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T-box transcription...
T-box transcription-factor-deficient mice display increased joint pathology and failure of infection control during staphylococcal arthritis.
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- Hultgren, Olof H., 1970 (author)
- Gothenburg University,Göteborgs universitet,Institutionen för laboratoriemedicin, Avdelningen för klinisk immunologi,Institute of Laboratory Medicine, Dept of Clinical Immunology
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- Verdrengh, Margareta, 1942 (author)
- Gothenburg University,Göteborgs universitet,Institutionen för invärtesmedicin, Avdelningen för reumatologi och inflammationsforskning,Institute of Internal Medicine, Dept of Rheumatology and Inflammation Research
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- Tarkowski, Andrej, 1951 (author)
- Gothenburg University,Göteborgs universitet,Institutionen för invärtesmedicin, Avdelningen för reumatologi och inflammationsforskning,Institute of Internal Medicine, Dept of Rheumatology and Inflammation Research
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(creator_code:org_t)
- Elsevier BV, 2004
- 2004
- English.
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In: Microbes and infection / Institut Pasteur. - : Elsevier BV. - 1286-4579. ; 6:6, s. 529-35
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Abstract
Subject headings
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- To study the impact of T-box transcription factor (T-bet) on initiation and progression of Staphylococcus aureus sepsis and arthritis, T-bet-deficient mice (T-bet(-/-)) and their wild-type controls (T-bet(+/+)) were intravenously inoculated with 8 x 10(6) S. aureus. Already 48 h after inoculation of S. aureus, T-bet-deficient mice displayed increased frequency (62% versus 19%, P = 0.002) as well as severity of arthritis compared with wild-type controls. The bacterial counts were significantly increased in T-bet(-/-) mice compared with T-bet(+/+) as measured in kidneys 72 h after the inoculation (4.3 +/- 1.8 x 10(7) versus 3.2 +/- 3.2 x 10(6) colony-forming units (CFU); P = 0.003). As expected, T-bet-deficient mice displayed significantly decreased production of IFN-gamma (10-15-fold) at 24 and 72 h after bacterial inoculation compared with wild-type mice. Interestingly, in the absence of T-bet, serum IL-4 was decreased at 24 h. IL-6 did not differ at early stage of infection but was sixfold increased in T-bet(-/-) mice over T-bet(+/+) animals at 72 h postinoculation. Ten days after the inoculation, T-bet(-/-) mice still displayed significantly more pronounced weight loss and increased serum IL-6 levels, probably due to increased bacterial burden compared with T-bet(+/+) mice. The cumulative mortality was 19% in T-bet mice (5/27) and 0% (0/27) in control animals (P = 0.05). In conclusion, T-bet plays an important role in early response to S. aureus infection, protecting against bacterial accumulation, cachexia and septic death. Furthermore T-bet downregulates joint inflammation in the early phase of disease.
Keyword
- Animals
- Arthritis
- Infectious
- immunology
- metabolism
- microbiology
- pathology
- Body Weight
- Colony Count
- Microbial
- Interferon Type II
- blood
- Interleukin-4
- blood
- Interleukin-6
- blood
- Joints
- pathology
- Kidney
- microbiology
- Mice
- Mice
- Inbred C57BL
- Sepsis
- immunology
- metabolism
- microbiology
- pathology
- Staphylococcal Infections
- immunology
- metabolism
- microbiology
- pathology
- Staphylococcus aureus
- growth & development
- T-Box Domain Proteins
- Transcription Factors
- deficiency
- physiology
Publication and Content Type
- ref (subject category)
- art (subject category)
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