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Fonseca MT. Hypothermia in sepsis: natural development and biological value. [Ph. D. Thesis (Immunology)]. São Paulo: Instituto de Ciências Biomédicas, Universidade de São Paulo; 2017. Sepsis is always accompanied by changes in body temperature, fever or hypothermia. The thermoregulatory response depends on the severity of the inflammation and the ambient temperature (TA), and the natural onset of hypothermia prevails in more severe cases of sepsis and affects approximately 10% of hospitalized patients. In most cases, this response is seen as something deregulated and progressive, even in the absence of a significant assessment of the natural course of this phenomenon in humans, since, experimental studies have shown that animals in endotoxic shock prefer to remain in a cold environment and develop hypothermia. The present study has as main objectives (i) to characterize the temporal course of hypothermia in a rare group of septic patients; (Ii) to develop a well-controlled experimental model of severe monobacterial sepsis; (iii) to assess how hypothermia, resulting from E. coli-induced peritonitis, alters the lung function of rats, with emphasis on the role of neutrophils and macrophages; and (iv) elucidate how hypothermia regulates the innate immune response and hence the infection control. Our results showed for the first time that hypothermia in septic patients is a transient, non-terminal phenomenon and that physiological dysfunctions or pharmacotherapy does not trigger the onset of this response. In addition, an experimental model of severe monobacterial sepsis was developed in which, when submitted to cold environments, the rats developed regulated hypothermia. Hypothermia preserved the pulmonary function of septic rats and decreased the neutrophil infiltrate to the lungs and peritoneum, and this cell expressed less the CCR2 receptor, involved in migration, and still had difficulty in motility. Despite all these setbacks, the infection was controlled in the lungs and peritoneum 20 h after sepsis, probably due to the increased microbicidal activity of macrophages in hypothermia. Therefore, we can conclude that hypothermia is a regulated, transient, self-limiting and non-terminal phenomenon in humans, unlike the deregulated and progressive response that was believed to exist. Furthermore, hypothermia decreases the inflammatory action of neutrophils at the same time as it potentiates the microbicidal activity of macrophages. These cells kill more at the same time as they favor a less inflammatory profile, showing that there is a selective mechanistic refinement of macrophages in hypothermia.

Hipotermia na sepse: desenvolvimento natural e valor biológico.