Role of chemokines and cytokines in a reactivation model of arthritis in rats induced by injection with streptococcal cell walls

Schrier, Denis J.; Schimmer, Ralph C.; Flory, Craig M.; Tung, David; Ward, Peter A.

doi:10.1002/jlb.63.3.359

Cited by 61 publications

(48 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The mean ankle circumference, an accurate way to monitor rat ankle inflammation, was significantly higher from day 14 to day 29 compared with controls. As shown in Figure 1C, the mean body weight of AIA rats increased on the days prior to inflammation (days 0-14) and after peak inflammation (days [18][19][20][21][22][23][24][25][26][27][28][29]. However, the body weight of AIA rats was down-regulated starting with the initial phases of inflammation (on day 14) until peak inflammation (on day 18).…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Chemokine receptor expression and in vivo signaling pathways in the joints of rats with adjuvant‐induced arthritis

Shahrara¹,

Amin²,

Woods³

et al. 2003

Arthritis & Rheumatism

View full text Add to dashboard Cite

Objective. This study was undertaken to characterize the role of CC chemokines and their receptors in rat adjuvant-induced arthritis (AIA), a model for rheumatoid arthritis (RA). Furthermore, we investigated the signaling pathways associated with CC receptors as well as the cell type distribution of the receptors.Methods. Using TaqMan real-time reverse transcription-polymerase chain reaction, Western blot analysis, and immunohistochemistry, we defined chemokine and chemokine receptor messenger RNA (mRNA) expression, CC chemokine receptor (CCR) protein activation during the disease course, CCRassociated signaling pathways, and immunopositive CCR5, phosphorylated signal transducer and activator of transcription 1 (p-STAT-1), and p-STAT-3 cells in rat AIA versus control joints.Results. We showed significant up-regulation of CCR1, CCR2, CCR5, and macrophage inflammatory protein 1␤/CCL4 mRNA in AIA on post-adjuvant injection day 18, coincident with peak inflammation. Additionally, increases in tyrosine phosphorylation of CCR1 (days 14, 18, 21, and 24), CCR2 (days 14 and 18), and CCR5 (days 14, 18, and 21) were detected in AIA rats compared with control (nonarthritic) rats. JAK-1, STAT-1, and STAT-3 were associated with CCR1 and were highly tyrosine phosphorylated on days 14 and 18. Rheumatoid arthritis (RA) is an inflammatory disorder characterized by infiltration of monocytes, T cells, and polymorphonuclear cells into the synovial joints. The CC chemokines monocyte chemoattractant protein 1 (MCP-1)/CCL2, macrophage inflammatory protein 1␣ (MIP-1␣)/CCL3, MIP-1␤/CCL4, and

show abstract

Section: Resultsmentioning

confidence: 99%

“…Administration of neutralizing antibodies against the CC chemokines MCP-1, MIP-1␣, and RANTES delayed the onset of arthritis and reduced the severity of the disease in rodents (9,(19)(20)(21). Leukocytes are believed to be recruited from the circulation to the synovial tissue and to migrate into the joint space (22).…”

mentioning

confidence: 99%

Chemokine receptor expression and in vivo signaling pathways in the joints of rats with adjuvant‐induced arthritis

Shahrara¹,

Amin²,

Woods³

et al. 2003

Arthritis & Rheumatism

View full text Add to dashboard Cite

show abstract

“…After all, it probably augments a pre-existing response that, to begin with, is not sufficient to entirely suppress the development of an autoimmune condition. Interestingly, targeting the function of a single proinflammatory mediator suppresses a disease regulated by various cytokines and chemokines (13,(43)(44)(45)(46)(47)(48)(49)(50). These results are very surprising since different chemokines bind and activate common chemokine receptors.…”

Section: Discussionmentioning

confidence: 99%

Targeting the Function of IFN-γ-Inducible Protein 10 Suppresses Ongoing Adjuvant Arthritis

Salomon¹,

Netzer²,

Wildbaum³

et al. 2002

The Journal of Immunology

122

115

View full text Add to dashboard Cite

IFN-γ-inducible protein 10 (IP-10) is a CXC chemokine that is thought to manifest a proinflammatory role because it stimulates the directional migration of activated T cells, particularly Th1 cells. It is an open question whether this chemokine is also directly involved in T cell polarization. We show here that during the course of adjuvant-induced arthritis the immune system mounts a notable Ab titer against self-IP-10. Upon the administration of naked DNA encoding IP-10, this titer rapidly accelerates to provide protective immunity. Self-specific Ab to IP-10 developed in protected animals, as well as neutralizing Ab to IP-10 that we have generated in rabbits, could inhibit leukocyte migration, alter the in vivo and in vitro Th1/Th2 balance toward low IFN-γ, low TNF-α, high IL-4-producing T cells, and adoptively transfer disease suppression. This not only demonstrates the pivotal role of this chemokine in T cell polarization during experimentally induced arthritis but also suggests a practical way to interfere in the regulation of disease to provide protective immunity. From the basic science perspective, this study challenges the paradigm of in vivo redundancy. After all, we did not neutralize the activity of other chemokines that bind CXCR3 (i.e., macrophage-induced gene and IFN-inducible T cell α chemoattractant) and yet significantly blocked not only adjuvant-induced arthritis but also the in vivo competence to mount delayed-type hypersensitivity.

show abstract

“…IL-1, TNF␣, and IL-4 are essential during the reactivation phase (59). The combined action of IL-4 and TNF␣ enhances T cell adhesion molecules and may thereby regulate part of the transition from an acute to a chronic T cell-mediated phase (56).…”

Section: Evaluation Of Therapeutic Targets In Animal Models Of Arthritismentioning

confidence: 99%

Evaluation of therapeutic targets in animal models of arthritis: How does it relate to rheumatoid arthritis?

Bevaart¹,

Vervoordeldonk²,

Tak³

2010

Arthritis & Rheumatism

232

193

View full text Add to dashboard Cite

There are accumulating data describing the association between diabetes and cancer mortality from Westernised populations. There are no data describing the relationship between diabetes and cancer mortality in African or South Asian populations from developing countries. We explored the relationship of abnormal glucose tolerance and diabetes on cancer mortality risk in a large, multi‐ethnic cohort from the developing nation of Mauritius. Population‐based surveys were undertaken in 1987, 1992 and 1998. The 9559 participants comprised 66% of South Asian (Indian), 27% of African (Creole), and 7% of Chinese descent. Cox's proportional hazards model with time varying covariates was used to obtain hazard ratios (HRs) and 95% confidence intervals (95% CI) for risk of cancer mortality, after adjustment for confounding factors. In men, but not women, cancer mortality risk increased with rising 2h‐PG levels with HR for the top versus bottom quintile of 2.77 (95%CI: 1.28 to 5.98). South Asian men with known diabetes had a significantly greater risk of cancer mortality than those with normal glucose tolerance (NGT) HR: 2.74 (95%CI: 1.00‐7.56). Overall, impaired glucose tolerance was associated with an elevated risk of cancer mortality compared to NGT (HR: 1.47, 95% CI: 0.98–2.19), though this was not significant. We have shown that the association between abnormal glucose tolerance and cancer extends to those of African and South Asian descent. These results highlight the importance of understanding this relationship in a global context to direct future health policy given the rapid increase in type 2 diabetes, especially in developing nations.

show abstract

Role of chemokines and cytokines in a reactivation model of arthritis in rats induced by injection with streptococcal cell walls

Cited by 61 publications

References 31 publications

Chemokine receptor expression and in vivo signaling pathways in the joints of rats with adjuvant‐induced arthritis

Chemokine receptor expression and in vivo signaling pathways in the joints of rats with adjuvant‐induced arthritis

Targeting the Function of IFN-γ-Inducible Protein 10 Suppresses Ongoing Adjuvant Arthritis

Evaluation of therapeutic targets in animal models of arthritis: How does it relate to rheumatoid arthritis?

Contact Info

Product

Resources

About