Interaction of Nippostrongylus brasiliensis and Influenza Virus in Mice. I. Influence of the Nematode on the Virus

Wescott, Richard B.; Todd, A. C.

doi:10.2307/3276478

Cited by 11 publications

(17 citation statements)

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“…We quantified the health of mice in our experiments using two measures that have proven informative during Pcc infection [ 49 ] and Pcc -nematode co-infection [ 50 ]: body mass and RBC density. To our knowledge, this is the first report demonstrating that murine Nb infection has a negative impact on both parameters, although reduced weight gain in young Nb -infected mice has previously been reported [ 40 ]. Nb caused a statistically significant, transient ~3% loss of body mass from approximately 2-4 days pi, and in other experiments using a higher dose (500 L3s), mice lost closer to 10% of their starting body mass (unpublished data).…”

Section: Discussionmentioning

confidence: 95%

“…Reported effects of Nb on the course of microparasite infections are likewise mixed: densities of T. gondii [ 60 ] and M. bovis BCG [ 62 ] are unaffected by the presence of the nematode, while C. abortus density increases dramatically [ 61 ]. Interestingly, the concurrent presence of influenza virus with migrating Nb larvae in the lung exacerbates the severity of lung disease compared to mice with influenza alone [ 40 ]. A two-week delay between Nb infection and influenza infection, or replacement of Nb with H. polygyrus , eliminates the added pathology, suggesting that the simultaneous presence of larvae and virus in the lungs is required [ 40 ].…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly, the concurrent presence of influenza virus with migrating Nb larvae in the lung exacerbates the severity of lung disease compared to mice with influenza alone [ 40 ]. A two-week delay between Nb infection and influenza infection, or replacement of Nb with H. polygyrus , eliminates the added pathology, suggesting that the simultaneous presence of larvae and virus in the lungs is required [ 40 ]. Such may also be the case for Pcc-Nb co-infection.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, we expected the lung and draining (thoracic) lymph nodes to be potential sites of strong interactions between Nb and Pcc . The idea that helminth-malaria co-infection may impose Type 1-Type 2 immunological conflict is not new [ 30 ], nor is the idea that parasitic co-infection may alter the severity of pulmonary disease [ 39 , 40 ], but our emphasis on the consequences of malaria for pulmonary Type 2 responses has not previously been explored.…”

Section: Introductionmentioning

confidence: 99%

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Plasmodium chabaudi limits early Nippostrongylus brasiliensis-induced pulmonary immune activation and Th2 polarization in co-infected mice

et al. 2009

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BackgroundLarvae of several common species of parasitic nematodes obligately migrate through, and often damage, host lungs. The larvae induce strong pulmonary Type 2 immune responses, including T-helper (Th)2 cells as well as alternatively activated macrophages (AAMφ) and associated chitinase and Fizz/resistin family members (ChaFFs), which are thought to promote tissue repair processes. Given the prevalence of systemic or lung-resident Type 1-inducing pathogens in geographical areas in which nematodes are endemic, we wished to investigate the impact of concurrent Type 1 responses on the development of these Type 2 responses to nematode larval migration. We therefore infected BALB/c mice with the nematode Nippostrongylus brasiliensis, in the presence or absence of Plasmodium chabaudi chabaudi malaria parasites. Co-infected animals received both infections on the same day, and disease was assessed daily before immunological measurements were taken at 3, 5, 7 or 20 days post-infection.ResultsWe observed that the nematodes themselves caused transient loss of body mass and red blood cell density, but co-infection then slightly ameliorated the severity of malarial anaemia. We also tracked the development of immune responses in the lung and thoracic lymph node. By the time of onset of the adaptive immune response around 7 days post-infection, malaria co-infection had reduced pulmonary expression of ChaFFs. Assessment of the T cell response demonstrated that the Th2 response to the nematode was also significantly impaired by malaria co-infection.ConclusionP. c. chabaudi co-infection altered both local and lymph node Type 2 immune activation due to migration of N. brasiliensis larvae. Given recent work from other laboratories showing that N. brasiliensis-induced ChaFFs correlate to the extent of long-term lung damage, our results raise the possibility that co-infection with malaria might alter pulmonary repair processes following nematode migration. Further experimentation in the co-infection model developed here will reveal the longer-term consequences of the presence of both malaria and helminths in the lung.

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Plasmodium chabaudi limits early Nippostrongylus brasiliensis-induced pulmonary immune activation and Th2 polarization in co-infected mice

et al. 2009

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“…Early studies showed that coinfection of mice with H. polygyrus and influenza virus decreased the lung consolidation caused by influenza virus infection. 19 , 20 Although the mechanisms underlying these changes were not fully addressed, the investigators speculated that this might be due to the immunosuppressive effect of H. polygyrus . Alternatively, the observed protection against pulmonary disease might be due to reduced infiltration of inflammatory immune cells into the lungs.…”

Section: Beneficial Outcomesmentioning

confidence: 99%

Helminth–virus interactions: determinants of coinfection outcomes

2021

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Viral infections are often studied in model mammalian organisms under specific pathogen-free conditions. However, in nature, coinfections are common, and infection with one organism can alter host susceptibility to infection with another. Helminth parasites share a long coevolutionary history with mammalian hosts and have shaped host physiology, metabolism, immunity, and the composition of the microbiome. Published studies suggest that helminth infection can either be beneficial or detrimental during viral infection. Here, we discuss coinfection studies in mouse models and use them to define key determinants that impact outcomes, including the type of antiviral immunity, the tissue tropism of both the helminth and the virus, and the timing of viral infection in relation to the helminth lifecycle. We also explore the current mechanistic understanding of how helminth-virus coinfection impacts host immunity and viral pathogenesis. While much attention has been placed on the impact of the gut bacterial microbiome on immunity to infection, we suggest that enteric helminths, as a part of the eukaryotic macrobiome, also represent an important modulator of disease pathogenesis and severity following virus infection.

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