Dear colleagues,

The response to inflammation after endotoxin exposure is a broad response that includes fever, anorexia, and a number of hormonal and metabolic changes which are necessary to adapt the body to this new situation. This complex response leads to an increase in catabolism and a decrease in anabolism. The global effect is an increased release of energy substrates stored in the liver, adipose tissue, and skeletal muscle in order to provide energy to the activated immune cells. In this response, glucocorticoids play an important role, but cytokines also exert important effects.   

Endotoxin is a well-known modulator of hypothalamic and anterior pituitary hormones. The acute phase of inflammation induces a decreased activity of the thyroid and gonadal axes, with an increased activity of the adrenal axis. Inflammation also affects the hypothalamic neurons that regulate feeding behavior and basal metabolism. Several data suggest that sepsis or high-grade hypothalamic inflammation is associated with anorexia, decreased fat mass, skeletal muscle wasting, and weakness. By contrast, low-grade hypothalamic inflammation has been associated to obesity and insulin resistance. Both conditions increase morbidity and mortality in several diseases. Therefore, it is important to understand the molecular mechanisms by which inflammation modifies the hypothalamic regulation of energy homeostasis.

In addition to the effects on the metabolic and neuroendocrine system, endotoxin produces severe dysfunction in major organ systems such as brain, liver, heart and kidney. Molecular mechanisms involved in the pathophysiology include glucocorticoids and pro-inflammatory mediators, epigenetic changes, gut dysbiosis and the expression and secretion (in exosomes) of microRNAs.

We invite investigators to contribute with original research articles, as well as meta-analyses and review articles that will stimulate the comprehension of the molecular mechanisms underlying the relevance of neuroendocrine and metabolic responses to endotoxin and the pathophysiology related to the major organs dysfunction.

Potential topics include but are not limited to:            
- Molecular mechanisms involve in the pathophysiology of sepsis;
- Metabolic endotoxemia;
- Inflammation-induced epigenetic changes;
- Adipose tissue: a site of inflammation, adipocyte dysfunction, and the pathogenesis of obesity;
- Inflammation, intestinal microbiota, and insulin resistance;
- Hypothalamic inflammation and energy balance disruption;
- Inflammation-induced body weight loss, muscle wasting, and cachexia;
- Role of microRNAs in the response to inflammation induced by endotoxin.

• Endotoxin
• Inflammation 
• Anorexia 
• Adipokines 
• Cachexia 
• Epigenetic 
• Microbiota 
• mirRNA