These results and the lower infiltration of inflammatory cells into perivascular and parabronchial areas observed in our histopathological study, as well as the lower expression of CD68 in pulmonary tissue due CPC treatment in OVA-induced asthma model, support the idea of a decrease in the number of macrophages in the pulmonary microenvironment, but the remaining cells may be a population of M2 macrophages, these anti-inflammatory cells are responsible for the overproduction of IL-10 and IL-4, quintessential anti-inflammatory cytokines in classical endotype T2-higer asthma. The gene discussed is IL10; the disease is asthma.