Date/Time
Date(s) - 25/07/2024
5:30 pm - 7:00 pm
Location
BT2 Détente / Kitchenette 1st Floor room 101
Categories
Do you like scientific discussion? And how about Pizza?
If we gained your attention with ‘scientific’, or at least with ‘Pizza’, then you are already looking forward to the right event!
Pizza Club is a regularly held Journal Club event co-organized by The Representatives of the Doctoral Programme in Systems and Molecular Biomedicine, part of the Doctoral School in Science and Engineering (DSSE); and the Uni.lu student association ISCB RSG Luxembourg.
In short, Students (PhD candidates) present a scientific paper (+- 20 mins) they find interesting or that inspired the development of their individual PhD project (doesn’t need to be authored by the speaker).
There will be a open discussion round after each scientific presentation (2-3 students per event), followed by informal and fun chatting with some pizzas around!
Moreover, each presentation of peer-reviewed papers will be rewarded by 0.5 ECTS!
Presenter: Bianca BRANDUS (https://researchportal.lih.lu/en/persons/bianca-brandus)
Presenter introduction: Bianca is in the last year of her PhD in Dr. Carole Devaux’s group working on the development of a new type of molecule, called CoMiX, targeting multidrug resistant Pseudomonas aeruginosa.
Paper presented: Factor H-related protein 1 promotes complement-mediated opsonization of Pseudomonas aeruginosa. (https://pubmed.ncbi.nlm.nih.gov/38510967/)
Paper description: This study demonstrates that Factor H-Related protein 1 (FHR-1) binds to Pseudomonas aeruginosa via OprG, an outer membrane protein. This binding competitively inhibits Factor H from attaching to the bacteria, thereby promoting C3b-deposition and enhanced C5a generation. Consequently, this paper adds to the growing body of evidence that FHR proteins function as complement activators, rather than complement inhibitors.
Presenter: Mónica MIRANDA (https://researchportal.lih.lu/en/persons/monica-miranda-de-la-maza)
Presenter introduction: Mónica is a 2nd year PhD student at the Luxembourg Center for Neuropathology. She is from Bilbao (Spain) and she is currently studying the interplay between microglia, astrocytes and infiltrating immune cells in neuroinflammatory mechanisms in Alzheimer’s disease (AD). AD displays multifaceted neuropathological features, including β-amyloid plaques (Aβ), neurofibrillary tangles (NFTs) and neuroimmunological alterations. The contribution of glial and immune cells to AD progression is still under debate. Indeed the role of microglia, the brain-resident immune cells, that typically aggregate around Aβ plaques, astrocytes and, even peripheral immune cells (e.g. T-cells and perivascular macrophages) that can infiltrate the parenchyma in neurodegenerative areas, yet remains controversial, with evidence for both protective and disease-enhancing contributions. They aim to generate high-content data on astrocytes, microglia and immune cells interplays to unveil new facets of neuroinflammation in AD.
Paper presented: Requirement of brain interleukin33 for aquaporin4 expression in astrocytes and glymphatic drainage of abnormal tau. (https://doi.org/10.1038/s41380-020-00992-0)
Paper description: Defective glymphatic drainage mediated by aquaporin4 (AQP4) has been associated with tauopathy and amyloid plaque formation in Alzheimer’s disease. In this paper, they found out that brain interleukin-33 (IL33) is crucial for regulating AQP4 expression in astrocytes, particularly in those with neuron-facing membrane domains (n-AQP4). In IL33-deficient (Il33−/−) mice, there was a notable decrease in n-AQP4 after middle age, accompanied by a rapid build-up of abnormal tau in neurons and reduced clearance of this tau to peripheral tissues. When recombinant IL33 was injected into Il33−/− brains, there was a significant increase in AQP4 expression at the perivascular end-foot (p-AQP4) of astrocytes, but not in n-AQP4. While the increased p-AQP4 significantly enhanced the drainage of injected peptides from the brain, it did not notably improve the clearance of abnormal tau. These findings suggest that p-AQP4 facilitates overall fluid flow towards the perivenous space (glymphatics), whereas n-AQP4 might help remove neuronal waste, such as abnormal tau. Moreover, they demonstrated that IL33 plays a role in DNA repair and autophagy in neurons under oxidative stress. This study shows that IL33 deficiency also disrupts glymphatic drainage. This suggests IL33’s crucial role in maintaining effective glymphatic function and preventing neurodegeneration and tauopathy.
If we attracted your interest by now, feel free to join the monthly Pizza Club, either as part of Audience or as a registered Speaker. For the latter, please kindly use this form to sign up as an upcoming Speaker, by choosing your category of paper and desired month to present. Looking forward to seeing you at the next Pizza Club!
