However, the observation of an infection-associated redistribution of the TfR receptor from the cytosol to the surface of AGS cells, coupled with an increase in transferrin uptake by infected MDCK cells [32] and a significant increase in ferritin-rich intracellular compartments in infected AGS cells (this study) strengthens the hypothesis that these bacteria have the potential to perturb cellular iron homeostasis. Here, TF is linked to infection.