Further development of the baboon as a model for acute schistosomiasis

Damian, Raymond T.; Rosa, Miguel A. De la; Murfin, Daniel J.; Rawlings, Clarence A.; Weina, Peter J.; Xue, Yang

doi:10.1590/s0074-02761992000800041

Cited by 23 publications

(15 citation statements)

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“…As the infection becomes "chronic", at 10-20 wks, the appearance of the animals improves and the cellular response to antigen is downregulated while egg laying by the parasite continues unchanged (Tawfik et al 1986, Damian et al1992. Particular efforts to study the toxemic phase have been made in baboons, which exhibit fever as well as the other features noted in mice and other animal models (Damian et al 1992(Damian et al , 1996. It is unclear, however, how to relate the experimental acute disease to that in humans.…”

Section: Acute Toxemic Schistosomiasismentioning

confidence: 99%

Experimental models of Schistosoma mansoni infection

Cheever

Lenzi²,

Lenzi³

et al. 2002

Mem. Inst. Oswaldo Cruz

120

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Section: Acute Toxemic Schistosomiasismentioning

confidence: 99%

Experimental models of Schistosoma mansoni infection

Cheever

Lenzi²,

Lenzi³

et al. 2002

Mem. Inst. Oswaldo Cruz

120

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“…Baboons are natural hosts for Schistosoma mansoni in East Africa (20) and wild-caught baboons with schistosomiasis mansoni have been reported with periportal fibrosis (21). Experimental infections of baboons with S. mansoni, however, have not been previously reported to stimulate development of periportal fibrosis (22)(23)(24). We previously observed that multiple compared with singly infected animals that are subsequently cured and reinfected produced increased levels of schistosome egg Ag (SEA) 3 -driven TGF-␤, IL-4, and IL-2 production by PBMC (25,26).…”

Section: Repeated Exposure Induces Periportal Fibrosis Inmentioning

confidence: 99%

Repeated Exposure Induces Periportal Fibrosis inSchistosoma mansoni-Infected Baboons: Role of TGF-β and IL-4

Farah

Mola

Kariuki

et al. 2000

The Journal of Immunology

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Recently, we observed that repeated Schistosoma mansoni infection and treatment boost Th2-associated cytokines and TGF-β production in baboons. Other studies have shown that some chronically infected baboons develop hepatic fibrosis. Because TGF-β, IL-2, and IL-4 have been shown to participate in development of fibrosis in murine schistosomiasis, the present study examined whether repeated exposure stimulates hepatic fibrosis in olive baboons. To test this hypothesis, animals were exposed to similar numbers of S. mansoni cercariae given once or repeatedly. After 19 wk of infection, animals were cured with praziquantel and reinfected once or multiple times. Hepatic granulomatous inflammation and fibrosis were assessed from serial liver biopsies taken at weeks 6, 9, and 16 after reinfection and egg Ag (schistosome egg Ag)-specific cytokine production by PBMC were measured simultaneously. Periportal fibroblast infiltration and extracellular matrix deposition (fibrosis), angiogenesis, and biliary duct hyperplasia developed in some animals. The presence and amount of fibrosis directly correlated with the frequency of exposure. Fibrosis was not associated with adult worm or tissue egg burden. The amount of fibrosis correlated with increased schistosome egg Ag-driven TGF-β at 6, 9, and 16 wk postinfection (rs = 0.9, 0.8, and 0.54, respectively, all p < 0.01) and IL-4 production (p = 0.02) at 16 wk postinfection and not IFN-γ, IL-2, IL-5, or IL-10. These data suggest that repeated exposure is a risk factor for periportal fibrosis by a mechanism that primes lymphocytes to produce increased levels of profibrotic molecules that include TGF-β and IL-4.

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“…Morbidity observed in schistosomiasis is essentially related to female worm fecundity, with production of hundreds of eggs daily, which are deposited mainly in the host liver and intestines or urinary bladder. Granuloma formation around eggs, particularly in the liver and bladder, can lead to the development of severe fibrotic and often irreversible lesions [3].Previous research has established that baboons (Papio species) are a good model for many aspects of human schistosomiasis mansoni [4][5][6][7][8]. They develop a human-like acute schistosomiasis syndrome after exposure to the infective stage (cercariae) of Schis-…”

mentioning

confidence: 99%

“…Previous research has established that baboons (Papio species) are a good model for many aspects of human schistosomiasis mansoni [4][5][6][7][8]. They develop a human-like acute schistosomiasis syndrome after exposure to the infective stage (cercariae) of Schis-…”

mentioning

confidence: 99%

Altered Levels of Hypothalamic‐Pituitary‐Adrenocortical Axis Hormones in Baboons and Mice during the Course of Infection withSchistosoma mansoni

et al. 2001

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Baboons with primary or secondary exposure to Schistosoma mansoni were compared with each other over a 12-week infection period and with baseline values obtained from uninfected baboons with respect to serum levels of the hypothalamic-pituitary-adrenal (HPA) axis hormones-corticotropin-releasing hormone, adrenocorticotropic hormone, dehydroepiandrosterone sulfate (DHEA-S), and cortisol. Baboons with primary infections, when worm recovery and oviposition rates were high and hepatic schistosome egg granulomas were large, had decreasing levels of these hormones as infection progressed, compared with both uninfected and reexposed baboons. The most reduced hormone level was that of DHEA-S. Reduction of DHEA-S and cortisol levels also occurred in primary murine infections. Reexposed baboons with low worm recovery and oviposition rates and small (modulated) hepatic granulomas showed the opposite pattern: HPA axis hormone levels were maintained at, or exceeded, the baseline values of uninfected baboons. These results suggest that HPA axis hormones may play a role in regulating the establishment, maturation, and oviposition of schistosomes and the progression of schistosomiasis.

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Further development of the baboon as a model for acute schistosomiasis

Cited by 23 publications

References 0 publications

Experimental models of Schistosoma mansoni infection

Experimental models of Schistosoma mansoni infection

Repeated Exposure Induces Periportal Fibrosis inSchistosoma mansoni-Infected Baboons: Role of TGF-β and IL-4

Altered Levels of Hypothalamic‐Pituitary‐Adrenocortical Axis Hormones in Baboons and Mice during the Course of Infection withSchistosoma mansoni

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