In histoplasmosis murine models, CCL2 was associated with IL-4 production through a coordinated action of its CCR2-receptor [86], whereas in pneumocystosis murine models CCL2 and other cytokines (CCL3, CCL5, and cytokine-induced neutrophil chemoattractant) promoted a hyperinflammatory state, causing considerable lung damage after infection [45]. This evidence concerns the gene CCL3 and infection.