Experimental model of type IV Streptococcus agalactiae (group B streptococcus) infection in mice with early development of septic arthritis

Tissi, Luciana; Marconi, P; Mosci, Paolo; Merletti, L; Cornacchione, Paola; Rosati, Emanuela; Recchia, Simona; Hunolstein, Christina von; Orefici, Graziella

doi:10.1128/iai.58.9.3093-3100.1990

Cited by 50 publications

(21 citation statements)

References 28 publications

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“…As previously described (10) and as summarized in Table 1, clinical signs of joint swelling were observed in 30% of the mice as early as 24 hours after infection with 1 ϫ 10 7 GBS IV. The incidence of arthritis increased to 80% by day 5.…”

Section: Clinical Course Of Arthritis and Effect Of Ifn␥ Blockadesupporting

confidence: 64%

“…We recently described a mouse model of hematogenously induced GBS arthritis (10) in which mice inoculated with the reference serotype IV GBS strain manifested clinical signs of arthritis characterized by early onset and evolution from an acute exudative synovitis to permanent lesions, with irreversible joint damage and/or ankylosis. In this model, the production of interleukin-6 (IL-6), IL-1␤, and tumor necrosis factor ␣ (TNF␣) increased in response to GBS infection in the sera and joints (11).…”

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confidence: 99%

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Influence of interferon-γ administration on the severity of experimental group B streptococcal arthritis

Puliti

Hunolstein

Bistoni

et al. 2000

Arthritis & Rheumatism

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Objective To assess the effect of interferon‐γ (IFNγ) administration on the evolution of systemic infection and septic arthritis induced by group B streptococci (GBS) in mice. Methods CD1 mice were inoculated intravenously with arthritogenic strain 1/82 of type IV GBS. Exogenous murine IFNγ or anti‐IFNγ monoclonal antibodies were administered intravenously either 2 hours (−2 hours) before or 18 hours after infection with 1 × 107 GBS. Mice were monitored daily for survival and for signs of arthritis. In a subsequent set of experiments, mice were killed at selected times for examination of bacterial clearance, joint histopathology, and cytokine production. Results Mortality in mice treated with IFNγ at −2 hours was 100%, compared with 20% in those treated at 18 hours and with 40% in controls. As indicated by the arthritis score, mice treated with IFNγ at −2 hours developed early and more severe arthritis, whereas those treated at 18 hours had milder arthritis compared with infected controls. Less severe joint pathology in the mice treated with IFNγ at 18 hours correlated with low levels of interleukin‐6 (IL‐6) and IL‐1β and a low bacterial load in the joints, whereas rapid onset and worsening of articular lesions in those treated at −2 hours corresponded to early and sustained levels of IL‐6. Conclusion The findings of this study demonstrate that the effects mediated by IFNγ on GBS‐induced arthritis may be detrimental or beneficial, depending on the time of administration of IFNγ in relation to infection with the antigen.

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Section: Clinical Course Of Arthritis and Effect Of Ifn␥ Blockadesupporting

confidence: 64%

mentioning

confidence: 99%

Influence of interferon-γ administration on the severity of experimental group B streptococcal arthritis

Puliti

Hunolstein

Bistoni

et al. 2000

Arthritis & Rheumatism

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show abstract

“…Although a fair number of GBS remained in the joints, this amount of bacteria was most likely not sufficient to trigger articular damage to the same extent as that observed in WT intact mice. In fact, as we have previously demonstrated, a consistently raised bacterial load in the joints is required to induce arthritis (8,10).…”

Section: Discussionmentioning

confidence: 53%

“…We have previously described an experimental mouse model of type IV GBS infection with clinical features that closely resemble the infection in humans (8). Mice given a single intravenous dose of GBS develop clinical signs of arthritis within 48 hours.…”

Section: Mulation Of Inflammatory Cells Proinflammatory Cytokine Promentioning

confidence: 99%

Contribution of matrix metalloproteinase 2 to joint destruction in group B Streptococcus–induced murine arthritis

Puliti¹,

Momi²,

Falcinelli³

et al. 2012

Arthritis & Rheumatism

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Objective. To assess the role of matrix metalloproteinase 2 (MMP-2) in the evolution of septic arthritis induced by group B streptococci (GBS) in mice.Methods. Mice deficient in MMP-2 (MMP-2 ؊/؊ ) and wild-type controls were injected intravenously with 1 ؋ 10 7 colony-forming units of type IV GBS (strain 1/82). Levels of MMP-2, mortality rates, evolution of arthritis, bacterial clearance, joint histopathologic features, and production of cytokines and chemokines were examined in both experimental groups of mice on days 3, 6, and 9 after infection.Results. MMP-2 was produced during GBS infection. Disruption of the gene for MMP-2 resulted in a decrease in the incidence and severity of arthritis, as demonstrated by both clinical and histologic findings, without affecting mortality rates. Amelioration of arthritis was accompanied by a dramatic reduction in the local production of interleukin-1␤ (IL-1␤), IL-6, macrophage inflammatory protein 1␣ (MIP-1␣), and MIP-2 and a reduced bacterial burden.Conclusion. MMP-2, produced early during GBS infection in mice, is involved in the degradation of extracellular matrix components at the level of the joint. This degradation is the first step in a cascade of events (joint invasion by GBS, extravasation and accumulation of inflammatory cells, proinflammatory cytokine production), all of which contribute to the damage of articular tissue. Thus, MMP-2 should be regarded as a potential therapeutic target in GBS-induced arthritis.

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“…Başka bir modelde Tissi ve ark. tip IV Streptokokkus agalactiae kullanarak sıçanlarda deneysel septik artrit modeli oluşturmuştur (13).…”

Section: Deneyhayvanlarındaoluşturulanenfeksiyon Modelleriunclassified

Infection Models and Imaging Techniques Used in Preclinical Studies

Gültekin¹,

Üstün²

2019

nts

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Experimental model of type IV Streptococcus agalactiae (group B streptococcus) infection in mice with early development of septic arthritis

Cited by 50 publications

References 28 publications

Influence of interferon-γ administration on the severity of experimental group B streptococcal arthritis

Influence of interferon-γ administration on the severity of experimental group B streptococcal arthritis

Contribution of matrix metalloproteinase 2 to joint destruction in group B Streptococcus–induced murine arthritis

Infection Models and Imaging Techniques Used in Preclinical Studies

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