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Project description

My research focuses on generation of new knowledge important to our understanding of staphylococcus aureus -host interplay. My ultimate goal is that the new knowledge will contribute to the design of early diagnosis and improved therapeutic strategies against S. aureus septic arthritis.

Virulence factors and host factors in S. aureus infections

The lab is studying the involvement of bacterial virulence factors, as well as some host immune cell types and cytokines, in the pathogenesis of infectious arthritis using our unique mouse model for S. aureus septic arthritis. Currently we are working on the role of complement factors in septic arthritis.

On the bacterial factor side, activation of fibrinolysis by staphylokinase (enzyme produced by S. aureus) blocks the bacterial attachment by cleaving off the host-derived adhesins on the surface of implants (unpublished data). We want to further design new preventive modalities against biofilm infections e.g. plasminogen activators immobilization on prosthetic implants.

Immunoregulation to ameliorate septic arthritis

Our earlier results suggest that via TNF receptor 1, antibiotic-killed S. aureus causes long-lasting joint inflammation that might lead to post-infectious complications of S. aureus septic arthritis. In the follow-up studies, my research group is investigating whether the combination therapy of antibiotics and immunomodulating biologics (including TNF-a, IL-6 inhibitors, CTLA-Ig, and JAK kinase inhibitors) minimizes post infectious sequelae, alleviates the bone/cartilage destruction, and in turn diminishes the joint dysfunction in mice and patients with S. aureus septic arthritis.

Yet, there are potential dangers associated with clinicians choosing inadequate antibiotics in combination with biologics due to deteriorated immune responses by immunomodulating biologics. My lab is also studying the possible side effects of biologics e.g. increased susceptibility to S. aureus infections.

Key Publications: 

Ali A, Zhu X, Kwiecinski J, Gjertsson I, Lindholm C, Iwakura Y, Wang X, Lycke N, Josefsson E, Pullerits R, Jin T.
Antibiotic-killed Staphylococcus aureus induces destructive arthritis in mice. Arthritis & Rheumatology. 2015.
Impact factor: 7.332 (PMID: 25302691).

Kwiecinski J, Jacobsson G, Karlsson M, Zhu X, Wang W, Bremell T, Josefsson E, Jin T.
Staphylokinase promotes the establishment of Staphylococcus aureus skin infections while decreasing disease severity. Journal of Infectious Diseases. 2014.
Impact factor: 6.410 (PMID: 23801604) 

Kwiecinski J, Rhost S, Löfbom L, Blomqvist M, Månsson J, Cardell S. L. and Jin T.
Sulfatide attenuates experimental Staphylococcal aureus sepsis through a CD1d dependent pathway. Infection and Immunity. 2013.
Impact factor: 4.165. (PMID: 23340309)

Fei Y, Wang W, Kwiecinski J, Josefsson E, Pullerits R, Jonsson IM, Magnusson M, Jin T.
Combination of Tumour Necrosis Factor inhibitor and antibiotics alleviates staphylococcal arthritis and sepsis in mice. Journal of Infectious Diseases. 2011.
Impact factor: 6.410 (PMID: 21742832)

Kwiecinski J, Magnusson M, Josefsson E, Mitchell J, Higgins J, Tarkowski A, Foster T, Jin T and Bokarewa M.
Activation of plasminogen by staphylokinase reduces severity of staphylococcus aureus systemic infection. Journal of Infectious Diseases. 2010.
Impact factor: 6.410 (PMID:20726765)

Kwiecinski J, Klak M, Trysberg E, Blennow K, Tarkowski A, Jin T.
Elevated levels of Plasminogen Activator Inhibitor-1 in Cerebrospinal Fluid relate to neuronal destruction in Patients with CNS Lupus. Arthritis & Rheumatism. 2009.
Impact factor: 7.332 (PMID:19565516)

Kontaktinformation

Tao Jin

Box 480, 405 30 Göteborg

Besöksadress:
Gulhedsgatan 10A

Telefon:
+46 31 342 64 76
+46 73 779 74 02

Sidansvarig: kommunikation@medicine.gu.se|Sidan uppdaterades: 2015-04-02
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