ABSTRACT
We have explored whether lipopolysaccharide (LPS, endotoxin) induces pancreatic injury on pancreatic acinar cells both in vivo and in vitro. Wistar male rats were treated with four intraperitoneal injections of 10 mg/kg LPS, and AR4-2J cells were exposed to increasing doses of LPS. Expression of pancreatitis-associated-protein (PAP) mRNA was strongly induced in AR4-2J cells exposed to LPS, while amylase mRNA was reduced. LPS also induced apoptosis and expression of TNF-alpha, IL-1beta, and IL-8 mRNA in AR4-2J cells. The in vivo effect of LPS showed structural signs of cellular damage, including numerous cytoplasmic vacuoles, severe nuclear alterations, and high expression of PAP mRNA. This study demonstrated that LPS induced pancreatic damage by directly affecting the pancreatic acinar cells. The role of LPS in the pathophysiology of acute pancreatitis may be partly due to the effect LPS has on the acinar cell.
Subject(s)
Antigens, Neoplasm , Biomarkers, Tumor , Lectins, C-Type , Lipopolysaccharides/toxicity , Pancreas/drug effects , Pancreatitis/physiopathology , Systemic Inflammatory Response Syndrome/physiopathology , Acute Disease , Acute-Phase Proteins/genetics , Animals , Apoptosis/drug effects , Cell Line , Gene Expression/drug effects , Humans , Injections, Intraperitoneal , Interleukin-1/genetics , Interleukin-8/genetics , Male , Pancreas/pathology , Pancreas/physiopathology , Pancreatitis/chemically induced , Pancreatitis/pathology , Pancreatitis-Associated Proteins , RNA, Messenger/genetics , Rats , Rats, Wistar , Systemic Inflammatory Response Syndrome/pathology , Tumor Necrosis Factor-alpha/geneticsABSTRACT
To elucidate whether pancreatic acinar cell submitted to stress is able to express TNF-alpha, we studied TNF-alpha mRNA expression by Northern blot and in situ hybridization in healthy pancreas, in tissue from caerulein-induced pancreatitis and after lipopolysaccharide (LPS) treatment. In specimens from normal pancreas, TNF-alpha mRNA expression, as judged by both Northern blot and in situ hybridization, was negative, whereas a strong but transient expression was observed in acinar cells from caerulein pancreatitis and LPS treatment. TNF-alpha mRNA appeared as rapidly as 30 min after treatment, and was maximal 6 h after. At this time, there was mild infiltration consisting mostly of polymorphonuclear leukocytes (PMNL) and no signal of TNF-alpha transcript was found in their cytoplasm. Our results strongly indicate that pancreatic acinar cell is the source of TNF-alpha early in the course of acute pancreatitis and LPS treatment, and suggest that the expression of this cytokine is a part of a general response of the acinar cell to aggression.
Subject(s)
Pancreas/metabolism , Tumor Necrosis Factor-alpha/genetics , Animals , Ceruletide , Gene Expression Regulation , In Situ Hybridization , Lipopolysaccharides/pharmacology , Male , Mice , Pancreas/cytology , Pancreatitis/chemically induced , Pancreatitis/metabolism , Pancreatitis/pathologyABSTRACT
Se describen 219 episodios de endocarditis infecciosa en válvula nativa. Los hemocultivos fueron positivos en el 80 por ciento; de éstos, los Streptococcus no enterococcus representaron el 53 por ciento (Streptococcus viridans 34,8 por ciento), los Staphylococcus el 27,4 por ciento (Staphylococcus aureus 22,8 por ciento), los Enterococcus el 13,7 por ciento y los Gram negativos el 5,9 por ciento. El 56 por ciento de los pacientes había recibido antibioticoterapia previa. La insuficiencia cardíaca (39 por ciento) y las embolias (24,7 por ciento) fueron las complicaciones más frecuentes. Endocarditis infecciosas en válvula nativa por Staphylococcus aureus presentaron una incidencia mayor de embolismo. La mortalidad hospitalaria fue del 24,1 por ciento
Subject(s)
Humans , Male , Female , Adult , Middle Aged , Endocarditis, Bacterial/complications , Endocarditis, Bacterial/etiology , Endocarditis, Bacterial/microbiology , Endocarditis, Bacterial/surgery , Hospital Mortality , Heart Failure , Pulmonary Embolism , Streptococcal InfectionsABSTRACT
Se describen 219 episodios de endocarditis infecciosa en válvula nativa. Los hemocultivos fueron positivos en el 80 por ciento; de éstos, los Streptococcus no enterococcus representaron el 53 por ciento (Streptococcus viridans 34,8 por ciento), los Staphylococcus el 27,4 por ciento (Staphylococcus aureus 22,8 por ciento), los Enterococcus el 13,7 por ciento y los Gram negativos el 5,9 por ciento. El 56 por ciento de los pacientes había recibido antibioticoterapia previa. La insuficiencia cardíaca (39 por ciento) y las embolias (24,7 por ciento) fueron las complicaciones más frecuentes. Endocarditis infecciosas en válvula nativa por Staphylococcus aureus presentaron una incidencia mayor de embolismo. La mortalidad hospitalaria fue del 24,1 por ciento (AU)
