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| Funder | Swedish Research Council |
|---|---|
| Recipient Organization | Karolinska Institutet |
| Country | Sweden |
| Start Date | Jan 01, 2025 |
| End Date | Dec 31, 2028 |
| Duration | 1,460 days |
| Number of Grantees | 1 |
| Roles | Principal Investigator |
| Data Source | Swedish Research Council |
| Grant ID | 2024-02468_VR |
Despite growing evidence for a bidirectional oral-gut axis, the mechanisms of remote interaction - particularly how gut disorders affect the oral cavity - remain elusive.
Filling this gap is urgent and critical because (i) about one in six patients with bowel disorders develops oral pathology such as xerostomia (dry mouth), (ii) such conditions can lead to oral dysbiosis and oral chronic wounds, which significantly decrease quality of life, (iii) oral dysbiosis can exacerbate lower gastrointestinal (GI) tract disorders, as translocation of oral microbes can exacerbate inflammation, impair therapeutic response, and lead to colorectal cancer.
I have unbiasedly interrogated the effects of colitis in the upper GI tract using a new method and spatial omics, which led me to discover a novel murine salivary gland (SG) and to find that colitis causes significant SG atrophy and dysfunction via autonomic sympathetic pathways. Given the critical role of saliva in upper GI physiology, I hypothesize that this link is key to the gut-to-oral axis.
Using state-of-the-art technologies, mouse models, and human SG organoids, I aim to: (I) Functionally analyze the newly discovered organ(II) Unravel the mechanisms causing colitis-induced SG pathology and identify salivary biomarkers for precision medicine(III) Evaluate novel regenerative therapies for colitis-related SG dysfunctionMy ultimate goal is to mitigate the impact of this bidirectional pathogenic loop on the course of related diseases.
Karolinska Institutet
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