Association of Tumor Necrosis Factor-.ALPHA. with Fever and Pulmonary Lesion Score in Pigs Experimentally Infected with Swine Influenza Virus Subtype H1N2

Kim, Bongtae; Ahn, Kwangseog; Ha, Yoon‐Cheol; Lee, Yong Hoon; Kim, Duyeol; Lim, Jeong Han; Kim, Sung Hoon; Kim, Miyoung; Cho, Kyung-Dong; Lee, Bog‐Hieu; Chae, Chanhee

doi:10.1292/jvms.71.611

Cited by 20 publications

(12 citation statements)

References 19 publications

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“…24 In our cases, expression in the lung of IFNc by small mononucleated cells and TNFa by macrophages and AECs was low. This finding may be supported by Kim and colleagues, 25 who described in S-OIV infection, maximal indices of TNFa expression in lungs of infected pigs in the first days of the infection and then a gradual decrease.…”

Section: Discussionsupporting

confidence: 70%

Pathological and ultrastructural analysis of surgical lung biopsies in patients with swine-origin influenza type A/H1N1 and acute respiratory failure

Capelozzi

Parra

Ximenes

et al. 2010

Clinics

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BACKGROUND:Cases of H1N1 and other pulmonary infections evolve to acute respiratory failure and death when co‐infections or lung injury predominate over the immune response, thus requiring early diagnosis to improve treatment.OBJECTIVE:To perform a detailed histopathological analysis of the open lung biopsy specimens from five patients with ARDS with confirmed H1N1.METHODS:Lung specimens underwent microbiologic analysis, and examination by optical and electron microscopy. Immunophenotyping was used to characterize macrophages, natural killer, T and B cells, and expression of cytokines and iNOS.RESULTS:The pathological features observed were necrotizing bronchiolitis, diffuse alveolar damage, alveolar hemorrhage and abnormal immune response. Ultrastructural analysis showed viral‐like particles in all cases.CONCLUSIONS:Viral‐like particles can be successfully demonstrated in lung tissue by ultrastructural examination, without confirmation of the virus by RT‐PCR on nasopharyngeal aspirates. Bronchioles and epithelium, rather than endothelium, are probably the primary target of infection, and diffuse alveolar damage the consequence of the effect of airways obliteration and dysfunction on innate immunity, suggesting that treatment should be focused on epithelial repair.

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Section: Discussionsupporting

confidence: 70%

Pathological and ultrastructural analysis of surgical lung biopsies in patients with swine-origin influenza type A/H1N1 and acute respiratory failure

Capelozzi

Parra

Ximenes

et al. 2010

Clinics

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“…TNF is an important antiviral cytokine which has been shown to inhibit influenza viral replication in porcine lung epithelial cells in vitro and have greater effect against influenza virus replication than IFN-α and IFN-γ [48]. The levels of TNF in the respiratory tract correlates with pulmonary lesion scores and clinical disease in pigs [17], [18] and with body temperature in humans [19], indicating an important link with the induction of clinical signs [17], [18]. Unfortunately, TNF was only investigated on mRNA level on the total mononuclear cell population and the relative contribution of NK cells cannot be concluded.…”

Section: Discussionmentioning

confidence: 99%

Early Responses of Natural Killer Cells in Pigs Experimentally Infected with 2009 Pandemic H1N1 Influenza A Virus

et al. 2014

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Natural killer (NK) cells are important players in the innate immune response against influenza A virus and the activating receptor NKp46, which binds hemagglutinin on the surface of infected cells, has been assigned a role in this context. As pigs are natural hosts for influenza A viruses and pigs possess both NKp46− and NKp46+ NK cells, they represent a good animal model for studying the role of the NKp46 receptor during influenza. We explored the role of NK cells in piglets experimentally infected with 2009 pandemic H1N1 influenza virus by flow cytometric analyses of cells isolated from blood and lung tissue and by immunostaining of lung tissue sections. The number of NKp46+ NK cells was reduced while NKp46− NK cells remained unaltered in the blood 1–3 days after infection. In the lungs, the intensity of NKp46 expression on NK cells was increased during the first 3 days, and areas where influenza virus nucleoprotein was detected were associated with increased numbers of NKp46+ NK cells when compared to uninfected areas. NKp46+ NK cells in the lung were neither found to be infected with influenza virus nor to be undergoing apoptosis. The binding of porcine NKp46 to influenza virus infected cells was verified in an in vitro assay. These data support the involvement of porcine NKp46+ NK cells in the local immune response against influenza virus.

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“…However, fever is the most significant clinical feature in influenza virus infection. It was predicted that the cause of fever would be pyrogenic cytokines including tumor necrosis factor-α, interleukin, and interferon [11]. …”

Section: Introductionmentioning

confidence: 99%

Association between nasal shedding and fever that influenza A (H3N2) induces in dogs

Song

Moon

Jung

et al. 2011

Virol J

188

136

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BackgroundAvian origin canine influenza virus was reported in Korea. The dog to dog contact transmission of the avian origin canine influenza virus (CIV) H3N2 and CIV H3N8 was shown by experimental contact transmission. This study was focused on viral excretion and fever in order to elucidate the epidemiological associations which might be helpful to control the disease transmissions in CIV outbreak in dogs.MethodsAn influenza seronegative 10-week-old Beagle dog was experimentally inoculated with the canine influenza virus A/canine/01/2007, subtype H3N2. Eight hours after inoculation, the infected dog was cohoused with seven uninfected Beagle dogs. Clinical signs including fever were recorded for 14 days post inoculation.ResultsThe infected dog and four of seven contact dogs in the study showed clinical signs (sneezing, nasal discharge and coughing) during the study. Viral shedding occurred in all of the animals tested and began on 1 to 6 DPI in dogs with clinical signs. Elevated body temperatures above 39.5°C (geometric mean temperature of 39.86°C±0.49) were observed in all symptomatic dogs. The mean viral titer during fever was 2.99 log EID50/ml, which was significantly higher than the viral titer detected in the non fever.ConclusionsThe data show that contact dogs with a canine influenza infected dog shed different levels of virus in their nasal excretions and demonstrate that clinical signs, including fever, significantly correlate with the viral shedding.

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Association of Tumor Necrosis Factor-.ALPHA. with Fever and Pulmonary Lesion Score in Pigs Experimentally Infected with Swine Influenza Virus Subtype H1N2

Cited by 20 publications

References 19 publications

Pathological and ultrastructural analysis of surgical lung biopsies in patients with swine-origin influenza type A/H1N1 and acute respiratory failure

Pathological and ultrastructural analysis of surgical lung biopsies in patients with swine-origin influenza type A/H1N1 and acute respiratory failure

Early Responses of Natural Killer Cells in Pigs Experimentally Infected with 2009 Pandemic H1N1 Influenza A Virus

Association between nasal shedding and fever that influenza A (H3N2) induces in dogs

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