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Allergic eosinophil-rich inflammation develops in lungs and airways of B cell-deficient mice.

Korsgren M, Erjefält JS, Korsgren O, Sundler F, Persson CG - J. Exp. Med. (1997)

Bottom Line: Immunoglobulins (Ig), particularly IgE, are believed to be crucially involved in the pathogenesis of asthma and, equally, in allergic models of the disease.The eosinophilia extended to the regional lymph nodes.TEM confirmed the subepithelial and perivascular localization of eosinophils.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology and Neuroscience, Lund University Hospital, Sweden.

ABSTRACT
Immunoglobulins (Ig), particularly IgE, are believed to be crucially involved in the pathogenesis of asthma and, equally, in allergic models of the disease. To validate this paradigm we examined homozygous mutant C57BL/6 mice, which are B cell deficient, lacking all Ig. Mice were immunized intraperitoneally with 10 micrograms ovalbumin (OVA) plus alum, followed by daily (day 14-20) 30 min exposures to OVA aerosol (OVA/OVA group). Three control groups were run: OVA intraperitoneally plus saline (SAL) aerosol (OVA/SAL group); saline intraperitoneally plus saline aerosol; saline intraperitoneally plus OVA aerosol (n = 6-7). Lung and large airway tissues obtained 24 h after the last OVA or SAL exposure were examined by light microscopy and transmission electron microscopy (TEM). The Ig-deficient mice receiving OVA/ OVA treatment had swollen and discolored lungs and exhibited marked eosinophilia both in large airway subepithelial tissue (49.2 +/- 12.0 cells/mm basement membrane [BM] versus OVA/ SAL control 1.2 +/- 0.3 cells/mm BM; P < 0.001), and perivascularly and peribronchially in the lung (49.3 +/- 9.0 cells/unit area versus OVA/SAL control 2.6 +/- 0.6 cells/unit area; P < 0.001). The eosinophilia extended to the regional lymph nodes. TEM confirmed the subepithelial and perivascular localization of eosinophils. Mucus cells in large airway epithelium increased from 1.5 +/- 0.8 (OVA/SAL mice) to 39.5 +/- 5.7 cells/mm BM in OVA/OVA treated mice (P < 0.001). OVA/SAL mice never differed from the other control groups. Corresponding experiments in wild-type mice (n = 6-7 in each group) showed qualitatively similar but less pronounced eosinophil and mucus cell changes. Macrophages and CD4+ T cells increased in lungs of all OVA/OVA-treated mice. Mast cell number did not differ but degranulation was detected only in OVA/OVA-treated wild-type mice. Immunization to OVA followed by OVA challenges thus cause eosinophil-rich inflammation in airways and lungs of mice without involvement of B cells and Ig.

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Transmission electron micrographs showing the  tracheal epithelium in Ig-deficient  mice. The tracheal epithelium in  SAL/SAL-treated animals (a) harbored only few scattered cells  containing mucus granules. In  contrast, OVA/OVA-treated  mice (b) exhibited an epithelium  with numerous mucus granule– containing cells (arrows), often  protruding into the airway lumen. Bars, 10 μm.
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Figure 3: Transmission electron micrographs showing the tracheal epithelium in Ig-deficient mice. The tracheal epithelium in SAL/SAL-treated animals (a) harbored only few scattered cells containing mucus granules. In contrast, OVA/OVA-treated mice (b) exhibited an epithelium with numerous mucus granule– containing cells (arrows), often protruding into the airway lumen. Bars, 10 μm.

Mentions: In OVA/OVA-treated animals (both B cell–deficient and wild-type mice) there was a marked increase in airway epithelial mucus cells (Table 1) and the height of the epithelium appeared to be increased (Fig. 3). The OVA/OVA-treated animals further differed from controls by partial or seemingly complete occlusion of many smaller airways with viscid PAS-positive mucus plugs (Fig. 4). TEM examination of SAL/SAL-treated animals revealed only few cells containing mucus granules (see Fig. 3 a), whereas OVA/OVA-treated mice (both B cell deficient and wild type) exhibited an epithelium with numerous mucus granule–containing cells protruding into the airway lumen (see Fig. 3 b).


Allergic eosinophil-rich inflammation develops in lungs and airways of B cell-deficient mice.

Korsgren M, Erjefält JS, Korsgren O, Sundler F, Persson CG - J. Exp. Med. (1997)

Transmission electron micrographs showing the  tracheal epithelium in Ig-deficient  mice. The tracheal epithelium in  SAL/SAL-treated animals (a) harbored only few scattered cells  containing mucus granules. In  contrast, OVA/OVA-treated  mice (b) exhibited an epithelium  with numerous mucus granule– containing cells (arrows), often  protruding into the airway lumen. Bars, 10 μm.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2196175&req=5

Figure 3: Transmission electron micrographs showing the tracheal epithelium in Ig-deficient mice. The tracheal epithelium in SAL/SAL-treated animals (a) harbored only few scattered cells containing mucus granules. In contrast, OVA/OVA-treated mice (b) exhibited an epithelium with numerous mucus granule– containing cells (arrows), often protruding into the airway lumen. Bars, 10 μm.
Mentions: In OVA/OVA-treated animals (both B cell–deficient and wild-type mice) there was a marked increase in airway epithelial mucus cells (Table 1) and the height of the epithelium appeared to be increased (Fig. 3). The OVA/OVA-treated animals further differed from controls by partial or seemingly complete occlusion of many smaller airways with viscid PAS-positive mucus plugs (Fig. 4). TEM examination of SAL/SAL-treated animals revealed only few cells containing mucus granules (see Fig. 3 a), whereas OVA/OVA-treated mice (both B cell deficient and wild type) exhibited an epithelium with numerous mucus granule–containing cells protruding into the airway lumen (see Fig. 3 b).

Bottom Line: Immunoglobulins (Ig), particularly IgE, are believed to be crucially involved in the pathogenesis of asthma and, equally, in allergic models of the disease.The eosinophilia extended to the regional lymph nodes.TEM confirmed the subepithelial and perivascular localization of eosinophils.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology and Neuroscience, Lund University Hospital, Sweden.

ABSTRACT
Immunoglobulins (Ig), particularly IgE, are believed to be crucially involved in the pathogenesis of asthma and, equally, in allergic models of the disease. To validate this paradigm we examined homozygous mutant C57BL/6 mice, which are B cell deficient, lacking all Ig. Mice were immunized intraperitoneally with 10 micrograms ovalbumin (OVA) plus alum, followed by daily (day 14-20) 30 min exposures to OVA aerosol (OVA/OVA group). Three control groups were run: OVA intraperitoneally plus saline (SAL) aerosol (OVA/SAL group); saline intraperitoneally plus saline aerosol; saline intraperitoneally plus OVA aerosol (n = 6-7). Lung and large airway tissues obtained 24 h after the last OVA or SAL exposure were examined by light microscopy and transmission electron microscopy (TEM). The Ig-deficient mice receiving OVA/ OVA treatment had swollen and discolored lungs and exhibited marked eosinophilia both in large airway subepithelial tissue (49.2 +/- 12.0 cells/mm basement membrane [BM] versus OVA/ SAL control 1.2 +/- 0.3 cells/mm BM; P < 0.001), and perivascularly and peribronchially in the lung (49.3 +/- 9.0 cells/unit area versus OVA/SAL control 2.6 +/- 0.6 cells/unit area; P < 0.001). The eosinophilia extended to the regional lymph nodes. TEM confirmed the subepithelial and perivascular localization of eosinophils. Mucus cells in large airway epithelium increased from 1.5 +/- 0.8 (OVA/SAL mice) to 39.5 +/- 5.7 cells/mm BM in OVA/OVA treated mice (P < 0.001). OVA/SAL mice never differed from the other control groups. Corresponding experiments in wild-type mice (n = 6-7 in each group) showed qualitatively similar but less pronounced eosinophil and mucus cell changes. Macrophages and CD4+ T cells increased in lungs of all OVA/OVA-treated mice. Mast cell number did not differ but degranulation was detected only in OVA/OVA-treated wild-type mice. Immunization to OVA followed by OVA challenges thus cause eosinophil-rich inflammation in airways and lungs of mice without involvement of B cells and Ig.

Show MeSH
Related in: MedlinePlus