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In vitro  studies have implicated the small heat shock protein HSPB1 in a range of physiological functions. However, its  in vivo  relevance is unclear as the phenotype of unstressed HSPB1 −/−  mice is unremarkable. To determine the impact of HSPB1 in injury, HSPB1 −/−  and wild type (WT) mice were subjected to cecal ligation and puncture, a model of polymicrobial sepsis. Ten-day mortality was significantly higher in HSPB1 −/−  mice following the onset of sepsis (65% vs. 35%).  Ex vivo  mechanical testing revealed that common carotid arteries from HSPB1 −/−  mice were more compliant than those in WT mice over pressures of 50–120 mm Hg. Septic HSPB1 −/−  mice also had increased peritoneal levels of IFN-γ and decreased systemic levels of IL-6 and KC. There were no differences in frequency of either splenic CD4 +  or CD8 +  T cells, nor were there differences in apoptosis in either cell type. However, splenic CD4 +  T cells and CD8 +  T cells from HSPB1 −/−  mice produced significantly less TNF and IL-2 following  ex vivo  stimulation. Systemic and local bacterial burden was similar in HSPB1 −/−  and WT mice. Thus while HSPB1 −/−  mice are uncompromised under basal conditions, HSPB1 has a critical function  in vivo  in sepsis, potentially mediated through alterations in arterial compliance and the immune response.

The small heat shock protein HSPB1 protects mice from sepsis