New production of eosinophils and the corresponding TH1/TH2 balance in the lungs after allergen exposure in BALB/c and C57BL/6 mice.
Allergic asthma is associated with eosinophilic inflammation in the airways. Animal models commonly used to elucidate allergic inflammation mechanisms include BALB/c and C57BL/6 mice. Our aim was to evaluate lung eosinophilia and the corresponding Th1/Th2 balance in the two strains after allergen exposure. BALB/c and C57BL/6 mice were subjected to ovalbumin-induced allergic airway inflammation using BrdU to label newly produced cells. The numbers of new eosinophils were evaluated by differential cell count and immunocytochemistry (MBP+BrdU+). Proliferation rate of lung eosinophils was measured by analysis of CD45+CCR3+BrdU+ cells by FACS. Distribution of newly produced eosinophils in the lung and the Th1/Th2 (CD4+T-bet+/CD4+GATA-3+) balance was evaluated by immunohistochemistry. Allergen challenge with ovalbumin induced comparable eosinophilia in bone marrow (BM), blood and lung tissue in both strains of mice compared to phosphate-buffered saline controls, which was confirmed by immunocytochemistry. There was a small increase in the number of lung MBP+BrdU(-) eosinophils in C57BL/6 mice compared to BALB/c mice, which suggests a basal increase in this strain following sensitization. While there was no difference in eosinophilic proliferation in the lung, the distribution of the newly produced eosinophils differs between the two strains. BALB/c mice showed staining primarily around vessels and airways, whereas C57BL/6 mice showed a more even distribution in the lung tissue. No difference in the Th1/Th2 balance was observed between two strains. This study shows that there is a difference in the distribution of eosinophils in the lung between the C57BL/6 and BALB/c mice, but no difference in eosinophil production or Th1/Th2 balance.
Lu
Y
Y
Krefting Research Centre, Department of Internal Medicine, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Sjöstrand
M
M
Malmhäll
C
C
Rådinger
M
M
Jeurink
P
P
Lötvall
J
J
Bossios
A
A
D000485:Allergens / Q000276:immunology*; D000818:Animals; D001249:Asthma / Q000276:immunology* / Q000473:pathology; D015704:CD4 Antigens / Q000276:immunology; D004804:Eosinophils / Q000276:immunology*; D050990:GATA3 Transcription Factor / Q000276:immunology; D017493:Leukocyte Common Antigens / Q000276:immunology; D008168:Lung / Q000276:immunology* / Q000473:pathology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D010047:Ovalbumin / Q000276:immunology; D011657:Pulmonary Eosinophilia / Q000276:immunology* / Q000473:pathology; D054397:Receptors, CCR3 / Q000276:immunology; D020825:T-Box Domain Proteins / Q000276:immunology; D018417:Th1 Cells / Q000276:immunology*; D018418:Th2 Cells / Q000276:immunology*; D000098815:T-bet Transcription Factor
D000485:Allergens; D015704:CD4 Antigens; C515351:Ccr3 protein, mouse; D050990:GATA3 Transcription Factor; D054397:Receptors, CCR3; D020825:T-Box Domain Proteins; D000098815:T-bet Transcription Factor; D010047:Ovalbumin; D017493:Leukocyte Common Antigens; C516770:Ptprc protein, mouse