RGD Reference Report - Pulmonary eosinophilia requires interleukin-5, eotaxin-1, and CD4+ T cells in mice immunized with respiratory syncytial virus G glycoprotein. - Rat Genome Database

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Pulmonary eosinophilia requires interleukin-5, eotaxin-1, and CD4+ T cells in mice immunized with respiratory syncytial virus G glycoprotein.

Authors: Johnson, TR  Rothenberg, ME  Graham, BS 
Citation: Johnson TR, etal., J Leukoc Biol. 2008 Sep;84(3):748-59. Epub 2008 Jun 2.
RGD ID: 4890941
Pubmed: PMID:18519743   (View Abstract at PubMed)
PMCID: PMC2516895   (View Article at PubMed Central)
DOI: DOI:10.1189/jlb.0907621   (Journal Full-text)

Severe illness, type 2 cytokine production, and pulmonary eosinophilia are adverse immune responses resulting from respiratory syncytial virus (RSV) challenge of vvGs-immunized mice. We have shown IL-4 and IL-13 activity must be simultaneously inhibited to reduce disease severity. We now address the contributions of IL-5, eotaxin-1, and CD4+ and CD8+ T cells to the induction of disease-enhancing immune responses. Depletion of CD4+ T cells during immunization prevented IL-4, IL-13, and eotaxin-1 production, diminished eosinophilia, and reduced weight loss. Conversely, CD8+ T cell depletion did not decrease eosinophilia, weight loss, or type 2 cytokines but did dramatically reduce mucus production and increase eotaxin production. Anti-IL-5 administration at immunization or challenge significantly decreased pulmonary eosinophilia. Strikingly, there were not concomitant decreases in weight loss. Following RSV challenge eotaxin-1-deficient mice immunized with vvGs exhibited significantly less eosinophilia without decreased weight loss or type 2 cytokine production. We conclude CD4+ T cell production of IL-5 and induction of eotaxin-1 are required for vvGs-induced eosinophilia following RSV challenge, while CD8+ T cells appear to down-regulate eotaxin-1 and mucus production. In summary, we demonstrate that pulmonary eosinophilia 1) is a by-product of memory CD4+ T cell activation, 2) does not necessarily correlate with mucus production, and, most importantly, 3) is not required for the RSV G-induced illness in mice. These findings have important implications for the evaluation of candidate RSV vaccines.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
IL5Humanpulmonary eosinophilia  ISOIl5 (Mus musculus)associated with respiratory syncytial virus infectionRGD 
Il5Ratpulmonary eosinophilia  ISOIl5 (Mus musculus)associated with respiratory syncytial virus infectionRGD 
Il5Mousepulmonary eosinophilia  IMP associated with respiratory syncytial virus infectionRGD 

Objects Annotated

Genes (Rattus norvegicus)
Il5  (interleukin 5)

Genes (Mus musculus)
Il5  (interleukin 5)

Genes (Homo sapiens)
IL5  (interleukin 5)


Additional Information