Journal:

Article Title: Therapeutic Effects of Benzoxazinorifamycin KRM-1648 Administered Alone or in Combination with a Half-Sized Secretory Leukocyte Protease Inhibitor or the Nonsteroidal Anti-Inflammatory Drug Diclofenac Sodium against Mycobacterium avium Complex Infection in Mice

doi:

Figure Lengend Snippet: Effects of 1/2 SLPI and diclofenac Na on production of TNF-α, IL-10, and TGF-β by MAC-stimulated Mφs a

Article Snippet: After rinsing of the wells with 0.1% BSA–PBS, either biotinylated rat anti-mouse TNF-α (Pharmingen) Ab, biotinylated rat anti-mouse IL-10 (Pharmingen) Ab, or chicken anti-human TGF-β Ab (R & D Systems Inc., Minneapolis, Minn.) was added as the detecting Ab and was allowed to react with the complex consisting of the corresponding cytokines and capture Abs.

Techniques: Infection

Journal: Environmental Health Perspectives

Article Title: Lead Increases Lipopolysaccharide-Induced Liver Injury through Tumor Necrosis Factor-α Overexpression by Monocytes/Macrophages: Role of Protein Kinase C and p42/44 Mitogen-Activated Protein Kinase

doi: 10.1289/ehp.8550

Figure Lengend Snippet: Expression of TNF-α ( A ), AST ( B ), and ALT ( C ) in A/J mice exposed to Pb, LPS, Pb+LPS, or saline (control). ND, not detectable. Blood was collected 1.5 hr after treatment to determine serum TNF-α ( A ). Serum AST ( B ) and ALT ( C ) were evaluated 24 hr posttreatment. n = 3 per treatment. * p < 0.05 compared with LPS.

Article Snippet: Cells were fixed and per-meabilized using a commercial kit (Cytofix/Cytoperm; PharMingen, San Diego, CA, USA) and stained for intracellular TNF-α using fluorescein isothiocyanate (FITC)-conjugated rat anti-mouse TNF-α Ab (PharMingen).

Techniques: Expressing

Journal: Environmental Health Perspectives

Article Title: Lead Increases Lipopolysaccharide-Induced Liver Injury through Tumor Necrosis Factor-α Overexpression by Monocytes/Macrophages: Role of Protein Kinase C and p42/44 Mitogen-Activated Protein Kinase

doi: 10.1289/ehp.8550

Figure Lengend Snippet: Effects of TNF-α inhibitor on liver damage in A/J mice intraperitoneally injected with PTX (100 mg/kg) or H 2 O as vehicle (control). One hour later, mice were stimulated with Pb, LPS, Pb+LPS, or saline only (control). ND, not detectable. Blood was collected either 1.5 hr after Pb, LPS, or Pb+LPS treatment to determine serum TNF-α ( A ), or 24 hr posttreatment to determine serum AST ( B ) and ALT ( C ). n = 3 per treatment. * p < 0.05 compared with Pb+LPS.

Article Snippet: Cells were fixed and per-meabilized using a commercial kit (Cytofix/Cytoperm; PharMingen, San Diego, CA, USA) and stained for intracellular TNF-α using fluorescein isothiocyanate (FITC)-conjugated rat anti-mouse TNF-α Ab (PharMingen).

Techniques: Injection

Journal: Environmental Health Perspectives

Article Title: Lead Increases Lipopolysaccharide-Induced Liver Injury through Tumor Necrosis Factor-α Overexpression by Monocytes/Macrophages: Role of Protein Kinase C and p42/44 Mitogen-Activated Protein Kinase

doi: 10.1289/ehp.8550

Figure Lengend Snippet: TNF-α expression in cultured whole blood of mice. Whole blood was stimulated in vitro with LPS (5 μg/mL) with or without Pb acetate (1 μM) for 1.5 hr. ND, not detectable. ( A ) TNF-α in serum measured by ELISA. ( B ) Density plot for blood cells from the Pb+LPS-treated group doubly stained for surface CD14 and intracellular TNF-α ( x -axis, TNF-α; y -axis, CD14) and analyzed using flow cytometric analysis; the percentage shown is the ratio of TNF-α + to CD14 + cells. ( C ) Mean percentage of TNF-α + cells in CD14 + population (mean ± SE) of groups treated with Pb, LPS, or Pb + LPS ( n = 3–5 per treatment). * p < 0.05 compared with LPS.

Article Snippet: Cells were fixed and per-meabilized using a commercial kit (Cytofix/Cytoperm; PharMingen, San Diego, CA, USA) and stained for intracellular TNF-α using fluorescein isothiocyanate (FITC)-conjugated rat anti-mouse TNF-α Ab (PharMingen).

Techniques: Expressing, Cell Culture, In Vitro, Enzyme-linked Immunosorbent Assay, Staining

Journal: Environmental Health Perspectives

Article Title: Lead Increases Lipopolysaccharide-Induced Liver Injury through Tumor Necrosis Factor-α Overexpression by Monocytes/Macrophages: Role of Protein Kinase C and p42/44 Mitogen-Activated Protein Kinase

doi: 10.1289/ehp.8550

Figure Lengend Snippet: Liver damage after inactivating monocytes/macrophages in A/J mice intravenously injected with GdCl 3 (40 mg/kg) or H 2 O as vehicle (control). After 24 hr, mice were stimulated with Pb, LPS, Pb+LPS, or saline only (control). ND, not detectable. Blood was collected either 1.5 hr posttreatment to determine serum TNF-α ( A ) or 24 hr posttreatment to determine serum AST ( B ) and ALT ( C ). n = 3 per treatment. * p < 0.05 compared with Pb+LPS.

Article Snippet: Cells were fixed and per-meabilized using a commercial kit (Cytofix/Cytoperm; PharMingen, San Diego, CA, USA) and stained for intracellular TNF-α using fluorescein isothiocyanate (FITC)-conjugated rat anti-mouse TNF-α Ab (PharMingen).

Techniques: Injection

Journal: Environmental Health Perspectives

Article Title: Lead Increases Lipopolysaccharide-Induced Liver Injury through Tumor Necrosis Factor-α Overexpression by Monocytes/Macrophages: Role of Protein Kinase C and p42/44 Mitogen-Activated Protein Kinase

doi: 10.1289/ehp.8550

Figure Lengend Snippet: PKC and p42/44 MAPK as inhibitors on TNF-α expression and liver damage in mice pretreated (intraperitoneal injection) with C 21 H 18 NO 4 Cl (Ch; 5 mg/kg, 30 min), U0126 (25 μmol/kg, 10 min), or H 2 O vehicle (control, 30 min) and then stimulated with Pb, LPS, Pb+LPS, or saline only (control). ND, not detectable. Blood was collected either 1.5 hr after treatment to determine serum TNF-α ( A ), or 24 hr posttreatment to determine serum AST ( B ) and ALT ( C ). n = 3 per treatment. * p < 0.05 Ch+Pb+LPS or U0126+Pb+LPS compared with Pb+LPS.

Article Snippet: Cells were fixed and per-meabilized using a commercial kit (Cytofix/Cytoperm; PharMingen, San Diego, CA, USA) and stained for intracellular TNF-α using fluorescein isothiocyanate (FITC)-conjugated rat anti-mouse TNF-α Ab (PharMingen).

Techniques: Expressing, Injection

Journal: Environmental Health Perspectives

Article Title: Lead Increases Lipopolysaccharide-Induced Liver Injury through Tumor Necrosis Factor-α Overexpression by Monocytes/Macrophages: Role of Protein Kinase C and p42/44 Mitogen-Activated Protein Kinase

doi: 10.1289/ehp.8550

Figure Lengend Snippet: PKC and p42/44 MAPK in the induction of TNF-α in peritoneal macrophages and RAW264.7 cells. ( A ) TNF-α measured by ELISA in conditioned medium from peritoneal macrophages cultured in a 24-well plate (5 × 10 5 cells/well). After 24 hr of attachment, cells were stimulated with LPS (0.1 or 1 ng/mL) combined with Pb (10 μM) for 3 hr. To evaluate the effect of kinase inhibitors, peritoneal macrophages were pretreated with U0126 ( B ) or C 21 H 18 NO 4 Cl (Ch) ( C ) for 30 min and then stimulated with 0.1 ng/mL LPS plus 10 μM Pb for 3 hr. ( D ) RAW264.7 cells were seeded in a 96-well plate (1 × 10 4 cells/well) and stimulated for 3 hr with Pb (0, 1, or 10 μM) combined with LPS at various concentrations. To evaluate the effect of kinase inhibitors, RAW264.7 cells were pretreated with U0126 ( E ) or C 21 H 18 NO 4 Cl ( F ) for 30 min and then stimulated with 10 ng/mL LPS plus 10 μM Pb for 3 hr. n = 3. * p < 0.05 compared with Pb+LPS.

Article Snippet: Cells were fixed and per-meabilized using a commercial kit (Cytofix/Cytoperm; PharMingen, San Diego, CA, USA) and stained for intracellular TNF-α using fluorescein isothiocyanate (FITC)-conjugated rat anti-mouse TNF-α Ab (PharMingen).

Techniques: Enzyme-linked Immunosorbent Assay, Cell Culture

Journal: Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology

Article Title: Immune Suppression of Glia Maturation Factor Reverses Behavioral Impairment, Attenuates Amyloid Plaque Pathology and Neuroinflammation in an Alzheimer’s disease Mouse Model

doi: 10.1007/s11481-020-09929-4

Figure Lengend Snippet: Effect of GMF-antibody administration in 5XFAD mice on pro-inflammatory cytokines production in the cortex and hippocampal CA1region of 5XFAD mice. ELISA assays of pro-inflammatory cytokines TNF-α, IL-1β, and IL-6 were performed using cortical homogenates following 4 weeks of anti-GMF-antibody injection (a-c). ELISA assays using hippocampal homogenates following 4 weeks of GMF-antibody injection (d-f). Data are expressed as mean ± SEM (n=6) per group and quantified as percentage changes compared with WT. *P< 0.05 versus WT, #P<0.05 versus 5XFAD mice.

Article Snippet: Then, each well was incubated with respective antibodies against TNF-α anti-rat (1:200, R&D Systems, Minneapolis, MN), IL-1β anti-rabbit (1:250, CST) and IL-6 anti-goat (1:200, R&D Systems, Minneapolis, MN) for 2 h at 37 °C.

Techniques: Enzyme-linked Immunosorbent Assay, Injection