Cellular mechanisms involved in protection and recovery from influenza virus infection in immunodeficient mice

Bot, Adrian; Reichlin, Amy; Isobe, H; Bot, Simona; Schulman, Jerome L.; Yokoyama, Wayne M.; Bona, Constantin A.

doi:10.1128/jvi.70.8.5668-5672.1996

Cited by 49 publications

(16 citation statements)

References 25 publications

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“…Although recent studies demonstrated that cytotoxic T cells closely contributed to the elimination of pulmonary virus in the late phase in mice infected with influenza virus (3,6), it was also reported that the cooperative responses with antibody and cytotoxic T cells effectively contributed to the virus elimination (21,26) and that antibody response could also contribute to recovery from a pulmonary influenza virus infection (31). The most recent study showed that H5N1 influenza virus, a virulent strain for human and mouse, caused the systemic lethal infection with drastic lymphocytopenia (37).…”

Section: Discussionmentioning

confidence: 99%

Inhibitory Role of Neutrophils on Influenza Virus Multiplication in the Lungs of Mice

Fujisawa

2001

Microbiology and Immunology

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Abstract:The protective role of neutrophils on intranasal infection of influenza virus was investigated in 3 strains of tumor-bearing mice with neutrophilic leukocytosis. In vitro multiplication of influenza virus was inhibited by neutrophils from both normal and tumor-bearing mice, and the inhibitory effect of neutrophils was augmented by an addition of fMLP to the culture. Pulmonary virus infectivities in the early phase after infection decreased in such ICR and BALB/c mice, and virus elimination in the late phase was accelerated in the ICR mice. However, no decrease in pulmonary virus infectivity was observed in tumor-bearing C57BU6 mice. Intranasal administration of fMLP into normal and tumor-bearing C57BU6 mice after infection significantly inhibited the virus propagation in the lungs. The decrease in neutrophil infiltration into the lung in tumor-bearing C57BLl6 mice was confirmed from histological observations of the lung and lung lavage after infection and from analysis of the neutrophil chemotactic activity induced by fMLP. This might be responsible for the high level of pulmonary virus titer in tumor-bearing C57BLl6 mice. Phagocytic activities of alveolar macrophages and productions of neutralizing antibody were suppressed in the 3 strains of tumor-bearing mice. These observations indicated that neutrophils could be significant effector cells as a host defense mechanism against influenza virus infection in vivo, and infiltration and functional activation of neutrophils could playa significant role in virus elimination from the infected site. Furthermore, the inhibition of virus propagation by neutrophils in vitro was almost completely abrogated by an addition of ZnS04' suggesting that calprotectin could inhibit influenza virus multiplication.

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Section: Discussionmentioning

confidence: 99%

Inhibitory Role of Neutrophils on Influenza Virus Multiplication in the Lungs of Mice

Fujisawa

2001

Microbiology and Immunology

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“…For investigating the immune response against influenza viruses, the HI assay determines protective humoral responses (8). Finally, in addition to HI assay results, assessment of the human T-cell responses against influenza virus infection has been reported previously to provide an important marker of protection (3,10,22). Until now, these assays have been performed mostly by applying live virus, hence necessitating the use of BSL-3 conditions for studying (potential) pandemic influenza virus.…”

Section: Introduction Of a New Influenza Virus In Humans Urges Quick mentioning

confidence: 99%

Influenza Virus Inactivation for Studies of Antigenicity and Phenotypic Neuraminidase Inhibitor Resistance Profiling

et al. 2010

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Introduction of a new influenza virus in humans urges quick analysis of its virological and immunological characteristics to determine the impact on public health and to develop protective measures for the human population. At present, however, the necessity of executing pandemic influenza virus research under biosafety level 3 (BSL-3) high-containment conditions severely hampers timely characterization of such viruses. We tested heat, formalin, Triton X-100, and ␤-propiolactone treatments for their potencies in inactivating human influenza A(H3N2) and avian A(H7N3) viruses, as well as seasonal and pandemic A(H1N1) virus isolates, while allowing the specimens to retain their virological and immunological properties. Successful heat inactivation coincided with the loss of hemagglutinin (HA) and neuraminidase (NA) characteristics, and ␤-propiolactone inactivation reduced the hemagglutination titer and NA activity of the human influenza virus 10-fold or more. Although Triton X-100 treatment resulted in inconsistent HA activity, the NA activities in culture supernatants were enhanced consistently. Nonetheless, formalin treatment permitted the best retention of HA and NA properties. Triton X-100 treatment proved to be the easiest-to-use influenza virus inactivation protocol for application in combination with phenotypic NA inhibitor susceptibility assays, while formalin treatment preserved B-cell and T-cell epitope antigenicity, allowing the detection of both humoral and cellular immune responses. In conclusion, we demonstrated successful influenza virus characterization using formalin-and Triton X-100-inactivated virus samples. Application of these inactivation protocols limits work under BSL-3 conditions to virus culture, thus enabling more timely determination of public health impact and development of protective measures when a new influenza virus, e.g., pandemic A(H1N1)v virus, is introduced in humans.

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“…Recovery from influenza infection is dependent on the recruitment of proinflammatory leukocytes to sites of infection [9,10]. In particular, virus-specific T cells are essential for the clearance of influenza virus.…”

Section: Introductionmentioning

confidence: 99%

Chemokine expression during the development and resolution of a pulmonary leukocyte response to influenza A virus infection in mice

Wareing

Lyon

Liu

et al. 2004

Journal of Leukocyte Biology

161

150

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Influenza A virus replicates in the respiratory epithelium and induces an inflammatory infiltrate comprised of mononuclear cells and neutrophils. To understand the development of the cell-mediated immune response to influenza and how leukocyte trafficking to sites of inflammation is regulated, we examined the chemokine expression pattern in lung tissue from A/PR/8/34-infected C57BL/6 mice using an RNase protection assay. Monocyte chemoattractant protein 1, macrophage inflammatory protein 1alpha (MIP-1alpha), MIP-1beta, MIP-3alpha, regulated on activation, normal T expressed and secreted (RANTES), MIP-2, and interferon-inducible protein 10 (IP-10) mRNA expression was up-regulated between days 5 and 15 after infection, consistent with a role for these chemokines in leukocyte recruitment to the lung. Low levels of expression were detected for the CC chemokine receptors (CCR)2 and CCR5, whereas CXC chemokine receptor (CXCR)3 was significantly up-regulated by day 10 after infection, coinciding with peak inflammatory cell infiltration in the airways. As RANTES, IP-10, and their receptors were up-regulated during influenza virus infection, we investigated leukocyte recruitment and viral clearance in mice deficient in RANTES or CXCR3, the receptor for IP-10. Leukocyte recruitment and viral replication in influenza-infected RANTES knockout(-/-) mice were similar to that in control mice, showing that RANTES is not essential for the immune response to influenza infection. Similarly, leukocyte recruitment and viral replication in CXCR3-/- mice were identical to control mice, except at day 8 postinfection, where fewer lymphocytes, neutrophils, and eosinophils were detected in the bronchoalveolar lavage of CXCR3-/- mice. These studies suggest that although the chemokines detected may play a role in regulating leukocyte trafficking to the lung during influenza infection, some may be functionally redundant.

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Cellular mechanisms involved in protection and recovery from influenza virus infection in immunodeficient mice

Cited by 49 publications

References 25 publications

Inhibitory Role of Neutrophils on Influenza Virus Multiplication in the Lungs of Mice

Inhibitory Role of Neutrophils on Influenza Virus Multiplication in the Lungs of Mice

Influenza Virus Inactivation for Studies of Antigenicity and Phenotypic Neuraminidase Inhibitor Resistance Profiling

Chemokine expression during the development and resolution of a pulmonary leukocyte response to influenza A virus infection in mice

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