Tissue influx of neutrophils and monocytes is delayed during development of trovafloxacin-induced tumor necrosis factor-dependent liver injury in mice

Keyphrases

• Tumor Necrosis Factor-α 100%
• Neutrophils 100%
• Monocytes 100%
• Liver Injury 100%
• Trovafloxacin 100%
• Idiosyncratic Drug-induced Liver Injury 40%
• Levofloxacin 30%
• Monocyte-derived Macrophages 20%
• Leukocytes 20%
• Interleukin-6 10%
• Apoptosis 10%
• Murine Model 10%
• Liver 10%
• Human Animals 10%
• Human Patients 10%
• Cytotoxic Effect 10%
• Stress Signaling 10%
• Acute Liver Injury 10%
• Innate Immune Cells 10%
• Anti-inflammatory Function 10%
• Alanine Aminotransferase Level 10%
• Immunological Changes 10%
• Inflammatory Stress 10%
• Hepatic Vessels 10%
• Severe Hepatotoxicity 10%

Pharmacology, Toxicology and Pharmaceutical Science

• Tumor Necrosis Factor 100%
• Liver Injury 100%
• Trovafloxacin 100%
• Toxic Hepatitis 40%
• Levofloxacin 30%
• Anti-Inflammatory Drug 10%
• Hepatotoxicity 10%
• Alanine Aminotransferase 10%
• Interleukin 6 10%
• Cytotoxicity 10%

Immunology and Microbiology

• Tumor Necrosis Factor 100%
• Neutrophil 100%
• Macrophage 33%
• Leukocyte 33%
• Interleukin 6 16%
• Cytotoxicity 16%
• Alanine Aminotransferase Level 16%
• Programmed Cell Death 16%
• Innate Immune Cell 16%