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Fcgamma receptors modulate pulmonary inflammation by activating innate immune cells in murine hypersensitivity pneumonitis.

Park HJ, Kim HS, Chung DH - Immune Netw (2010)

Bottom Line: The family of Fcgamma receptors (FcgammaRs) has emerged as central regulators for modulating both pro-and anti-inflammatory responses.However, the role of FcgammaRs in the development of HP has not been investigated yet.These results demonstrate that activating Fcgamma receptors play an important role in activating neutrophils and macrophages in pulmonary inflammation and inducing Th1 differentiation by regulating cytokine expression in SR-induced HP.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, Seoul National University College of Medicine, Seoul, Korea.

ABSTRACT

Background: Hypersensitivity pneumonitis (HP) is an interstitial lung disease that develops following repeated exposure to inhaled particulate antigens. The family of Fcgamma receptors (FcgammaRs) has emerged as central regulators for modulating both pro-and anti-inflammatory responses. However, the role of FcgammaRs in the development of HP has not been investigated yet.

Methods: To explore the functional roles of FcgammaRs in HP, FcgammaR(-/-) and B6 mice were challenged with Saccharopolyspora rectivirgula (SR) antigen intranasally, and compared these mice in terms of the histological change, infiltrated immune cells in BALF and in vitro immune responses.

Results: FcgammaR(-/-) mice exhibited attenuation of HP in terms of histological alterations, and reduced numbers of neutrophils and macrophages in and the increased CD4:CD8 ratio of bronchoalveolar lavage fluid. The lungs of FcgammaR(-/-) mice showed high production of Th2 cytokine such as IL-4 and slightly low production of Th1 cytokine, INF-gamma compared to those of B6 mice. However, SR-specific adaptive immune responses of FcgammaR(-/-) mice were similar to those of B6 mice.

Conclusion: These results demonstrate that activating Fcgamma receptors play an important role in activating neutrophils and macrophages in pulmonary inflammation and inducing Th1 differentiation by regulating cytokine expression in SR-induced HP.

No MeSH data available.


Related in: MedlinePlus

Hypersensitivity pneumonitis is attenuated in FcγR-/- mice compared to B6 mice in terms of histological alteration. In B6 and FcγR-/- mice, hypersensitivity pneumonitis was induced by inoculating SR antigen intranasally. These mice were sacrificed 3 weeks after HP induction. (A) The lungs were removed from the B6 and FcγR-/- mice, and paraffin sections were stained with H&E. Original magnification, ×100 or ×400. The photographs are representative of the three mice in each group. (B) Inflammatory responses in the lungs of B6 and FcγR-/- mice were graded. 0 (n=3, *p<0.05, B6 mice versus FcγR-/- mice).
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Figure 2: Hypersensitivity pneumonitis is attenuated in FcγR-/- mice compared to B6 mice in terms of histological alteration. In B6 and FcγR-/- mice, hypersensitivity pneumonitis was induced by inoculating SR antigen intranasally. These mice were sacrificed 3 weeks after HP induction. (A) The lungs were removed from the B6 and FcγR-/- mice, and paraffin sections were stained with H&E. Original magnification, ×100 or ×400. The photographs are representative of the three mice in each group. (B) Inflammatory responses in the lungs of B6 and FcγR-/- mice were graded. 0 (n=3, *p<0.05, B6 mice versus FcγR-/- mice).

Mentions: To compare the phenotypes of the B6 and FcγR-/- mice with HP, we investigated the histological alterations in the lungs 3 weeks after the first SR antigen exposure. SR antigen induced multifocal pulmonary lesions characterized with peribronchial lymphocytic infiltration, alveolitis, interstitial fibrosis in B6 mice (Fig. 2A). In particular, the infiltration of neutrophils and macrophages in alveolar spaces and interstitium of B6 mice was prominent compared with FcγR-/- mice. In contrast, peribronchial hyperplasia of lymphoid follicles was more frequently found in FcγR-/- mice than in B6 mice. Consistent with histological alteration in these mice, the histological scorings of the pulmonary lesions revealed significant attenuation of HP in FcγR-/- mice compared with B6 mice (Fig. 2B).


Fcgamma receptors modulate pulmonary inflammation by activating innate immune cells in murine hypersensitivity pneumonitis.

Park HJ, Kim HS, Chung DH - Immune Netw (2010)

Hypersensitivity pneumonitis is attenuated in FcγR-/- mice compared to B6 mice in terms of histological alteration. In B6 and FcγR-/- mice, hypersensitivity pneumonitis was induced by inoculating SR antigen intranasally. These mice were sacrificed 3 weeks after HP induction. (A) The lungs were removed from the B6 and FcγR-/- mice, and paraffin sections were stained with H&E. Original magnification, ×100 or ×400. The photographs are representative of the three mice in each group. (B) Inflammatory responses in the lungs of B6 and FcγR-/- mice were graded. 0 (n=3, *p<0.05, B6 mice versus FcγR-/- mice).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2837154&req=5

Figure 2: Hypersensitivity pneumonitis is attenuated in FcγR-/- mice compared to B6 mice in terms of histological alteration. In B6 and FcγR-/- mice, hypersensitivity pneumonitis was induced by inoculating SR antigen intranasally. These mice were sacrificed 3 weeks after HP induction. (A) The lungs were removed from the B6 and FcγR-/- mice, and paraffin sections were stained with H&E. Original magnification, ×100 or ×400. The photographs are representative of the three mice in each group. (B) Inflammatory responses in the lungs of B6 and FcγR-/- mice were graded. 0 (n=3, *p<0.05, B6 mice versus FcγR-/- mice).
Mentions: To compare the phenotypes of the B6 and FcγR-/- mice with HP, we investigated the histological alterations in the lungs 3 weeks after the first SR antigen exposure. SR antigen induced multifocal pulmonary lesions characterized with peribronchial lymphocytic infiltration, alveolitis, interstitial fibrosis in B6 mice (Fig. 2A). In particular, the infiltration of neutrophils and macrophages in alveolar spaces and interstitium of B6 mice was prominent compared with FcγR-/- mice. In contrast, peribronchial hyperplasia of lymphoid follicles was more frequently found in FcγR-/- mice than in B6 mice. Consistent with histological alteration in these mice, the histological scorings of the pulmonary lesions revealed significant attenuation of HP in FcγR-/- mice compared with B6 mice (Fig. 2B).

Bottom Line: The family of Fcgamma receptors (FcgammaRs) has emerged as central regulators for modulating both pro-and anti-inflammatory responses.However, the role of FcgammaRs in the development of HP has not been investigated yet.These results demonstrate that activating Fcgamma receptors play an important role in activating neutrophils and macrophages in pulmonary inflammation and inducing Th1 differentiation by regulating cytokine expression in SR-induced HP.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, Seoul National University College of Medicine, Seoul, Korea.

ABSTRACT

Background: Hypersensitivity pneumonitis (HP) is an interstitial lung disease that develops following repeated exposure to inhaled particulate antigens. The family of Fcgamma receptors (FcgammaRs) has emerged as central regulators for modulating both pro-and anti-inflammatory responses. However, the role of FcgammaRs in the development of HP has not been investigated yet.

Methods: To explore the functional roles of FcgammaRs in HP, FcgammaR(-/-) and B6 mice were challenged with Saccharopolyspora rectivirgula (SR) antigen intranasally, and compared these mice in terms of the histological change, infiltrated immune cells in BALF and in vitro immune responses.

Results: FcgammaR(-/-) mice exhibited attenuation of HP in terms of histological alterations, and reduced numbers of neutrophils and macrophages in and the increased CD4:CD8 ratio of bronchoalveolar lavage fluid. The lungs of FcgammaR(-/-) mice showed high production of Th2 cytokine such as IL-4 and slightly low production of Th1 cytokine, INF-gamma compared to those of B6 mice. However, SR-specific adaptive immune responses of FcgammaR(-/-) mice were similar to those of B6 mice.

Conclusion: These results demonstrate that activating Fcgamma receptors play an important role in activating neutrophils and macrophages in pulmonary inflammation and inducing Th1 differentiation by regulating cytokine expression in SR-induced HP.

No MeSH data available.


Related in: MedlinePlus