Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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GENE EXPRESSION OF AN ANTI-INFLAMMATORY PENTAPEPTIDE ON CIA MURINE DEVELOPMENT

ABSTRACT: Monocyte Locomotion Inhibitory Factor (MLIF), an amoebic peptide, has an anti-inflammatory role, delaying the arrival of mononuclear cells to inflammatory sites, down regulating adhesin molecules and chemokines. We used microarrays to detail the global gene expression underlying anti-inflammatory effect of MILF in an inflammatory model. Collagen type II (CII) emulsified on complet Freund adjuvant, was injected on the tail of the base of DBA1J mice, 8 weeks older, and booster with CII emulsified in incomple Freund adjuvant three weeks later. MLIF was administrated intranasally weekly since one week before induction. Keywords: comparison effect Articular tissues of all mices were collected at the peak time of clinical severity (four weeks before booster), for RNA extraction and hybridization on Affymetrix microarrays. We induces CIA with chicken collagen type II, emulsified with Complet Adjuvant of Freund, and the controls were mice induced only with Complet Adjuvant of Freund with or without MLIF

ORGANISM(S): Mus musculus

SUBMITTER: Juan Velazquez

PROVIDER: E-GEOD-14721 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:The pathogenesis of rheumatoid arthritis (RA) is complicated and involves both innate and adaptive immunity [5]. The innate immunity such as macrophages or fibroblast-like synoviocytes (FLS) in the synovium can generate inflammatory mediators, including TNF-α, IL-1, IL-6, IL-17, IFN-γ, and chemo kines that lead to synovial inflammation, bone erosion, and cartilage damage [6-8]. The IL-17 signaling mediates the autoantibody production in collagen-induced arthritis (CIA) model [9]. However, the treatment response with an anti-IL17 monoclonal antibody in RA patients shows a high degree of heterogeneity [10]. The inhibitors of the Janus kinase (JAK) pathway are approved for RA patients [11]. These data suggest that the targeted multiple cytokines through the JAK pathway are useful for RA treatment. Disturbance of type I IFNs (IFNs-I) signaling and production drive autoimmune development [12]. The presymptomatic RA patients display an increase of IFNs-I before the onset of symptoms [13]. The RA patients also show the elevation of IFN- α in the synovial fluid and high expression of IFNs-I regulated gene in peripheral blood mononuclear cells (PBMC) [14]. However, the role of IFNs-I in arthritis and bone homeostasis has suggested the accelerating effect of arthritis and bone damage. The interferon-alpha receptor knockout mice develop arthritis severity higher than wild-type mice in the model of antigen-induced arthritis [15]. IFNs-I also affects the bone homeostasis by inhibiting osteoclastogenesis via receptor activator of nuclear factor-kappa B (RANK) pathway, and reduction of c-FOS expression [16-18]. Therefore, the goal of RA treatment with antagonizing the IFNs-I pathway has to be optimized between efficacy and potentially adverse effect. STING is a cytosolic DNA sensor that initiates the production of IFNs-I. STING functions have been reported as both pro-inflammatory signaling and negative regulator against inflammation [19-21]. The mutation in exon 5 of the STING gene results in gain function leading to initiate inflammation and cause the Sting associated vasculopathy with onset in infancy (SAVI) [22]. Loss of STING function rescues DNaseII-deficient mice from lethality and polyarthritis [23]. However, Sting-deficient lupus mice (MRL/Lpr mice) show higher and earlier mortality than Sting-sufficient MRL/Lpr mice [24]. The pathology also shows lymphoid hypertrophy with a higher amount of macrophages and granulocytes infiltration, autoantibodies, and cytokine [24]. The objective of this study was to identify the role of STING in the pathogenesis of rheumatoid arthritis using collagen-induced arthritis (CIA) model as a representative model of the human RA.

Project description:Methods: During the last trimester of the gestation, 12 heifers were immunized using intramuscular injection with heat-killed E. coli P4 emulsified in Montanide ISA 61VG® oil adjuvant (SEPPIC), as recommended by the manufacturer. Two months later, half of the heifers (IM group, n=6) got a second injection as a booster. Others received 50 µg of protein concentrate prepared from E. coli P4 supernate in two quarters (IMM group, n=6). Cows of the control group (CONT, n=6) were injected intramuscularly with adjuvant only at the same dates. Cows were then challenged on average at 49 days in milk in one healthy quarter by infusion of a E. coli P4 bacterial suspension (10e3 bacteria). Blood was collected before experiment, and seven days after the first and the second injection (immunization phase), and then at 0, 12 and 40 hours after infection (challenge phase). Results : Whole blood transcriptome through RNA-seq identifies the main biological functions altered during an E. coli mastitis. Systemic and mammary routes of E. coli immunization elicit different gene expression profiles that correlated with the levels of protection Conclusions: Intramuscular immunization is correlated with a high systemic Th1 response that is not as protective as the local route of immunization. During the last trimester of the gestation, 12 heifers were immunized using intramuscular injection with heat-killed E. coli P4 emulsified in Montanide ISA 61VG® oil adjuvant (SEPPIC), as recommended by the manufacturer. Two months later, half of the heifers (IM group, n=6) got a second injection as a booster. Others received 50 µg of protein concentrate prepared from E. coli P4 supernate in two quarters (IMM group, n=6). Cows of the control group (CONT, n=6) were injected intramuscularly with adjuvant only at the same dates. Cows were then challenged on average at 49 days in milk in one healthy quarter by infusion of a E. coli P4 bacterial suspension (10e3 bacteria). Blood was collected before experiment, and seven days after the first and the second injection (immunization phase), and then at 0, 12 and 40 hours after infection (challenge phase).

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GENE EXPRESSION OF AN ANTI-INFLAMMATORY PENTAPEPTIDE ON CIA MURINE DEVELOPMENT

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