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Defective pro-IL-1β responses in macrophages from aged mice

Alejandro Ramirez, Vijay Rathinam, Katherine A Fitzgerald, Douglas T Golenbock and Anuja Mathew*

Author Affiliations

Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, S6-862, 55 Lake Avenue North, Worcester, MA, 01655, USA

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Immunity & Ageing 2012, 9:27  doi:10.1186/1742-4933-9-27

Published: 11 December 2012



Cytokines regulated by the inflammasome pathway have been extensively implicated in various age-related immune pathologies. We set out to elucidate the contribution of the nod-like receptor protein 3 (NLRP3) inflammasome pathway to the previously described deficiencies in IL-1β production by macrophages from aged mice. We examined the production of pro-IL-1β and its conversion into IL-1β as two separate steps and compared these cytokine responses in bone marrow derived macrophages from young (6–8 weeks) and aged (18–24 months) C57BL/6 mice.


Relative to macrophages from young mice, macrophages from aged mice produced less pro-IL-1β after TLR4 stimulation with LPS. However upon activation of the NLRP3 inflammasome with ATP, macrophages from young and aged mice were able to efficiently convert and secrete intracellular pro-cytokines as functional cytokines.


Lower levels of IL-1β production are a result of slower and lower overall production of pro-IL-1β in macrophages from aged mice.

Ageing; Macrophages; Aged mice; NLRP3; Inflammasome; IL-1β