RESUMEN
AIM: This study aimed to evaluate the effect of two platelet preparations used in the clinic, pure platelet-rich plasma (P-PRP) and the supernatant of calcium-activated P-PRP (S-PRP), on the phenotype of human macrophages. MATERIALS & METHODS: Surface markers and cytokine production of human monocyte-derived macrophages were analyzed after 24 h stimulation with P-PRP or S-PRP. RESULTS: P-PRP and S-PRP present no difference in the expression of CD206, a M2 tissue-repair macrophage-related marker. However, these same macrophages presented different levels of CD163, CD86 as well as different IL-10 secretion capacities after 24 h incubation. CONCLUSION: These platelet preparations do not have an equivalent biological effect over macrophages, which suggest that they may present different clinical regenerative potentials.
Asunto(s)
Antígenos CD/biosíntesis , Calcio/farmacología , Interleucina-10/sangre , Macrófagos/citología , Macrófagos/metabolismo , Plasma Rico en Plaquetas , Adolescente , Adulto , Células Cultivadas , Femenino , Humanos , Masculino , Persona de Mediana EdadRESUMEN
Neisseria gonorrhoeae (Ngo) has developed multiple immune evasion mechanisms involving the innate and adaptive immune responses. Recent findings have reported that Ngo reduces the IL-1ß secretion of infected human monocyte-derived macrophages (MDM). Here, we investigate the role of adenosine triphosphate (ATP) in production and release of IL-1ß in Ngo-infected MDM. We found that the exposure of Ngo-infected MDM to ATP increases IL-1ß levels about ten times compared with unexposed Ngo-infected MDM (P < 0.01). However, we did not observe any changes in inflammasome transcriptional activation of speck-like protein containing a caspase recruitment domain (CARD) (ASC, P > 0.05) and caspase-1 (CASP1, P > 0.05). In addition, ATP was not able to modify caspase-1 activity in Ngo-infected MDM but was able to increase pyroptosis (P > 0.01). Notably ATP treatment defined an increase of positive staining for IL-1ß with a distinctive intracellular pattern of distribution. Collectively, these data demonstrate that ATP induces IL-1ß secretion by a mechanism not related to the NLRP3/ASC/caspase-1 axis and likely is acting at the level of vesicle trafficking or pore formation.