Expression of macrophage inflammatory protein-1α in alveolar macrophage in rat subjecting mechanical ventilation

Abstract

Objective To explore the role of alveolar macrophage(AM)activation in ventilator induced lung injury(VILI)by measuring macrophage inflammatory protein-1α(MIP-1α)and nuclear factorkappa B(NF-κB)p65 expressed in AM of rats with different tidal volume ventilations.Methods Thirty-two male Wistar rats were randomly divided into four groups:control group,low tidal volume group,conventional tidal volume group and high tidal volume group.The levels of MIP-1α and NF-κB p65 expressed in AM in BALF were measured by SABC method respectively and the ultrastructures of AM were observed with 100-CX transmission electron microscope.Results The percentages of AM in BALF stained positively with MIP-1α and NF-κB p65 both in high and conventional tidal volume groups were significantly higher than those in control and low tidal volume groups(P＜0.01).The percentages of AM in BALF stained positively with MIP-1α and NF-κB p65 in high tidal volume group were also significantly higher than those in conventional tidal volume group(P＜0.05),but no statistical differences existed between low tidal volume group and control group.Under transmission electron microscope the AM in high and conventional tidal vol ume groups appeared in active state.Conclusions AM is one of the starting cells to inducing VILI and plays an important role in VILI.AM activation and releasing MIP-1α is one of the main reasons leading to neutrophils aggregated and activated in the lungs and so to developing VILI.AM expression and releasing MIP-1α may be regulated by NF-κB to some extent. Key words: Mechanical ventilation; Acute lung injury; Alveolar macrophage; Nuclear factor-kappa B; Macrophage inflammatory protein-1α