Analysis of the local and systemic immune responses induced in BALB/c mice by experimental respiratory syncytial virus infection

Anderson, James; Norden, Jean; Saunders, David; Toms, G. L.; Scott, Ron

doi:10.1099/0022-1317-71-7-1561

Cited by 64 publications

(47 citation statements)

References 31 publications

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“…Previous studies have indicated that RSV antigen is found only in the alveoli, but not the bronchiolar epithelium, of BALB\c mice (Taylor et al, 1984). A mild cellular infiltration of mononuclear cells and polymorphs was also observed (Anderson et al, 1990). The time-scale of infection of mice with PVM strain J3666 was similar to that reported for HRSV infection ; however, mice infected with HRSV showed no clinical signs of disease (Anderson et al, 1990 ;Taylor et al, 1984).…”

Section: Discussionsupporting

confidence: 55%

“…A mild cellular infiltration of mononuclear cells and polymorphs was also observed (Anderson et al, 1990). The time-scale of infection of mice with PVM strain J3666 was similar to that reported for HRSV infection ; however, mice infected with HRSV showed no clinical signs of disease (Anderson et al, 1990 ;Taylor et al, 1984). In our study only a few HRSV-infected alveolar and bronchial epithelium cells were seen by in situ hybridization.…”

Section: Discussionmentioning

confidence: 55%

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Pathogenesis of pneumovirus infections in mice: detection of pneumonia virus of mice and human respiratory syncytial virus mRNA in lungs of infected mice by in situ hybridization.

Cook

Eglin

Easton³

1998

Journal of General Virology

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The pathogenesis of pneumonia virus of mice (PVM) and human respiratory syncytial virus (HRSV) in BALB/c mice were investigated by using in situ hybridization to detect virus mRNA in fixed lung sections. Following intranasal inoculation with 120 p.f.u. PVM the pattern of hybridization showed that virus mRNA was initially detected within 2 days in alveolar cells. As the infection progressed the number of hybridizing alveolar cells increased and signal was also detected in cells lining the terminal bronchioles. By days 4 to 5 post-infection areas of morphological abnormality could be seen, particularly in the strongly hybridizing regions of the lung, and this correlated with the appearance of clinical

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Section: Discussionsupporting

confidence: 55%

Section: Discussionmentioning

confidence: 55%

Pathogenesis of pneumovirus infections in mice: detection of pneumonia virus of mice and human respiratory syncytial virus mRNA in lungs of infected mice by in situ hybridization.

Cook

Eglin

Easton³

1998

Journal of General Virology

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“…The most abundant cytokine in clinical specimens from RSVinfected children is IFN-␥, and most RSV infections likely resolve via a typical antiviral Th-1-type response (2). In BALB/c mice, RSV A2 strain infection causes an increase in the number of IFN-␥-producing NK cells in bronchoalveolar lavage fluid (BALF) that precedes the BALF appearance of abundant IFN-␥-producing CD8 cells and cytotoxic T lymphocytes (CTLs) (5)(6)(7). Both CD4 ϩ and CD8 ϩ T cells exacerbate RSV-induced illness and contribute to virus clearance in primary infection of BALB/c mice (8).…”

mentioning

confidence: 99%

Differential Regulation of GM1 and Asialo-GM1 Expression by T Cells and Natural Killer (NK) Cells in Respiratory Syncytial Virus Infection

et al. 2008

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We previously reported that respiratory syncytial virus (RSV) infection increases lung CD8 ϩ T cell GM1 expression. The related lipid asialo-GM1 (ASGM1) is expressed by T cells in viral infection and by natural killer (NK) cells. The in vivo co-expression of GM1 and ASGM1 by immune cells is not defined. Here we analyzed lung lymphocyte GM1 and ASGM1 expression in RSV-infected mice. GM1 and ASGM1 were coordinately upregulated by activated CD8 ϩ T cells in RSV-infected BALB/c and C57BL/6 mice. In contrast, RSV infection had no effect on constitutively high NK cell GM1 expression, while increasing NK cell ASGM1 expression. GM1 and ASGM1 co-localized in lipid raft structures in NK and CD8 ϩ T cells sorted from the lungs of RSV-infected mice. Anti-ASGM1 Ab treatment of RSV-infected BALB/c mice depleted GM1/ASGM1-expressing NK cells and GM1/ASGM1-expressing T cells, reduced lung IFN-␥ levels, increased viral load, delayed viral clearance, and reduced illness. STAT1 Ϫ/Ϫ mice are more susceptible to RSV replication and disease than wild-type mice. In RSV-infected STAT1 Ϫ/Ϫ mice, anti-ASGM1 Ab altered cytokine levels, but in contrast to BALB/c mice, antibody treatment had no effect on viral load or illness. Taken together, GM1 and ASGM1 expression are differentially regulated by T and NK cells in RSV infection. Also, GM1/ASGM1-expressing cells are important for control of RSV in BALB/c mice, whereas STAT1 Ϫ/Ϫ mice clear RSV by an alternative pathway. 327

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“…No changes in the spleen were found after primary infection with RSV. The latter finding corresponds to the absence of RSVspecific cytotoxic T cells in the spleen until 3-4 weeks after infection [18]. The following hypothesis is suggested.…”

Section: Discussionmentioning

confidence: 94%

“…RSV-specific, MHC-restricted, cytotoxic T cells can be found in the lungs and nasal turbinates of mice or cotton rats infected with live virus [4,[16][17][18]. The cytotoxic response is maximal 7-9 days after infection [18], mainly carried by CD8+ cells [4,9] and of major importance for both viral clearance and pathogenesis of disease [8,9]. Recently, flow cytometry studies defined in more detail the phenotypic characteristics ofthe T cells activated and attracted to the lungs after primary infection with RSV [5,6,19].…”

Section: Discussionmentioning

confidence: 99%

T cell redistribution kinetics after secondary infection of BALB/c mice with respiratory syncytial virus

Kimpen

Ogra

1993

Clinical and Experimental Immunology

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SUMMARYBALB/c mice were infected intranasally with live respiratory syncytial virus (RSV) and reinfected 4 weeks later. At regular intervals thereafter groups of animals were killed and T cell subsets were determined in blood, spleen and bronchoalveolar lavage (BAL) with flow cytometry employing T cell subset-specific MoAbs. Total lymphocyte counts in the peripheral blood decreased 1-3 days after infection, returning to preinfection levels on day 8 (/" = 00111). Simultaneously, a marked increase of lymphocytes was noted in the BAL, reaching a maximum at day 8 (/'<0 0001). Both CD4+ and CD8 + T cells decreased in the blood on day 1 -3 (P < 0 0097 and P = 0 003 respectively), and increased in the BAL progressively towards a maximum at day 8 (/'<0 0001). In BAL, CD4+ cells increased 35-fold and CD8+ cells 27-fold during the first week after reinfection. On the other hand, in the spleen a significant decline of CD4+ and CD8+ cells was noted 1 day post-infection (P = 0 0002). It is concluded that a strong T cell redistribution response among systemic and mucosal tissues occurs after reinfection with RSV. The kinetics of this response differ both quantitatively and qualitatively from the T cell response after primary infection. The magnitude of cell traffic is more pronounced in blood, spleen and BAL than after primary infection. CD4+ T cells are more intensively distributed to the lungs than after primary infection.

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Analysis of the local and systemic immune responses induced in BALB/c mice by experimental respiratory syncytial virus infection

Cited by 64 publications

References 31 publications

Pathogenesis of pneumovirus infections in mice: detection of pneumonia virus of mice and human respiratory syncytial virus mRNA in lungs of infected mice by in situ hybridization.

Pathogenesis of pneumovirus infections in mice: detection of pneumonia virus of mice and human respiratory syncytial virus mRNA in lungs of infected mice by in situ hybridization.

Differential Regulation of GM1 and Asialo-GM1 Expression by T Cells and Natural Killer (NK) Cells in Respiratory Syncytial Virus Infection

T cell redistribution kinetics after secondary infection of BALB/c mice with respiratory syncytial virus

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