Host Immunosenescence Impairs Tuberculosis Clearance | Aging

Aging-US #published this #research paper on May 4, 2026, in Volume 18, titled “Host immunosenescence compromises Mycobacterium tuberculosis clearance" by #researchers from the Translational Health Group, International Centre for Genetic Engineering and Biotechnology, New Delhi, 110067, India; Bio-experimentation Facility, International Centre for Genetic Engineering and Biotechnology, New Delhi, 110067, India. @ICGEB #aging #tuberculosis #immunosenescence #proteomics #openaccess #openscience #PaperSpotlight #peerreview #journal #publishing #meded DOI - https://doi.org/10.18632/aging.206374 Corresponding author - Ranjan Kumar Nanda - ranjan@icgeb.res.in Authors interview - https://www.youtube.com/watch?v=bSaJaB751kM Abstract Immunosenescence increases susceptibility to infectious diseases like tuberculosis (TB) in older adults (≥60 years) and hinder effective containment of Mycobacterium tuberculosis (Mtb) during therapeutic intervention. A comprehensive understanding of the cellular and molecular changes underlying age-associated immune alterations may inform development of strategies to improve treatment outcomes. Here, we monitored the immunopathology, frequency, and functionality of immune cells across extreme age groups of C57BL/6 mice following low aerosol dose infection (100-120 cfu) with Mtb H37Rv and treatment with rifampicin and isoniazid (RIF-INH). Up to 6 weeks post infection, mycobacterial load in tissues (lung, spleen, and liver) of old (17-19 months; M) and aged (31M) C57BL/6 mice was similar to that of young (2-4M) mice. However, at two weeks post-treatment, older mice showed a slower rate of Mtb clearance in the lungs. Mtb-infected old mice had higher splenic T-follicular cytotoxic (TFC)-like cells, and proteomic analysis of flow-sorted CD4+CD44+ T cells revealed deregulated mitochondrial proteins (4-hydroxy-2-oxoglutarate aldolase, aspartate aminotransferase, and prostaglandin E synthase), suggesting impaired mitochondrial function. Collectively, these findings suggest that age-associated immune alterations may disrupt immunometabolic pathways, thereby contributing to the delayed Mtb clearance. Targeting immunometabolic dysfunction therefore represents a promising strategy to enhance TB treatment efficacy and reduce disease burden in older populations. Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206374 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, tuberculosis, immunosenescence, TFH cells, proteomics To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM