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The role of macrophage-epithelial transition for mycobacterial granuloma progression and disease outcome

2024-11-25Master thesis Embargoed access
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dc.contributor.advisorResende, Mariana
dc.contributor.advisorNova, Manuel Vila
dc.contributor.advisorVieira, Mónica
dc.contributor.authorSantos, Débora Alexandra Costa dos
dc.date.accessioned2025-02-18T14:04:49Z
dc.date.available2025-02-18T14:04:49Z
dc.date.issued2024-11-25
dc.date.submitted2024-11-25
dc.description.abstractMucobacterial infections, primarily caused by Mycobacterium tuberculosis (Mtb) and Mycobacterium avium (M. avium) represent a global health problema. Following infection, bactéria are phagocytosed by macrophages, initiating na imune response that recruits additional imune cells to the site of infection, resulting in the formation of granulomas. Granulomas are organized structures consisting of a core of macrophages surrounded by B and T lymphocytes, that contain the bactéria. However, granulomas can envolve in ways that cause tissue damage and facilitate bacterial dissemination. Within these structures, macrophages undergo an epitelial transformation, acquiring epitelial-like properties suc as E-cadherin expression. The current study aims to elucidate the role of macrophage epithelization in shaping granuloma architecture, infection containment, and disease progression. To this end, we employed a mouse model with conditional disruption of E-cadherin expression in macrophages (Lyz2Cre x Cdh1fl/fl), wich was subsequently infected with either M. avium 2447 or M. avium 25291. Our initial objectives included analyzing the livers, spleens, and lungs to assess granuloma morphology, celular composition, E-cadherin expression, and bacterial growth. However animals did not become properly infected, altering the course of the project. Thus, we worked to understand the reasons behind the results obtained. It’s still nuclear why the animals do not develop the infection, but it become evidente that we cannot purpose with our initial aim using our Lyz2Cre x Cdh1fl/fl mouse colony. Nonetheless, it is important to refer that understanding the underlying mechanisms ofmacrophage epithelization remains crucial for identifying molecular targets to modulate granuloma Dynamics and develop therapeutic strategies for mycobacterial diseases.por
dc.description.sponsorshipNORTE-01-0145-FEDER-000039
dc.identifier.tid203852834
dc.identifier.urihttp://hdl.handle.net/10400.22/29555
dc.language.isoeng
dc.rights.uriN/A
dc.subjectMycobacterial infections
dc.subjectM. avium
dc.subjectGranuloma architecture
dc.subjectMacrophage epithelization
dc.subjectE-cadherin
dc.titleThe role of macrophage-epithelial transition for mycobacterial granuloma progression and disease outcomepor
dc.typemaster thesis
dspace.entity.typePublication

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