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Expression of adhesion molecules in lungs of mice infected with Paracoccidioides brasiliensis conidia
Angel Gonzalez1, Henrique L Lenzi, Ester M Motta
1Medical and Experimental Mycology Group, Corporación para Investigaciones Biológicas (CIB); Carrera 72 A No 78 B 141, A.A. 73 78, Medellín, Colombia, South America. agonzalezm@cib.org.co
Abstract:
In infected tissues, leukocyte recruitment is mediated by interactions between adhesion molecules, expressed on activated vascular endothelial cells, and ligands present on circulating cells. We evaluated the inflammatory response and the expression of cellular adhesion molecules (ICAM-1, VCAM-1, CD18, LFA-1 and Mac-1) in lungs of BALB/c mice infected with Paracoccidioides brasiliensis conidia. When compared with uninfected animals, infected mice had a significant increase in the inflammatory response during the first 4 days, peaking 2-3 days post-challenge, 40.3% vs. 0.0% and 41.8% vs. 0.7%, respectively. This inflammatory infiltrate was composed mainly of neutrophils and macrophages with a few eosinophils and lymphocytes. An increase in the intensity of immunofluorescence (IF) for ICAM-1 was also observed during days 1-4. ICAM-1 was present in bronchiolar epithelium, type II pneumocytes, and macrophages, as well as on vascular endothelium. The control animals presented ICAM-1 constitutively. In infected mice, VCAM-1 was only observed on vascular endothelium during the first 2 days, with some macrophages expressing this molecule throughout the study periods. CD18 and Mac-1 but not LFA-1 were expressed with a high intensity on neutrophils and macrophages present in the inflammatory infiltrate. In addition, we observed a significant decrease in Colony forming units (CFUs) after the first 2 days post-challenge. These findings suggest that during these early stages, up-regulation of ICAM-1, VCAM-1, CD18 and Mac-1 expression occurs, participating in the inflammatory process and as such, in the pathogenesis of paracoccidioidomycosis (PCM).
Insights
Leukocyte adhesion molecules like ICAM-1 and VCAM-1 increase in mouse lungs after infection with Paracoccidioides brasiliensis. This suggests their role in the early inflammatory response and pathogenesis of paracoccidioidomycosis (PCM).
Area of Science:
- Immunology
- Pathology
- Microbiology
Background:
- Leukocyte recruitment to infected tissues relies on adhesion molecule interactions.
- Understanding these interactions is crucial for deciphering inflammatory processes in infectious diseases.
Purpose of the Study:
- To investigate the inflammatory response and cellular adhesion molecule expression in mouse lungs infected with Paracoccidioides brasiliensis.
- To elucidate the role of ICAM-1, VCAM-1, CD18, LFA-1, and Mac-1 in the early pathogenesis of paracoccidioidomycosis (PCM).
Main Methods:
- BALB/c mice were infected with Paracoccidioides brasiliensis conidia.
- Inflammatory infiltrate and expression of adhesion molecules (ICAM-1, VCAM-1, CD18, LFA-1, Mac-1) were assessed using immunofluorescence.
- Colony forming units (CFUs) were quantified to evaluate fungal burden.
Main Results:
- Infected mice showed a significant increase in inflammatory response, peaking 2-3 days post-infection, with neutrophils and macrophages as primary cells.
- Up-regulation of ICAM-1, VCAM-1, CD18, and Mac-1 was observed on vascular endothelium and inflammatory cells.
- A decrease in CFUs was noted after the first 2 days, indicating early control of fungal load.
Conclusions:
- Early stages of paracoccidioidomycosis involve increased expression of ICAM-1, VCAM-1, CD18, and Mac-1.
- These adhesion molecules play a significant role in mediating leukocyte recruitment and the inflammatory process during PCM.
- The findings highlight the involvement of specific adhesion molecules in the early pathogenesis of paracoccidioidomycosis.
