Introduction More than 210, 000 people die from sepsis in the United States each year, with an annual cost of more than 16 billion dollars. Despite continued advances in treatment and prevention, sepsis is a growing problem, with a significant mortality rate of 28% to 50%. In the past, death from sepsis was thought be due to uncontrolled inflammation, and as a result, numerous anti-inflammatory therapeutics were developed. Uncontrolled inflammation leading to death may be true in sepsis due to certain types of pathogens (e. g., Neisseria meningitides, Clostridium perfringens) and in these patients anti-inflammatory therapies may help. However, large-scale clinical trials of anti-inflammatory therapies in septic patients have failed to reduce patient mortality. Recent research into the host' s immune response in sepsis has led to a fundamental change in the way clinicians and researchers think about this disease. After an initial hyper-inflammatory phase, septic patients may descend into a period of prolonged immune suppression, and it is during this period that the majority of patients die. Death usually occurs from multiorgan system failure brought on by the host' s inability to clear the primary infection or from a second opportunistic or nosocomial infection. One important hallmark of sepsis is widespread cell death in multiple organ systems due to both apoptosis and necrosis. This chapter reviews the cell types that undergo apoptosis and necrosis, the known inciting factors and mechanisms of cell death, and the impact of sepsis-induced apoptosis on morbidity and mortality, especially focusing on the importance of the lymphocyte.
|Title of host publication||Apoptosis|
|Subtitle of host publication||Physiology and Pathology|
|Publisher||Cambridge University Press|
|Number of pages||9|
|State||Published - Jan 1 2011|