Angiogenesis in mice with chronic airway inflammation: strain-dependent differences

Area of Science:

• Immunology
• Vascular Biology
• Respiratory Medicine

Background:

• Chronic inflammation is linked to blood vessel changes, including proliferation and enlargement.
• These vascular alterations may represent distinct forms of angiogenesis influenced by the stimulus.
• Understanding these processes is crucial for managing inflammatory diseases.

Purpose of the Study:

• To investigate if vascular changes in chronic airway inflammation are different types of angiogenesis.
• To determine if these vascular changes are dependent on the host's immune response.
• To compare angiogenesis in resistant versus susceptible mouse strains during Mycoplasma pulmonis infection.

Main Methods:

• Inducing chronic airway inflammation via Mycoplasma pulmonis infection in C57BL/6 (resistant) and C3H (susceptible) mice.
• Assessing tracheal vascularity using Lycopersicon esculentum lectin staining in whole mounts.
• Quantifying vessel number, length, diameter, endothelial cell proliferation, and capillary-to-venule conversion.

Main Results:

• Both mouse strains showed increased tracheal vascularity post-infection.
• C57BL/6 mice exhibited a doubling of vessel number, with increased capillaries and venules.
• C3H mice showed no change in vessel number or length, but increased diameter, endothelial cells, and venule proportion.

Conclusions:

• The same inflammatory stimulus can induce either blood vessel proliferation or enlargement based on host susceptibility.
• Endothelial cell proliferation occurs in both responses.
• Angiogenesis can manifest as new capillary formation or the conversion of capillaries to venules.