Publication: The role of sepiolite and palygorskite on the migration of leukocyte cells to an inflammation site
Full text at PDC
Advisors (or tutors)
Sepiolite and palygorskite have shown beneficial health effects but understanding human cell-clay interactions has yet to become unveiled. This paper reports on the effects of sepiolite (Vallecas, Spain) and palygorskite (Torrejon El Rubio, Spain) on the infiltration of human blood leukocytes to an infiltration site. Quantification of human blood leukocyte cells under pro- and anti-inflammatory conditions was conducted, and cells visualized in an Axioscope (Carl Zeiss; Oberkochen, Germany). Images were recorded with an Axiocam Mrm monochromatic camera and ZEN Pro software (Carl Zeiss). The distribution of human blood leukocyte cells at the inflammation site varied before and after adding the clay. The relative proportion of PMN-to-monocytes(MN) (PMN/MN) exposed to the inflammatory activity by 12-O-tetradecanoylphorbol-13-acetate (TPA) changed in the presence of sepiolite (TPA + sepiolite) or palygorskite (TPA + palygorskite) either after 4 or 24 h, namely, 0.60, 2.5, and 2.33; and 4.33, 1.53, and 2.8, respectively. PMN/MN values compared in the presence of TPA or TPA and palygorskite, however decreased sharply in the presence of TPA and sepiolite. Proposedly, decreases in PMN/MN values caused by adding sepiolite may alter PMN and MN immunological functions, by lessening the destruction extent of invasive bacteria via phagocytosis and the conversion of MN to macrophages. Proposedly, limiting a conversion of MN to macrophages impedes resolving inflammation because of an incomplete digestion of aged cells. Evidently, shifting from pro- to anti-inflammatory conditions due to the addition of the clay altered the mechanism of infiltration of different leukocyte cells to an inflammation site. Finally, the presence of few macrophages at the inflammation site was attributed to resolution of inflammation, whereby macrophages participated in anti-inflammatory mechanisms leading to the return to homeostasis in tissues.