{'fraction_non_alphanumeric': 0.033863165169315826, 'fraction_numerical': 0.0082930200414651, 'mean_word_length': 5.241379310344827, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Deficiency in Heat Shock Factor 1 (HSF-1) Expression Exacerbates Sepsis-induced Inflammation and Cardiac Dysfunction.

In the present study, we investigated whether absence of heat shock factor 1 (HSF-1) and inability to increase myocardial expression of heat shock proteins alter septic responses of inflammatory cytokines and myocardial contractility. HSF-1 knockout (hsf -/-) mice and wild type litter mates underwent a sterile (lipopolysaccharide; LPS) or infectious (Streptococcus pneumoniae or Klebsiella pneumoniae) septic challenge. Production of cytokines, TNF, IL-1β, IL-6 and IL-10, in the blood and from cardiomyocytes was exaggerated in the hsf -/- mice compared to responses measured in wild type mice given an identical septic challenge. This enhanced compartmentalized myocardial inflammation was associated with significantly decreased cardiac contraction and diminished relaxation in the hsf -/- mice. However, lacking HSF-1 expression did not affect intracellular calcium and sodium responses in cardiomyocytes isolated from septic challenged mice, suggesting that ion loading was not a major or sustaining cause of the greater myocardial contractile defects in hsf -/- mice. In conclusion, our data indicated that HSF-1 and downstream heat shock proteins are essential components to support cardiac function in sepsis. Further studies are warranted to further define the precise mechanisms of HSF-1 mediated cardiac protection.