Mononuclear-cell pulmonary vasculitis in NZB/W mice. I. Histopathologic evaluation of spontaneously occurring pulmonary infiltrates
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Abstract:
This report describes the spontaneous occurrence of pulmonary vasculitis in NZB/W mice, a well-characterized autoimmune strain of mice. These mice develop pulmonary vasculitis in an age-related fashion. Mild perivascular and peribronchiolar lymphoid hyperplasia is first seen at 4 months of age and progresses into severe hyperplasia by 8 months. This precedes the development of angiodestructive lesions, which are first noticeable at 10 months. By 12 months of age all mice show multilobe disease characterized by transmural infiltration of the vascular walls by plasma cells, histiocytes, and mature lymphocytes. Mitotic figures and necrosis are rare to absent. Vessel lumens are markedly narrowed and obliterated in severe cases, with focal disruption of the limiting elastic membranes. In mice older than 10 months of age, there is extension of the infiltrate into the interstitium in a manner similar to that of lymphoid interstitial pneumonia. Arteries and veins are equally affected. The cellular infiltrates and pattern of involvement bears similarity to various pulmonary vasculitides in humans. This is the first report of spontaneous pulmonary vasculitis in NZB/W mice.
Insights
This study reports spontaneous pulmonary vasculitis in NZB/W mice, an autoimmune model. The age-related condition mimics human pulmonary vasculitis, offering insights into autoimmune lung disease.
Area of Science:
- Immunology
- Pathology
- Veterinary Medicine
Background:
- NZB/W mice are a well-established model for autoimmune diseases.
- Pulmonary involvement in autoimmune conditions can be severe and progressive.
- Spontaneous models are crucial for understanding disease pathogenesis.
Purpose of the Study:
- To document the spontaneous development of pulmonary vasculitis in NZB/W mice.
- To characterize the age-related progression of this autoimmune lung disease.
- To compare the murine model to human pulmonary vasculitis.
Main Methods:
- Histopathological examination of lung tissue from NZB/W mice at various ages (4, 8, 10, 12 months).
- Assessment of lymphoid hyperplasia, angiodestructive lesions, and cellular infiltrates.
- Evaluation of vascular changes including lumen narrowing and elastic membrane integrity.
Main Results:
- Age-related pulmonary vasculitis observed in NZB/W mice.
- Progression from lymphoid hyperplasia (4-8 months) to angiodestructive lesions (≥10 months).
- Severe vasculitis by 12 months, characterized by transmural infiltration and vascular narrowing, resembling human pulmonary vasculitis.
Conclusions:
- NZB/W mice spontaneously develop age-related pulmonary vasculitis.
- The observed pathology shares similarities with human pulmonary vasculitides.
- This model provides a valuable platform for studying autoimmune lung disease mechanisms.