Loss of Bid does not alter the cytokine and chemokine milieu of the joint

<p><b>Copyright information:</b></p><p>Taken from "Pro-apoptotic Bid is required for the resolution of the effector phase of inflammatory arthritis"</p><p>http://arthritis-research.com/content/9/3/R49</p><p>Arthritis Research & Therapy 2007;9(3):R49-R49.</p><p>Published online 17 May 2007</p><p>PMCID:PMC2206343.</p><p></p> Pro-inflammatory cytokine production in ankle joints following transfer of K/BxN serum. Untreated wild-type (Wt) and Bid-/- mice were euthanized at three, five, or seven days post-serum transfer. Ankles from each mouse (days 3, = 6 (Wt) and n= 8 (Bid-/-); day 5, = 10; day 7, = 12 (Wt) and = 8 (Bid-/-)) were isolated, snap frozen, ground into a fine powder, lysed, and examined for production of tumor necrosis factor (TNF)α and IL-1β using sandwich ELISAs. Chemokine production in ankle joints following transfer of K/BxN serum. Ankles lysates as described above were examined for production of CXC chemokine (KC) and monocyte chemoattractant protein (MCP)-1 using ELISA. Data are shown as μg/μl per joint. Values represent the mean ± standard error, which were compared by Student's -test

Histological scores of ankle sections from wild-type (Wt) and Bid-/- mice

<p><b>Copyright information:</b></p><p>Taken from "Pro-apoptotic Bid is required for the resolution of the effector phase of inflammatory arthritis"</p><p>http://arthritis-research.com/content/9/3/R49</p><p>Arthritis Research & Therapy 2007;9(3):R49-R49.</p><p>Published online 17 May 2007</p><p>PMCID:PMC2206343.</p><p></p> Bid-/- mice have increased inflammation and joint destruction compared to Wt mice. Ankles isolated from mice (Wt, = 9; Bid-/- = 7) were prepared as described in Figure 2. Ankle sections were evaluated and scored by a pathologist blinded to the study as described in the Materials and methods section. Values represent the mean ± standard error of ankles/time point, which were compared by Student's -test. Increased numbers of lymphocytes and polymorphonuclear (PMNs) cells in inflamed Bid-/- joints. Ankles were prepared as described above. Values represent the mean ± standard error of ankles/time point, which were compared by Student's -test. Arthritic Bid-/- mice have more macrophages in the pannus and in the whole joint. Ankles were examined for F4/80 antigen as described in Materials and methods. The number of positive cells for F4/80 in pannus, synovial lining, and whole joint was determined by a pathologist blinded to the study. Values represent the mean ± standard error of ankles/time point, which were compared by Student's -test

Additional file 1: Figure S1. of Genetic deficiency of Wnt5a diminishes disease severity in a murine model of rheumatoid arthritis

Gene expression of Wnt5a and ROR2 during the development of STIA. Figure S2. Characteristics of the baseline phenotype of control and Wnt5a cKO mice. Figure S3. Histology of the baseline phenotype of control and Wnt5a cKO mice. Figure S4. Baseline osteoclast phenotype of control and Wnt5a cKO mice. Figure S5. Additional histopathological scoring of arthritis in Wnt5a cKO mice. Figure S6. Gene expression of cytokines and osteoclast genes in paws of control and Wnt5a cKO mice undergoďťżing STIA. Figure S7. Characteristics of fusing osteoclasts in the absence and presence of Wnt5a-treated medium. Figure S8. Gene expression of osteoclast markers during BMDM differentiation to osteoclasts. Figure S9. Gene expression of NFATa1 markers during BMDM differentiation to osteoclasts. (PDF 4647 kb

Rosuvastatin does not alter the clinical course of influenza A infection in mice.

<p>We treated mice with rosuvastatin or control therapy starting 3 days before they were infected with either Udorn or WSN strains of influenza A virus and measured (<b>A</b>) WSN-associated mortality and (<b>B</b>) Udorn- and (<b>C</b>) WSN-associated changes in daily weight.</p

Rosuvastatin does not modify the severity of influenza A-induced lung injury.

<p>We treated mice with rosuvastatin or control starting 3 days before they were infected with either Udorn or WSN strains of influenza A virus. (<b>A, B</b>) Four days after influenza A infection, we collected lungs for assessment of lung histology. Representative low (×100) and high (×1,000) magnification images of lung sections from mice treated with either the (<b>A</b>) Udorn or (<b>B</b>) WSN strains. (<b>C, D</b>) BALF protein concentrations in mice 4 days after infection with either the (<b>C</b>) Udorn or (<b>D</b>) WSN strains. (<b>E</b>) Wet-to-dry weight ratio of lungs from mice 6 days after infection with the WSN strain. *P<0.05 Udorn vs. PBS, WSN vs. PBS. NS; not significant (Rosuvastatin vs. Control treatment).</p

Rosuvastatin does not alter the influenza A-induced expression of activation markers on inflammatory cells in the lungs.

<p>We treated mice with rosuvastatin or control therapy starting 3 days before they were infected with WSN strains of influenza A virus. Four days after influenza A infection, we performed flow cytometry in digested lung tissue to determine the effect of rosuvastatin on activation markers expressed on (<b>A</b>) alveolar macrophages and (<b>B</b>) interstitial macrophages. *P<0.05 WSN vs. PBS. NS; not significant (Rosuvastatin vs. Control treatment).</p

Rosuvastatin does not affect the influenza A-induced changes in pro-inflammatory cytokines in the lungs.

<p>We treated mice with rosuvastatin or control starting 3 days before they were infected with either Udorn or WSN strains of influenza A virus. Four days after influenza A infection, we collected bronchoalveolar lavage fluid (BALF) and measured (<b>A, B</b>) TNF-α and (<b>C, D</b>) IL-6 levels. *P<0.05 Udorn vs. PBS, WSN vs. PBS. NS; not significant (Rosuvastatin vs. Control treatment).</p

Rosuvastatin does not have an effect on influenza A-induced changes in inflammatory cell count and differential in the lungs.

<p>We treated mice with rosuvastatin or control therapy starting 3 days before they were infected with either Udorn or WSN strains of influenza A virus. Four days after influenza A infection, (<b>A</b>, <b>B</b>) we measured cell count in the bronchoalveolar lavage fluid (BALF). (<b>C</b>) We also performed flow cytometry in digested lung tissue from mice treated with WSN strain of influenza A virus to determine differential count of inflammatory cells including alveolar and interstitial macrophages, monocytes and neutrophils. *P<0.05 Udorn vs. PBS, WSN vs. PBS. NS; not significant (Rosuvastatin vs. Control treatment).</p

MOESM3 of ApoE deficiency exacerbates the development and sustainment of a semi-chronic K/BxN serum transfer-induced arthritis model

Additional file 3. Alteration of levels of circulating cytokines/chemokines in C57BL/6 and ApoE−/− mice with induction of arthritis. Serum levels from non-arthritic and arthritic C57BL/6 (control, n = 2 non-arthritic and n = 13 arthritic) and ApoE−/− (n = 3 non-arthritic and n = 6 arthritic) mice at 4–6 months. Data are represented as mean ± SEM. * denotes statistically significant differences. *p < 0.05, **p < 0.01,***p < 0.001

Additional file 2: Table S2. of Conditional deletion of caspase-8 in macrophages alters macrophage activation in a RIPK-dependent manner

ANOVA comparison data from Affymetrix QuantiGene 2.0 custom panel 21522 for analysis of macrophage polarization. (XLS 68 kb