The analysis reveals hip fracture injury alters macrophage phenotype and immune responses in older adults, suggesting chronic inflammation persists post-injury.
Description Healthy elderly individuals are particularly prone to catastrophic events at any moment of their lives. One stressful event for individuals aged 65 and older is a fall that results in a fracture of the hip (HF). HF causes a state of inflammation that may affect immune responses. To assess the impact of HF on macrophage phenotypes. Distribution, functions (chemotaxis, phagocytosis, superoxide production and cytokine production)and phenotype were evaluated in polarized macrophages by GM-CSF and M-CSF before surgery and 6 weeks and 6 months after the event. In healthy older (HO) subjects (n-12) the monocytes under GM-CSF normally polarized towards MI (CD86, CD80, IFN-gamma and IL-12) toward MII under M-CSF (CD163,Arginase, IL-10, Il-4). The use of autologous sera in HO shifted the macrophages towards M1 phenotype which remained during the 6 months follow up in the hip fracture (HF) group (n = 22). Interestingly, when the monocytes from HF patients were treated by heterologous (HO) autologous sera they polarized towards MII even after 6 months. The phagocytosis decreased, however the chemotaxis and ROS production increasing in macrophages during the 6 months followup in HF patients. These data indicate that HF polarizes macrophages towards mainly Mii phenotype and except their phagocytosis all their other functions are increasing creating a sort of permanent inflammatory setting after 6 months HF followup despite the MII phenotype.
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Tamás Fülöp (2025) studied this question.
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