Other diseases
Human and mouse macrophages trained by low-dose LPS attenuate the
inflammatory phenotype of endometriotic cells via an IL-10-dependent
pathway, and significantly upregulated H3K4me3 on the IL-10 promoter and
altered inflammatory cytokine production have been observed
simultaneously in endometriosis 78. In addition,
evidence of macrophage memory has also been obtained with respect
neurodegenerative disorders, such as Alzheimer’s disease, Parkinson’s
disease, and autism spectrum disorder 55. In a mouse
model of Alzheimer’s pathology, LPS-induced immune training has been
demonstrated to exacerbate cerebral β-amyloidosis, whereas this could be
alleviated by immune tolerance, attributable to microglial
(brain-resident macrophage) memory, along with altered inflammatory
cytokine production and H3K4me1 and H3K27ac enrichment79. Furthermore, in respiratory diseases such as
allergic asthma, allergen-triggered macrophages have been observed to
acquire a TNF-dependent inflammatory memory and show an excessive
mediator response upon stimulation, thereby resulting in a shift toward
an M2-like macrophage phenotype and the production of diverse
inflammatory cytokines. Conversely, TNF blockade or genetic ablation has
been found to prevent the inflammatory imprinting of macrophages80. The concept of macrophage memory presents a new
perspective for better understanding of disease pathology, and
elucidating the precise underlying mechanisms may provide relevant
insights for the development of novel therapeutic strategies.