Abstract
The cytokine migration inhibitory factor (MIF) has recently emerged as an important effector molecule of innate immune responses and sepsis. Two functional MIF promoter polymorphisms, a 5–8 CATT tetranucleotide repeat at -794 (CATT5–8) and a -173*G/C single nucleotide polymorphism, have been associated with susceptibility to and/or severity of rheumatoid arthritis, atopy and ulcerative colitis. Our objective was to study the impact of MIF gene polymorphisms on susceptibility to Neisseria meningitidis sepsis and to analyze the functional and biological effects of MIF polymorphisms in vitro.
Highlights
The pathogenesis of endotoxemic tubular dysfunction with failure in urine concentration is poorly understood
To clarify the role of cytokines and renal ischemia in the regulation of renal urea transporters, experiments were performed with cytokine knockout mice, mice treated with low-dose LPS (1, 5 mg/kg) as a sepsis model without induction of hypotension, glucocorticoid-treated mice, and mice with renal artery clipping serving as a model for renal ischemia
Our aim is to study the mechanisms involved in the resis- two-dose 100–200 ml hyperimmune plasma per day prevented a tance of CCR4–/– mice subjected to severe sepsis by cecal ligation following decrease of antibody levels, and in 98% of cases and puncture (CLP) and how Treg cells modulate this effect
Summary
The pathogenesis of endotoxemic tubular dysfunction with failure in urine concentration is poorly understood. Materials and methods Retrospective collection of data for all obstetric patients with severe sepsis and septic shock admitted to the intensive care unit over an 11-year period (May 1996–May 2007) in a maternity hospital (IASO). The ZnPPIX pretreatment prevents the failure of neutrophil endothelium rolling, adhesion and migration observed in vehicle-pretreated mice subjected to S-CLP As consequence, these mice presented reduced bacteremia, low levels of seric TNFα and lung neutrophil sequestration, reduced liver, kidney and cardiac injury and improved mean arterial pressure, resulting in an increase of the survival rate. Materials and methods TLR2-deficient (TLR2–/–) and C57BL/6 (WT) mice were subjected to severe polymicrobial sepsis by the cecal ligation and puncture (CLP) model, and neutrophil migration, bacteremia, CXCR2 expression and cytokines levels were evaluated.
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