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Salvaging impaired inflammasome function in elderly mice with flu

The innate immune system depends upon encoded pattern recognition receptors, such as the NOD-like receptor (NLR) family, to mount an appropriate immune response against microbial threats. Members of the NLR family, including NLRP3/NALP3, are critical components of the inflammasome, which links danger-signals to caspase-1 activation and subsequent processing and release of the pro-inflammatory cytokines IL-1β and IL-18. Dr. Heather W. Stout-Delgado of the Lovelace Respiratory Research Institute, Albuquerque, NM and colleagues demonstrated that elderly influenza A virus-infected mice produced lower levels of IL-1β (Stout-Delgado et al (2012) J Immunol;188(6):2815-24). Dendritic cells from elderly mice exhibited decreased expression of ASC, NLRP3, and capase-1 but increased expression of pro–IL-1β, pro–IL-18, and pro–IL-33, compared with cells from young infected mice. Treatment with nigericin during infection augmented IL-1β production, increased caspase-1 activity, and decreased morbidity and mortality in the elderly mice. The study provides one possible mechanism for why the elderly are more susceptible to influenza infection and suggests new approaches to enhancing immune response, thereby reducing morbidity and mortality in this population.

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