Distinctive and critical roles for cellular immunity and immune-inflammatory response in the immunopathology of Sendai virus infection in mice

Simon, Ayo Yila; Sasaki, Nobuya; Ichii, Osamu; Kajino, Kiichi; Kon, Yasuhiro; Agui, Takashi

doi:10.1016/j.micinf.2011.04.003

Cited by 6 publications

(10 citation statements)

References 49 publications

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“…As has been previously described, DBA/2 mice are highly susceptible to lethal infection with SeV [11,13-15]. Specifically, we found that DBA/2 mice which received a higher titer virus inoculum (1.6x10 5 IU of SeV) sustained greater weight loss and mortality than the mice that received the lower inoculum (1.6x10 3 IU of SeV).…”

Section: Discussionsupporting

confidence: 79%

“…Differences in susceptibility to SeV infection among mouse strains exist, with C57BL/6 mice being more resistant and DBA/2 mice being more susceptible to infection [11,13,14]. SeV is known to be a strong inducer of various cytokines/chemokines, including interferon-Υ, IL-2, TNF-α, IL-6, and IL-10 [12].…”

Section: Introductionmentioning

confidence: 99%

“…Simon and colleagues showed that SeV infection in the susceptible DBA/2 mice resulted in a vigorous inflammatory response, specifically with increased production of IL-1β, IL-2, IL-6, interferon-γ, and TNF-α, with subsequent mortality from severe lung injury. Similarly, in comparison to the resistant C57BL/6 mice, up-regulation of CCL3 and CCL11 was seen in the SeV-infected DBA/2 mice [11]. …”

Section: Introductionmentioning

confidence: 99%

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Local production of CCL3, CCL11, and IFN-γ correlates with disease severity in murine parainfluenza virus infection

Suryadevara

Bonville

Rosenberg

et al. 2013

Virol J

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BackgroundUsing a murine model of parainfluenza virus infection (mPIV1 or Sendai virus; SeV), we compared the inflammatory responses to lethal and sub-lethal infections in inbred DBA/2 mice.MethodsMice were intranasally inoculated with either 1.6×103 or 1.6×105 infectious units (IU) of SeV or diluent control. Clinical data including daily weights, oxygen saturation, and lung function via whole body plethysmography were collected on days 0, 3–7, and 9–14. Clarified whole lung homogenates were evaluated for inflammatory markers by enzyme-linked immunoassay (ELISA). Data were analyzed using ANOVA or Student t-tests, as appropriate.ResultsMice inoculated with 1.6×105 IU of SeV developed a lethal infection with 100% mortality by day 7, while mice inoculated with 1.6×103 IU developed a clinically significant infection, with universal weight loss but only 32% mortality. Interestingly, peak virus recovery from the lungs of mice inoculated with 1.6×105 IU of SeV did not differ substantially from that detected in mice that received the 100-fold lower inoculum. In contrast, concentrations of CCL5 (RANTES), CCL11 (eotaxin), interferon-γ, CXCL10 (IP-10), and CCL3 (MIP-1α) were significantly higher in lung tissue homogenates from mice inoculated with 1.6×105 IU (p < 0.05). In the lethal infection, levels of CCL11, interferon- γ and CCL3 all correlated strongly with disease severity.ConclusionWe observed that severity of SeV-infection in DBA/2 mice was not associated with virus recovery but rather with the levels of proinflammatory cytokines, specifically CCL11, interferon- γ and CCL3, detected in lung tissue in response to SeV infection.

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Section: Discussionsupporting

confidence: 79%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Local production of CCL3, CCL11, and IFN-γ correlates with disease severity in murine parainfluenza virus infection

Suryadevara

Bonville

Rosenberg

et al. 2013

Virol J

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“…Virus preparations were evaluated for purity by electron microscopy and quantified using a latex sphere standard as previously described. 28 To derive the virus particle number per milliliter using an alternate method that was determined comparable to electron microscopy, total viral RNA was extracted for quantitative reverse transcription-polymerase chain reaction (qRT-PCR) analysis 29 using the reported molecular weight of the genome RNA (3.3 3 10 6 ). The DENV viability was measured by Vero cell infectivity using standard plaque assays.…”

Section: Denv Purificationmentioning

confidence: 99%

“…Two-step qRT-PCR was conducted as previously described 29 except DENV RNA was extracted from homogenized platelet pellets using TRIzol reagent. DENV RNA was purified with RNeasy Micro Kit and further incubated with Turbo DNase to digest and eliminate DNA.…”

Section: Dengue Virus Rna Quantificationmentioning

confidence: 99%

Dengue virus binding and replication by platelets

Simon

Sutherland

Pryzdial

2015

Blood

143

161

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Key Points• Platelets replicate and produce infectious DENV.• DENV binds directly to platelets using DC-SIGN and heparan sulfate proteoglycan as primary receptors.Dengue virus (DENV) infection causes ∼200 million cases of severe flulike illness annually, escalating to life-threatening hemorrhagic fever or shock syndrome in ∼500 000. Although thrombocytopenia is typical of both mild and severe diseases, the mechanism triggering platelet reduction is incompletely understood. As a probable initiating event, direct purified DENV-platelet binding was followed in the current study by quantitative reverse transcription-polymerase chain reaction and confirmed antigenically. Approximately 800 viruses specifically bound per platelet at 37°C. Fewer sites were observed at 25°C, the blood bank storage temperature (∼350 sites), or 4°C, known to attenuate virus cell entry (∼200 sites). Dendritic cell-specific intercellular adhesion molecule-3-grabbing nonintegrin (DC-SIGN) and heparan sulfate proteoglycan were implicated as coreceptors because only the combination of anti-DC-SIGN and lowmolecular-weight heparin prevented binding. Interestingly, at 37°C and 25°C, platelets replicated the positive sense single-stranded RNA genome of DENV by up to ∼4-fold over 7 days. Further time course experiments demonstrated production of viral NS1 protein, which is known to be highly antigenic in patient serum. The infectivity of DENV intrinsically decayed in vitro, which was moderated by plateletmediated generation of viable progeny. This was shown using a transcription inhibitor and confirmed by freeze-denatured platelets being incapable of replicating the DENV genome. For the first time, these data demonstrate that platelets directly bind DENV saturably and produce infectious virus. Thus, expression of antigen encoded by DENV is a novel consideration in the pathogen-induced thrombocytopenia mechanism. These results furthermore draw attention to the possibility that platelets may produce permissive RNA viruses in addition to DENV. (Blood. 2015;126(3):378-385)

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Verification of genetic loci responsible for the resistance/susceptibility to the Sendai virus infection using congenic mice

Abbas

Torigoe

Kameda

et al. 2018

Infection, Genetics and Evolution

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Sendai virus (SeV) is one of the most important pathogens in the specific-pathogen free rodents. It is known that there are some inbred mouse strains susceptible or resistant to SeV infection. The C57BL/6 (B6) and DBA/2 (D2) mice are representative of the resistant and susceptible strains, respectively. Previous study with the quantitative trait locus (QTL) analysis identified three QTLs responsible for resistance or susceptibility to SeV infection on different chromosomes and indicated that resistance or susceptibility to SeV infection was almost predicted by genotypes of these three QTLs. In this paper, to verify the above hypothesis, congenic lines were generated as follows; B6-congenic lines carrying one of the D2 alleles of three QTLs and combination of these three QTLs, and D2-congenic lines carrying single or combination of B6 alleles of three QTLs. All these congenic lines were then challenged with SeV infection. D2 congenic lines introgressed single or combination of B6 alleles of QTLs changed to resistance to SeV infection. Especially, a D2 triple-congenic line became resistant as similar level to B6-parental strain. However, B6-congenic lines introgressed single or combination of D2 alleles of QTLs all remained to be resistant to SeV infection. Both IL-6 and TNF-α in broncho-alveolar lavage fluid of D2 triple-congenic line were decreased to the similar level of B6 mice, suggesting that this is a part of factors that D2 triple-congenic line became resistant to the similar level of B6 mice. Data obtained from these congenic mice verified that three QTLs identified previously were indeed responsible for the resistance/susceptibility to SeV infection in B6 and D2 mice.

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Distinctive and critical roles for cellular immunity and immune-inflammatory response in the immunopathology of Sendai virus infection in mice

Cited by 6 publications

References 49 publications

Local production of CCL3, CCL11, and IFN-γ correlates with disease severity in murine parainfluenza virus infection

Local production of CCL3, CCL11, and IFN-γ correlates with disease severity in murine parainfluenza virus infection

Dengue virus binding and replication by platelets

Verification of genetic loci responsible for the resistance/susceptibility to the Sendai virus infection using congenic mice

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