent cations had little effect on TbMCP-1 activity but increasing amounts of Co2+ inhibited the enzyme. Despite having similar tertiary structure, both protozoan MCPs display different substrate specificity with respect to P1 position. Thus, TcMCP-1 enzyme cleaved Abz-FVK-(Dnp)-OH substrate (where Abz: o-aminobenzoic acid and Dnp: 2,4-dinitrophenyl) whereas TbMCP-1 had no activity on this substrate. Comparative homology models and sequence alignments using TcMCP-1 as a template led us to map several residues that could explain this difference. To verify this hypothesis, site-directed mutagenesis was undertaken replacing the TbMCP-1 residues by those present in TcMCP-1. We found that the substitution A414M led TbMCP-1 to gain activity on Abz-FVK-(Dnp)-OH, thus showing that this residue is involved in specificity determination, probably being part of the S1 sub-site. Moreover, the activity of both protozoan MCPs was explored on two vasoactive compounds such as bradykinin and angiotensin I resulting in two different hydrolysis patterns.

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“…T. vivax produces immunosuppression, which has also been demonstrated in goats 43 . Thrombocytopenia, microthrombus formation and hemorrhage suggestive of disseminated intravascular coagulation (DIC) have been observed in goats infected with T. vivax 44,45 …”

Section: T Vivaxmentioning

confidence: 97%

Trypanosomosis in Goats

Gutiérrez

Corbera

Morales

et al. 2006

Annals of the New York Academy of Sciences

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Trypanosomosis is a major constraint on ruminant livestock production in Africa, Asia, and South America. The principal host species affected varies geographically, but buffalo, cattle, camels, and horses are particularly sensitive. Natural infections with Trypanosoma congolense, T. vivax, T. brucei, and T. evansi have been described in goats. Trypanosomosis in goats produces acute, subacute, chronic, or subclinical forms, being T. vivax, T. congolense, and T. evansi, the most invasive trypanosomes for goats. However, the role of goats in the epidemiology of trypanosomosis is largely discussed and not well understood. Thus, it has commonly been assumed that trypanosomosis presents a subclinical course and that goats do not play an important role in the epidemiology of the disease. This can partially be due to parasitemia caused by trypanosomes which has been considered low in goats. However, this assumption is currently undergoing a critical reappraisal because of goats may also serve as a reservoir of trypanosome infection for other species, including the human beings in the case of T. brucei rhodesiense. The present article describes the current status of trypanosomosis in goats in Africa, Asia, and South America. Pathogenesis, clinical features, diagnosis, and treatment of the different trypanosomes are also described. The possible role in the epidemiology of the disease in the different areas is also discussed.

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A comparison of the role of kinins and serotonin in endotoxin induced fever and Trypanosoma vivax infections in the goat

Cited by 31 publications

References 28 publications

Pro‐inflammatory cytokines in a ruminant model: Pathophysiological, pharmacological, and therapeutic aspects

Pro‐inflammatory cytokines in a ruminant model: Pathophysiological, pharmacological, and therapeutic aspects

Characterization of the M32 metallocarboxypeptidase of Trypanosoma brucei: Differences and similarities with its orthologue in Trypanosoma cruzi

Trypanosomosis in Goats

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