This study aimed to investigate the role of palmitic acid (PA) in modulating the neutrophil response during Trichomonas vaginalis infection. A human neutrophil-like cell model (nHL-60) was established by differentiating the human promyelocytic leukemia cell line HL-60 with 1.3% dimethyl sulfoxide. The expressions of the genes IL-8, NF-κB, MyD88, and TLR4 and the production of reactive oxygen species (ROS) of differentiated cells were compared, using end-point RT-PCR and nitroblue tetrazolium reduction, in the presence or absence of 1 mM PA and 100 μM of docosahexaenoic acid. Additionally, oxidative burst activity was also evaluated in response to T. vaginalis stimulation in the presence of either PA or docosahexaenoic acid. nHL-60 cells showed increased expression of key mediators of the TLR4 signaling pathway, and enhanced ROS production upon phorbol 12-myristate 13-acetate stimulation. Peripheral blood neutrophils exposed to T. vaginalis in the presence of PA exhibited higher ROS production than neutrophils stimulated by the parasite only. These findings indicate that PA enhances neutrophil activation to a secondary stimulus with T. vaginalis. They provide new insights into the role of metabolic factors in host-pathogen interactions.
Neutrophils are important effector cells against protozoan extracellular parasite Entamoeba histolytica, which causes amoebic colitis and liver abscess in human beings. Apoptotic cell death of neutrophils is an important event in the resolution of inflammation and parasite's survival in vivo. This study was undertaken to investigate the ultrastructural aspects of apoptotic cells during neutrophil death triggered by Entamoeba histolytica. Isolated human neutrophils from the peripheral blood were incubated with or without live trophozoites of E. histolytica and examined by transmission electron microscopy (TEM). Neutrophils incubated with E. histolytica were observed to show apoptotic characteristics, such as compaction of the nuclear chromatin and swelling of the nuclear envelop. In contrast, neutrophils incubated in the absence of the amoeba had many protrusions of irregular cell surfaces and heterogenous nuclear chromatin. Therefore, it is suggested that Entamoeba-induced neutrophil apoptosis contribute to prevent unwanted tissue inflammation and damage in the amoeba-invaded lesions in vivo.
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