Humans ; Microcirculation ; Sepsis ; physiopathology

Humans ; Intestinal Diseases ; physiopathology ; Sepsis ; physiopathology

Gastrointestinal Tract ; physiopathology ; Humans ; Infection ; physiopathology ; Sepsis ; physiopathology ; Shock, Septic ; physiopathology

Humans ; Kidney Diseases ; etiology ; physiopathology ; Sepsis ; complications ; physiopathology ; Shock, Septic ; complications ; physiopathology

Severe sepsis provokes significant abnormalities in host neuroendocrine system, and they are hallmarked by the glucocorticoid and growth hormone resistance, vasopressin deficiency, and compromised vagal activity. As a consequence, the increased stress hormones result in a hyperdynamic circulation, hypermetabolic state, and the hyperglycemia/insulin resistance in sepsis. The cardiac autonomic dysfunction also occurs as a consequence of depressed vagal activity. Current therapeutic strategies include insulin therapy to control hyperglycemia, physiologic doses of corticosteroids to improve immunity, growth hormone to reverse negative nitrogen balance, and vasopressin to raise blood pressure. Non-specific beta-adrenergic blockade has also been attempted to either attenuate the hypermetabolism or to reduce the inflammatory response. Future therapy may be directed at both central and peripheral immune system so as to alleviate the hyperdynamic inflammatory state and possibly encephalopathy in severe sepsis.
Autonomic Nervous System ; physiopathology ; Humans ; Neurosecretory Systems ; physiopathology ; Sepsis ; physiopathology ; therapy

OBJECTIVESepsis is defined as life-threatening organ dysfunction due to a dysregulated host response to infection. In this article, we reviewed the correlation between neutrophil dysfunction and sepsis.

DATA SOURCESArticles published up to May 31, 2016, were selected from the PubMed databases, with the keywords of "neutrophil function", "neutrophil dysfunction", and "sepsis".

STUDY SELECTIONArticles were obtained and reviewed to analyze the neutrophil function in infection and neutrophil dysfunction in sepsis.

RESULTSWe emphasized the diagnosis of sepsis and its limitations. Pathophysiological mechanisms involve a generalized circulatory, immune, coagulopathic, and/or neuroendocrine response to infection. Many studies focused on neutrophil burst or cytokines. Complement activation, impairment of neutrophil migration, and endothelial lesions are involved in this progress. Alterations of cytokines, chemokines, and other mediators contribute to neutrophil dysfunction in sepsis.

CONCLUSIONSSepsis represents a severe derangement of the immune response to infection, resulting in neutrophil dysfunction. Neutrophil dysfunction promotes sepsis and even leads to organ failure. Mechanism studies, clinical practice, and strategies to interrupt dysregulated neutrophil function in sepsis are desperately needed.

Endothelial Cells ; metabolism ; pathology ; Humans ; Sepsis ; metabolism ; physiopathology

Adrenal Cortex Diseases ; etiology ; Child ; Humans ; Sepsis ; complications ; physiopathology ; Shock, Septic ; complications ; physiopathology

Anticoagulants ; classification ; therapeutic use ; Child ; Humans ; Sepsis ; drug therapy ; physiopathology ; Treatment Outcome

OBJECTIVE: To investigate the functional pathways enriched and differentially expressed genes (DEGs) in peripheral blood mononuclear cells (PBMCs) of patients with gram-positive and gram-negative sepsis. METHODS: Dataset GSE9960 obtained from NCBI GEO database containing PBMC samples from 16 non-infectious systematic inflammatory response syndrome (SIRS) patients, 17 gram-positive septic patients and 18 gram-negative septic patients were included in the study. Functional pathway annotations were conducted by gene set enrichment analysis and weighted gene co-expression network analysis. DEGs were filtered and master DEGs were then validated in PBMCs of gram-positive septic, gram-negative septic and non-infectious SIRS patients. RESULTS: The enriched gene sets in gram-positive sepsis and gram-negative sepsis were significantly different. The results indicated the opposite co-expression networks in SIRS and gram-negative sepsis, and the entirely different co-expression networks in gram-positive and gram-negative sepsis. Furthermore, we validated that CONCLUSIONS The results indicate that there are differences in the mechanism and pathogenesis of gram-positive and gram-negative sepsis, which may provide potential markers for sepsis diagnosis and empirical antimicrobial therapy.
Biomarkers/analysis* ; Gene Expression Profiling ; Gram-Negative Bacterial Infections/physiopathology* ; Gram-Positive Bacterial Infections/physiopathology* ; Humans ; Leukocytes, Mononuclear/pathology* ; Sepsis/physiopathology*