Effects of experimental Salmonella dublin infection in cattle given Fasciola hepatica thirteen weeks previously

Aitken, Maureen M.; Jones, Phillip W.; Hall, G.A.; Hughes, D.L.; Collis, K.A.

doi:10.1016/0021-9975(78)90063-4

Cited by 34 publications

(18 citation statements)

References 10 publications

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“…Previous co‐infection studies have shown that Schistosoma mansoni and Nippostrongylus brasiliensis co‐infection in mice increased the bacterial burden and growth of M. tuberculosis, respectively. F. hepatica infection in cattle induced higher excretion rates in concurrent infection with Salmonella Dublin and more disseminated bacterial infection in the organs . Similarly, another study in mice showed that co‐infection with F. hepatica and Bordetella pertussis delayed bacterial clearance in the co‐infected groups .…”

Section: Discussionmentioning

confidence: 92%

“…This reduced sensitivity of the diagnostic tests was hypothesized to be due to an immunosuppression induced by F. hepatica infection. A downregulation of the Th1 immune response in other co‐infection models has been associated with an increase in bacterial loads . Thus, we proposed that these changes in F. hepatica‐ infected animals might also result in an increase in the M. bovis numbers in co‐infected animals.…”

Section: Introductionmentioning

confidence: 83%

“…Parasitic helminths, ubiquitous in grazing livestock and common in humans in many parts of the world, typically use immunoregulatory strategies to achieve persistent infections, while reducing inflammatory pathology in the host . They also have the potential, through bystander immunoregulation, to alter the pathology and course of other infections in the same host . Here, we model some aspects of the interaction between a helminth and a bacterial pathogen, both of which cause economically important diseases of livestock.…”

Section: Introductionmentioning

confidence: 99%

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Fasciola hepatica infection reduces Mycobacterium bovis burden and mycobacterial uptake and suppresses the pro‐inflammatory response

Garza-Cuartero

O'Sullivan

Blanco

et al. 2016

Parasite Immunology

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SUMMARYBovine tuberculosis (BTB), caused by Mycobacterium bovis, has an annual incidence in cattle of 0.5% in the Republic of Ireland and 4.7% in the UK, despite long-standing eradication programmes being in place. Failure to achieve complete eradication is multifactorial, but the limitations of diagnostic tests are significant complicating factors. Previously, we have demonstrated that Fasciola hepatica infection, highly prevalent in these areas, induced reduced sensitivity of the standard diagnostic tests for BTB in animals co-infected with F. hepatica and M. bovis. This was accompanied by a reduced M. bovis-specific Th1 immune response. We hypothesized that these changes in co-infected animals would be accompanied by enhanced growth of M. bovis. However, we show here that mycobacterial burden in cattle is reduced in animals co-infected with F. hepatica. Furthermore, we demonstrate a lower mycobacterial recovery and uptake in blood monocyte-derived macrophages (MDM) from F. hepatica-infected cattle which is associated with suppression of pro-inflammatory cytokines and a switch to alternative activation of macrophages. However, the cell surface expression of TLR2 and CD14 in MDM from F. hepatica-infected cattle is increased. These findings reflecting the bystander effect of helminth-induced downregulation of pro-inflammatory responses provide insights to understand host-pathogen interactions in co-infection.

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Section: Discussionmentioning

confidence: 92%

Section: Introductionmentioning

confidence: 83%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Fasciola hepatica infection reduces Mycobacterium bovis burden and mycobacterial uptake and suppresses the pro‐inflammatory response

Garza-Cuartero

O'Sullivan

Blanco

et al. 2016

Parasite Immunology

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“…hepatica can be long lived and accompanied by parasite-specific and non-specific immunosuppression [8, 43, 44]. As the host progresses from a Th2 type response to a more regulatory response it is assumed that secretion of IL-10 and TGF-β increases as a result of either T-cell phenotypic changes or the expansion of T-regulatory cells.…”

Section: Discussionmentioning

confidence: 99%

A Trematode Parasite Derived Growth Factor Binds and Exerts Influences on Host Immune Functions via Host Cytokine Receptor Complexes

et al. 2016

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The trematode Fasciola hepatica is responsible for chronic zoonotic infection globally. Despite causing a potent T-helper 2 response, it is believed that potent immunomodulation is responsible for rendering this host reactive non-protective host response thereby allowing the parasite to remain long-lived. We have previously identified a growth factor, FhTLM, belonging to the TGF superfamily can have developmental effects on the parasite. Herein we demonstrate that FhTLM can exert influence over host immune functions in a host receptor specific fashion. FhTLM can bind to receptor members of the Transforming Growth Factor (TGF) superfamily, with a greater affinity for TGF-β RII. Upon ligation FhTLM initiates the Smad2/3 pathway resulting in phenotypic changes in both fibroblasts and macrophages. The formation of fibroblast CFUs is reduced when cells are cultured with FhTLM, as a result of TGF-β RI kinase activity. In parallel the wound closure response of fibroblasts is also delayed in the presence of FhTLM. When stimulated with FhTLM blood monocyte derived macrophages adopt an alternative or regulatory phenotype. They express high levels interleukin (IL)-10 and arginase-1 while displaying low levels of IL-12 and nitric oxide. Moreover they also undergo significant upregulation of the inhibitory receptor PD-L1 and the mannose receptor. Use of RNAi demonstrates that this effect is dependent on TGF-β RII and mRNA knock-down leads to a loss of IL-10 and PD-L1. Finally, we demonstrate that FhTLM aids newly excysted juveniles (NEJs) in their evasion of antibody-dependent cell cytotoxicity (ADCC) by reducing the NO response of macrophages—again dependent on TGF-β RI kinase. FhTLM displays restricted expression to the F. hepatica gut resident NEJ stages. The altered fibroblast responses would suggest a role for dampened tissue repair responses in facilitating parasite migration. Furthermore, the adoption of a regulatory macrophage phenotype would allow for a reduced effector response targeting juvenile parasites which we demonstrate extends to an abrogation of the ADCC response. Thus suggesting that FhTLM is a stage specific evasion molecule that utilises host cytokine receptors. These findings are the first to clearly demonstrate the interaction of a helminth cytokine with a host receptor complex resulting in immune modifications that facilitate the non-protective chronic immune response which is characteristic of F. hepatica infection.

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“…In cattle, fasciolosis is a risk factor for Salmonella dublin infection on dairy farms (Vaessen et al, 1998), though the results of co-infection experiments are equivocal (Aitken et al, 1978;Hall et al, 1981). Another important effect of F. hepatica, which has been explored much more cattle in than in sheep, is its role in immunomodulation (Naranjo Lucena et al, 2017).…”

Section: Cattlementioning

confidence: 99%

Liver fluke infections in cattle and sheep

Forbes

2017

Livestock

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The trematode, Fasciola hepatica, is a cosmopolitan parasite of temperate regions that can infect a wide variety of wild and domestic mammalian species, including man. Host-responses differ amongst different species and this article focuses on the contrast between cattle and sheep, the two classes of livestock in which fasciolosis assumes the greatest economic importance. In the sheep, acute fasciolosis resulting from parenchymal damage to the liver and haemorrhage caused by migrating juvenile flukes is a severe and potentially fatal disease. In contrast, the parenchymal stages have limited effects in cattle and the acute form of the disease is extremely rare. Though there is no evidence for a functional, acquired immune response to Fasciola hepatica, cattle provide a less hospitable environment, probably due to the profound changes in parasitised bile ducts, which render them as unsuitable habitats for feeding fluke. Consequently, in untreated cattle, many liver fluke die within 18 months of infection, though some can survive for 2 years or more. In the sheep, essentially, the fluke can live as long as the sheep; up to 11 years has been reported. These differences lead to the need for different treatment approaches in cattle and sheep with respect to juvenile fluke, but do also provide some opportunities for novel control approaches, based on the relative tolerance of cattle and their ability to limit parasitic damage to the liver parenchyma.

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Effects of experimental Salmonella dublin infection in cattle given Fasciola hepatica thirteen weeks previously

Cited by 34 publications

References 10 publications

Fasciola hepatica infection reduces Mycobacterium bovis burden and mycobacterial uptake and suppresses the pro‐inflammatory response

Fasciola hepatica infection reduces Mycobacterium bovis burden and mycobacterial uptake and suppresses the pro‐inflammatory response

A Trematode Parasite Derived Growth Factor Binds and Exerts Influences on Host Immune Functions via Host Cytokine Receptor Complexes

Liver fluke infections in cattle and sheep

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