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Tao Jin

Researcher

Tao Jin
Researcher , Avd-/sektionschef, bitr, inst
tao.jin@rheuma.gu.se
+46 31-342 6476

Postal Address: Box 480, 40530 Göteborg
Visiting Address: Guldhedsgatan 10 , 41346 Göteborg


Department of Rheumatology a Inflammation Research at Institute of Medicine (More Information)
Box 480
405 30 Göteborg
0313421000
Fax: +46 31823925
Visiting Address: Medicinaregatan 3, plan 5 , 413 90 Göteborg

About Tao Jin

MD, Associate professor
Deputy Head of Department of Rheumatology and Inflammation Research, Institute of Medicine

  • MD, Suzhou Medical College, China (1995)
  • Phd, Department of Rheumatology and Inflammation
  • Research, Sahlgrenska Academy, University of Gothenburg (2005)
  • Associate professor in Rheumatology (2010)
    Rheumatologist (2015)

Research

Septic arthritis remains one of the most dangerous joint diseases due to its rapidly progressive and destructive disease character. Despite advances in the use of antibiotics, permanent reductions in joint function occur in up to 50% of patients who may need joint replacement surgery. 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.

Specifically, there are two main questions that I want to answer:
1. how do bugs reach the joint cavity?
2. which bacterial factor causes joint damage?

My group found that depletion of coagulases (two S. aureus products promoting clotting of plasma or blood) totally abolished the capability of S. aureus to invade joint cavity and greatly reduced joint inflammation and bone destruction, while it did not affect the bacterial load in other organs. This suggests that we are very close to the core mechanism of this disease. Other important observation is that one single intraarticular injection of lipoprotein (bacterial cell wall component) causes long-lasting and destructive joint damage. We plan to further understand the underlying mechanism and develop the new vaciccins 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.

Group members

Abukar Ali
Postdoctoral Fellow

Anders Jarneborn
PhD student

Majd Mohammed
PhD student

Manli Na
Postdoctoral Fellow

 

Latest publications

Complement Consumption in Systemic Lupus Erythematosus Leads to Decreased Opsonophagocytosis In Vitro.
Amanda Mitander, Ying Fei, Estelle Trysberg, Majd Mohammad, Zhicheng Hu et al.
The Journal of rheumatology, Journal article 2018
Journal article

Human skin commensals augment Staphylococcus aureus pathogenesis.
Emma Boldock, Bas G J Surewaard, Daria Shamarina, Manli Na, Ying Fei et al.
Nature microbiology, Journal article 2018
Journal article

Impact of cell wall peptidoglycan O-acetylation on the pathogenesis of Staphylococcus aureus in septic arthritis.
Gaurav Baranwal, Majd Mohammad, Anders Jarneborn, Bommana Raghunath Reddy, Archana Golla et al.
International journal of medical microbiology : IJMM, Journal article 2017
Journal article

Showing 1 - 10 of 43

2019

2018

Complement Consumption in Systemic Lupus Erythematosus Leads to Decreased Opsonophagocytosis In Vitro.
Amanda Mitander, Ying Fei, Estelle Trysberg, Majd Mohammad, Zhicheng Hu et al.
The Journal of rheumatology, Journal article 2018
Journal article

Human skin commensals augment Staphylococcus aureus pathogenesis.
Emma Boldock, Bas G J Surewaard, Daria Shamarina, Manli Na, Ying Fei et al.
Nature microbiology, Journal article 2018
Journal article

2017

Impact of cell wall peptidoglycan O-acetylation on the pathogenesis of Staphylococcus aureus in septic arthritis.
Gaurav Baranwal, Majd Mohammad, Anders Jarneborn, Bommana Raghunath Reddy, Archana Golla et al.
International journal of medical microbiology : IJMM, Journal article 2017
Journal article

2016

Showing 1 - 10 of 43

Page Manager: Karin Allander|Last update: 9/19/2019
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