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Amebic monocyte locomotion inhibitory factor peptide ameliorates inflammation in CIA mouse model by downregulation of cell adhesion, inflammation/chemotaxis, and matrix metalloproteinases genes
Amebic monocyte locomotion inhibitory factor peptide ameliorates inflammation in CIA mouse model by downregulation of cell adhesion, inflammation/chemotaxis, and matrix metalloproteinases genes
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Amebic monocyte locomotion inhibitory factor peptide ameliorates inflammation in CIA mouse model by downregulation of cell adhesion, inflammation/chemotaxis, and matrix metalloproteinases genes
Amebic monocyte locomotion inhibitory factor peptide ameliorates inflammation in CIA mouse model by downregulation of cell adhesion, inflammation/chemotaxis, and matrix metalloproteinases genes

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Amebic monocyte locomotion inhibitory factor peptide ameliorates inflammation in CIA mouse model by downregulation of cell adhesion, inflammation/chemotaxis, and matrix metalloproteinases genes
Amebic monocyte locomotion inhibitory factor peptide ameliorates inflammation in CIA mouse model by downregulation of cell adhesion, inflammation/chemotaxis, and matrix metalloproteinases genes
Journal Article

Amebic monocyte locomotion inhibitory factor peptide ameliorates inflammation in CIA mouse model by downregulation of cell adhesion, inflammation/chemotaxis, and matrix metalloproteinases genes

2010
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Overview
Objective and design Monocyte locomotion inhibitory factor (MLIF), an amebic peptide with antiinflammatory properties, was evaluated in collagen-induced arthritis (CIA) to test its effects on the onset and acute inflammatory response of arthritis. Material DBA1/J mice at 8-10 weeks of age were divided into four groups (eight mice per group). Treatment The adjuvant group received Freund adjuvant, the CIA group was immunized with collagen II, the MLIF/CIA group received collagen II and MLIF, and the MLIF group received MLIF and Freund adjuvant. Methods All groups were evaluated clinically. Seven weeks after the collagen injection, at the peak of the clinical arthritis score, limb specimens were collected and histological studies and gene expression analysis using microarrays were performed. Results MLIF administered weekly as a preventive scheme delayed and reduced the severity of acute arthritis. MLIF induced gene changes in functional categories including adhesion molecules, matrix metalloproteinases, and inflammatory cytokines. Conclusions MLIF could be an interesting new molecule to investigate in the field of rheumatoid arthritis pathogenesis research for its potential to prevent inflammation.

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