Doctoral ceremony takes place at the university again for the first time since the pandemic
The two doctoral award winners Christian Niehaus, MD (left), and Liart Pollmann, MD. Copyright: Karin Kaiser / MHH
08.05.2023
MHH has awarded a total of 105 doctoral degrees since November 2022: 76 female and 29 male doctoral students of Hannover Medical School (MHH) received their doctoral certificates on Friday. Among them are 48 young female and 21 male physicians, eleven male and two female dentists, eleven male and three female natural scientists, four male and three female human biologists, and two female doctoral students in population medicine (public health). A total of 17 of them graduated "with honor," and two received the doctoral prizes of the Society of Friends of the MHH of 2,500 euros each as an outstanding honor.
For the first time after a longer pandemic-related break, MHH President Professor Dr. Michael P. Manns again personally presented the doctoral certificates to the doctoral candidates during a ceremony at the university. Together with Professor Dr. Frank Bengel, Dean of Research at the university, Professor Dr. Siegfried Piepenbrock, Chairman of the Society of Friends of the MHH e.V., awarded the two doctoral prize winners: Christian Niehaus, MD, MHH Clinic for Gastroenterology, Hepatology, Infectiology and Endocrinology, and Liart Pollmann, MD, Clinic for Cardiology and Pneumology at the University Medical Center Göttingen (UMG).
Mucosa-associated invariant T (MAIT) cells as a new potential therapeutic target in advanced liver cirrhosis
Christian Niehaus, MD, has submitted his dissertation "Mucosal-associated invariant T cells in patients with liver cirrhosis" to Professor Markus Cornberg, MD, Department of Gastroenterology, Hepatology, Infectious Diseases and Endocrinology. The data of his dissertation work provide extensive new results in patients with advanced liver cirrhosis and open up mucosa-associated invariant T (MAIT) cells as a new potential therapeutic target.
Liver cirrhosis corresponds to the end stage of chronic liver disease. The main complication is the occurrence of abdominal fluid. Patients still have a mortality rate of about 50 percent within one year despite improved medical care. The main cause is infection, including inflammation of the abdominal fluid, known as spontaneous bacterial peritonitis (SBP).
In his doctoral thesis, Dr. med Christian Niehaus investigated the role of mucosa-associated invariant T (MAIT) cells, a subset of immune cells that combine properties of the innate and the acquired immune system, in patients with advanced liver cirrhosis and characterized them in more detail with regard to their immune response. He was able to show that although this group of immune cells is reduced in the blood of patients with liver cirrhosis, it is increased in the abdominal fluid of these patients and exhibits an activated, tissue-resident phenotype here. Likewise, these cells isolated from the abdominal fluid were able to produce anti-inflammatory messenger substances after stimulation with the bacterium Escherichia coli. Compared to MAIT cells obtained from the blood of the same patients, this response was higher, demonstrating that despite severe impairment of MAIT cells in the blood, they are highly functional in the abdominal fluid and have the ability to significantly respond to pathogens and participate in immune responses.
Furthermore, the PhD student found that MAIT cells are actively recruited to the abdominal cavity during abdominal fluid infection by certain soluble messengers and thus may play an important overall role in infection defense.
The original paper by Dr. Christian Niehaus can be found here: https://journals.lww.com/hep/Fulltext/2020/10000/MAIT_Cells_Are_Enriched_and_Highly_Functional_in.19.aspx
Hope for young patients with a severe form of Mendelian Susceptibility to Mycobacterial Disease (MSMD)
Liart Pollmann, MD, PhD, has completed his doctoral thesis entitled "Human Lentiviral Gene Therapy Restores the Cellular Phenotype of Autosomal Recessive CompleteIFN-γR1 Deficiency" with Professor Nico Lachmann, MD, MHH Department of Pediatric Pneumology, Allergology and Neonatology. As part of the experimental research project, he tested novel gene ferries. In doing so, he successfully demonstrated the correction of the IFN-γR1 signaling protein in human target cells.
In addition to mycobacteria causing tuberculosis, so-called non-tuberculous mycobacteria (NTM) are increasingly coming into the focus of science, as they can cause life-threatening infections in some people. Mendelian Susceptibility to Mycobacterial Disease (MSMD) is a rare genetic immunodeficiency in which young patients have an increased susceptibility to contracting NTM or Bacillus Calmette-Guérin (BCG). A large proportion of them can be treated with medication, but for some of the young children only bone marrow transplantation is an option. This particularly severe form of MSMD due to mutations in the IFN-γR1 gene is therefore the focus of the development of new forms of therapy.
Current treatment methods are administration of anti-infectives (symptomatic) or stem cell transplantation (causal). However, due to recurrent infections, success is not satisfactory. A long-lasting solution would be the development of a gene therapy to treat this disease, which is called autosomal recessive complete IFN-γR1 deficiency. In Professor Lachmann's research group, gene shuttles were successfully developed, which were tested for their function by Liart Pollmann. He successfully introduced the missing gene into target cells by means of the gene shuttles and was able to demonstrate the restoration of the signaling cascade in cell lines and in patient cells by means of different biochemical methods.
This research, which was also supported by the German Center for Infection Research (DZIF), enabled the development of the first steps towards a new form of therapy for patients with autosomal recessive complete IFN-γR1 deficiency.
The original paper by Dr. Liart Pollmann can be found here: https://www.sciencedirect.com/science/article/pii/S2329050120300620?via%3Dihub