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

Immunity & Ageing

Anuja Mathew¹  Douglas T Golenbock¹  Katherine A Fitzgerald¹  Vijay Rathinam¹  Alejandro Ramirez¹ 

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

关键词: IL-1β;    Inflammasome;    NLRP3;    Aged mice;    Macrophages;    Ageing;   

Others  :  815171
DOI  :  10.1186/1742-4933-9-27

 received in 2012-07-20, accepted in 2012-12-05,  发布年份 2012

【 摘 要 】

Background

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.

Findings

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.

Conclusions

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

【 授权许可】

   
2012 Ramirez et al.; licensee BioMed Central Ltd.

【 图 表 】

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