Page 109 - Ebook-Book JCMS 2025

Mycobacterium abscessus Survives in Human Dermal
Fibroblasts and Induces High Levels of IL-6
Rawipas Saisuwan, Pattanan Smosorn, Nuttawan Kassaket, Wiwit Tantibhedhyangkul*
Department of Immunology, Faculty of Medicine Siriraj Hospital
*Corresponding Author E-mail: wiwat.tan@mahidol.ac.th
Background: Abstract
Mycobacterium abscessus is a rapidly growing non-tuberculous mycobacterium that
often causes disseminated infections in individuals producing anti-interferon-gamma
autoantibodies. While most studies have focused on macrophage responses, little is known
about how fibroblasts—non-immune cells capable of producing high levels of IL-6—
respond to mycobacterial infections. This study aims to investigate the interaction between
M. abscessus and human dermal fibroblasts.
Methods: M. abscessus was cultured in Middlebrook 7H9 broth supplemented with albumin, dextrose,
and catalase. Human dermal fibroblasts were maintained in DMEM supplemented with 12%
fetal bovine serum and basic fibroblast growth factor. Intracellular bacterial growth was
assessed using a colony-forming unit (CFU) assay. Intracellular localization was verified by
immunofluorescence and confocal microscopy. Cytokine gene expression was analyzed by
quantitative RT-PCR, and protein levels were measured by ELISA.
Results: The CFU assay revealed that M. abscessus survived and replicated slowly within fibroblasts.
Confocal imaging confirmed intracellular colocalization of the bacteria with lysosome-
associated membrane protein 1 (LAMP-1), indicating localization to late endosomal/
lysosomal compartments. qRT-PCR showed high IL-6 gene expression, while TNF was
undetectable and IL-10 levels remained unchanged. ELISA confirmed that uninfected fibroblasts
secreted high basal levels IL-6, which significantly increased at 9 and 24 hours post-infection
Conclusion: Human dermal fibroblasts support intracellular survival of M. abscessus and respond with
robust IL-6 production. Given previous findings that IL-6 from macrophages promotes B
cell differentiation into plasmablasts, this study suggests fibroblasts may also contribute to
B cell activation and potentially to the development of autoantibody production.
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