Ficolin A and ficolin B aggravate poly(I:C) secondary LPS stimulation-induced acute lung injury by modulating...

Area of Science:

• Immunology
• Pathology
• Microbiology

Background:

• Respiratory viral infections, such as influenza, frequently lead to secondary bacterial infections, a major cause of mortality.
• These secondary infections can result in severe pneumonia and lung injury, even after mild viral infections.

Purpose of the Study:

• To investigate the role of ficolin A/B in the pathogenesis of secondary Gram-negative bacterial pneumonia following respiratory RNA virus infection.
• To explore ficolin A/B as a potential therapeutic target for severe pneumonia.

Main Methods:

• Mice were intranasally stimulated with polyinosinic-polycytidylic acid [poly(I:C)] followed by lipopolysaccharide (LPS) to model secondary bacterial infection.
• Evaluated body weight loss, lung pathological injury, immune cell recruitment (neutrophils, macrophages), and ficolin A/B expression.
• Utilized ficolin A/B knockout mice to assess its functional role.

Main Results:

• Poly(I:C) and LPS co-stimulation exacerbated weight loss, lung injury, and inflammatory cell infiltration.
• Ficolin A/B expression was elevated in neutrophils and macrophages in the lungs.
• Ficolin A/B knockout attenuated lung injury, reduced weight loss, and decreased interstitial macrophage recruitment and alveolar macrophage exhaustion.

Conclusions:

• Ficolin A/B plays a critical role in mediating severe pneumonia following respiratory viral and secondary Gram-negative bacterial infections.
• Targeting ficolin A/B may offer a therapeutic strategy to mitigate lung injury and inflammation in such conditions.