The Generation of ‘Cytotoxic’ Macrophages in Mice during Infection with Influenza A or Sendai Virus

Mak, Nai‐Ki; Leung, Ka Nang; Ada, G. L.

doi:10.1111/j.1365-3083.1982.tb00683.x

Cited by 22 publications

(8 citation statements)

References 18 publications

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“…or i.n. inoculation of mice with influenza virus 12 . BJx109, but not PR8, induced the recruitment and activation of MΦ in the peritoneal cavity as indicated by (i) the tumouricidal activity of day 5 PECs from BJx109‐injected mice against the MΦ‐sensitive P815 cell line (Figure 5a), (ii) the ability of day 5 PECs from BJx109‐inoculated mice to produce high levels of nitrite (as a measure of NO production) following overnight culture (Figure 5b), and (iii) enhanced expression of Class II MHC and co‐stimulatory molecules CD80 and CD86 (Figure 5c) on F4/80 + MΦ from BJx109‐inoculated mice.…”

Section: Resultsmentioning

confidence: 99%

Influenza viruses differ in ability to infect macrophages and to induce a local inflammatory response following intraperitoneal injection of mice

et al. 2010

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Strains of influenza A virus show marked differences in their ability to infect murine macrophages (MU) such that strain A/PR/8/34 (PR8; H1N1) infects MU poorly while strain BJx109 (H3N2) infects MU to high levels. Given the central role of MU in initiating and regulating inflammatory responses, we hypothesized that virus strains that infect MU poorly may also be poor at initiating inflammatory responses. Studies to compare the inflammatory response of mice after intranasal inoculation with either BJx109 or PR8 were confounded by the rapid growth of the PR8 virus in lung tissues. Consequently, we have characterized the cellular inflammatory response following inoculation into the peritoneal cavity, as influenza viruses do not replicate at this site. Herein, we report marked differences in the local inflammatory response to BJx109 or PR8 in the peritoneal cavity with strain PR8 being particularly poor in its ability to recruit and activate peritoneal leukocytes, including NK cells and MU. In vitro BJx109, but not PR8, stimulated release of high levels of type I IFNs and TNF-a from PEC MU, and treatment of mice with neutralizing antibodies to either cytokine inhibited the ability of BJx109 to recruit and activate NK cells and MUs in the peritoneal cavity. Together, these data suggest that the ability of influenza virus strains to infect MU and stimulate cytokine release is an important factor governing the nature of the acute inflammatory response.

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Section: Resultsmentioning

confidence: 99%

Influenza viruses differ in ability to infect macrophages and to induce a local inflammatory response following intraperitoneal injection of mice

et al. 2010

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“…The pathology of influenza in the mouse is immune mediated (32), with a substantial contribution from delayed-type hypersensitivity T lymphocytes (15), whereas other categories of cells, i.e., NK cells (11), "cytotoxic" macrophages (16), and cytotoxic T lymphocytes (34) …”

Section: Discussionmentioning

confidence: 99%

Enhancement of bronchoalveolar cell recovery and stimulation of alveolar macrophage chemiluminescence and resistance to influenza virus after treatment with RU 41821 aerosol

Rudent¹,

Michel²,

Labarre³

et al. 1987

Antimicrob Agents Chemother

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Aerosol treatment with RU 41821, a glycoprotein extract from Klebsiella pneumoniae, was tested in mice for its effect on the kinetics of the induction of bronchoalveolar cells (i.e., alveolar macrophages, monocytes, lymphocytes, and polymorphonuclear leukocytes). RU 41821 led to an increase in the total number of bronchoalveolar celis. The largest increase was observed for polymorphonuclear leukocytes, and more moderate increases occurred in the numbers of alveolar macrophages, monocytes, and lymphocytes. The alveolar macrophages recruited in response to RU 41821 were activated, as indicated by luminol-dependent chemiluminescence in response to stimulation by opsonized zymosan. The effects of five RU 41821 aerosol treatments and those of a single treatment were further examined in vivo by aerosol infection of mice inoculated with a mouse-pathogenic influenza virus. The maximum protective effect was obtained after five once-a-day treatments and was correlated with the largest increase in the total number of bronchoalveolar cells.

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“…The virus causes the activation and maturation of dendritic cells and stimulates plasmacytoid dendritic cells to secrete large amounts of type I IFNs (López et al 2004;Cella et al 2000). Influenza virus activates macrophages to secrete IL-1, 6 and 12 and TNF-a (Mak et al 1982;Pirhonen et al 1999). IL-12 in turn induces IFN-g production by NK cells.…”

Section: Innate Immunitymentioning

confidence: 96%

Pandemic Influenza Vaccines

DiMenna

Ertl

2009

Current Topics in Microbiology and Immunology

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Since their compositions remain uncertain, universal pandemic vaccines are yet to be created. They would aim to protect globally against pandemic influenza viruses that have not yet evolved. Thus they differ from seasonal vaccines to influenza virus, which are updated annually in spring to incorporate the latest circulating viruses, and are then produced and delivered before the peak influenza season starts in late fall and winter. The efficacy of seasonal vaccines is linked to their ability to induce virus-neutralizing antibodies, which provide subtype-specific protection against influenza A viruses. If pandemic vaccines were designed to resemble current vaccines in terms of composition and mode of action, they would have to be developed, tested, and mass-produced after the onset of a pandemic, once the causative virus had been identified. The logistic problems of generating a pandemic vaccine from scratch, conducting preclinical testing, and producing billions of doses within a few months for global distribution are enormous and may well be insurmountable. Alternatively, the scientific community could step up efforts to generate a universal vaccine against influenza A viruses that provides broadly cross-reactive protection through the induction of antibodies or T cells to conserved regions of the virus.

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The Generation of ‘Cytotoxic’ Macrophages in Mice during Infection with Influenza A or Sendai Virus

Cited by 22 publications

References 18 publications

Influenza viruses differ in ability to infect macrophages and to induce a local inflammatory response following intraperitoneal injection of mice

Influenza viruses differ in ability to infect macrophages and to induce a local inflammatory response following intraperitoneal injection of mice

Enhancement of bronchoalveolar cell recovery and stimulation of alveolar macrophage chemiluminescence and resistance to influenza virus after treatment with RU 41821 aerosol

Pandemic Influenza Vaccines

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