Chronic Systemic Infection of Mice with Leishmania infantum Leads to Increased Bone Mass.

This article investigates the impact of chronic infection with the protozoan parasite *Leishmania infantum* on bone homeostasis using a mouse model of visceral leishmaniasis. The study found that, contrary to typical infection-induced bone loss, chronic *L. infantum* infection led to increased trabecular bone mass characterized by enhanced osteoblast differentiation and reduced osteoclast maturation and function. The parasite was detected within bone marrow macrophages and osteoclasts but not osteoblasts, and infected macrophages secreted elevated levels of the chemokine CCL5 (also known as RANTES), which was shown to inhibit osteoclast differentiation; neutralization of CCL5 restored osteoclastogenesis in vitro. These findings suggest that *L. infantum* modulates bone remodeling by directly infecting osteoclasts and indirectly impairing their development via macrophage-derived CCL5, resulting in increased bone formation during chronic visceral leishmaniasis.