ALA formation following depletion of Kupffer cells by clodronate liposomes.

<p>(A) Gating strategy to define resident CD11b⁺F4/80^hi (subset 1) and transient inflammatory CD11b^hiF4/80^lo (subset 2) Kupffer cells in the livers of mice five days after a single intravenous (i.v.) administration of clodronate liposomes (clod) or empty liposomes (ctrl) three days post-infection. Data represent the mean ± SEM of three independent experiments (n = 3 animals/group). (B) Gating strategy to define CD11b⁺CD68⁺ (region 1) and CD11b⁺CD68⁻ (region 2) Kupffer cells following treatment with clodronate liposomes (clod) or empty liposomes (ctrl) three days post-infection. (C) Immunohistochemical staining of liver tissue sections two days post i.v. administration of empty liposomes (ctrl) or clodronate liposomes (clod) using an anti-F4/80 antibody; Kupffer cells are indicated by the brown staining. (D) Gating strategy to define CD11b⁺Ly6G⁻Ly6C⁺ inflammatory monocytes derived from total liver and blood leukocytes five days post-clodronate treatment and three days post-infection. Data represent the mean ± SEM of three independent experiments (n = 3 animals/group). (E) Abscess size in wild-type (WT), clodronate-treated (clod), and control (ctrl) mice was monitored by MRI at the indicated times post-infection. Data represent the mean ± SEM of two experiments (3–4 mice/group). (F) PAS staining of abscessed liver tissue sections from control (ctrl) or clodronate-treated mice three days post-treatment and one day post-infection. Arrows indicate <i>E. histolytica</i> trophozoites. Data represent the mean ± SEM; <i>P</i>-values were determined by the Mann-Whitney U and unpaired Student's t test (^*<i>P</i><0.05).