Väitös (lääketieteellinen mikrobiologia ja immunologia): MSc Madhukar Vedantham
MSc Madhukar Vedantham esittää väitöskirjansa ”Gut inflammation: physiological and molecular insights on poly(adp-ribose) polymerase 14 in inflammatory bowel disease and salmonellosis” julkisesti tarkastettavaksi Turun yliopistossa perjantaina 24.10.2025 klo 12.00 (Turun yliopisto, Calonia, Cal1, Caloniankuja 3, Turku).
Yleisön on mahdollista osallistua väitökseen myös etäyhteyden kautta: https://echo360.org.uk/section/6ce57e3d-ed97-438a-9a43-c25532e04c00/public (kopioi linkki selaimeen).
Vastaväittäjänä toimii professori Tuure Kinnunen (Itä-Suomen yliopisto) ja kustoksena dosentti Arto Pulliainen (Turun yliopisto). Tilaisuus on englanninkielinen. Väitöksen alana on lääketieteellinen mikrobiologia ja immunologia.
Väitöskirja yliopiston julkaisuarkistossa: https://urn.fi/URN:ISBN:978-952-02-0375-7 (kopioi linkki selaimeen).
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Tiivistelmä väitöstutkimuksesta:
Gut inflammation is a serious health issue worldwide. It appears in long-term diseases such as inflammatory bowel disease (IBD), which includes Crohn’s disease and ulcerative colitis, and in acute infections such as salmonellosis caused by Salmonella bacteria. In both cases, the protective lining of the intestine is damaged, leading to pain, diarrhea, and in severe situations, lasting complications.
My doctoral research focused on a protein called PARP14, which had not been well studied in gut diseases before. I examined its role using human colon tissue and experimental mouse models of chemically induced colitis and Salmonella infection.
The findings show that PARP14 is more active in the gut during inflammation and infection, especially in the cells that form the intestinal lining. When PARP14 was absent in mice, gut damage from chemically induced colitis or Salmonella infection became more severe. These mice lost protective mucus-producing cells, their gut lining eroded more extensively, and inflammatory reactions were stronger. This suggests that PARP14 contributes to protecting the intestine by helping to control inflammation and supporting tissue repair.
This research provides new information about how the gut maintains its barrier and responds to injury in both chronic and infectious inflammation. It highlights PARP14 as a protein worth further study, both for understanding gut biology and as a possible marker or target for future treatments.
In summary, the work shows that PARP14 helps the intestine cope with inflammation in experimental models. These insights may support the development of better strategies to protect patients with IBD and serious gut infections in the future.
Yleisön on mahdollista osallistua väitökseen myös etäyhteyden kautta: https://echo360.org.uk/section/6ce57e3d-ed97-438a-9a43-c25532e04c00/public (kopioi linkki selaimeen).
Vastaväittäjänä toimii professori Tuure Kinnunen (Itä-Suomen yliopisto) ja kustoksena dosentti Arto Pulliainen (Turun yliopisto). Tilaisuus on englanninkielinen. Väitöksen alana on lääketieteellinen mikrobiologia ja immunologia.
Väitöskirja yliopiston julkaisuarkistossa: https://urn.fi/URN:ISBN:978-952-02-0375-7 (kopioi linkki selaimeen).
***
Tiivistelmä väitöstutkimuksesta:
Gut inflammation is a serious health issue worldwide. It appears in long-term diseases such as inflammatory bowel disease (IBD), which includes Crohn’s disease and ulcerative colitis, and in acute infections such as salmonellosis caused by Salmonella bacteria. In both cases, the protective lining of the intestine is damaged, leading to pain, diarrhea, and in severe situations, lasting complications.
My doctoral research focused on a protein called PARP14, which had not been well studied in gut diseases before. I examined its role using human colon tissue and experimental mouse models of chemically induced colitis and Salmonella infection.
The findings show that PARP14 is more active in the gut during inflammation and infection, especially in the cells that form the intestinal lining. When PARP14 was absent in mice, gut damage from chemically induced colitis or Salmonella infection became more severe. These mice lost protective mucus-producing cells, their gut lining eroded more extensively, and inflammatory reactions were stronger. This suggests that PARP14 contributes to protecting the intestine by helping to control inflammation and supporting tissue repair.
This research provides new information about how the gut maintains its barrier and responds to injury in both chronic and infectious inflammation. It highlights PARP14 as a protein worth further study, both for understanding gut biology and as a possible marker or target for future treatments.
In summary, the work shows that PARP14 helps the intestine cope with inflammation in experimental models. These insights may support the development of better strategies to protect patients with IBD and serious gut infections in the future.
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