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Acta Physiologica Congress

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Acta Physiologica 2011; Volume 203, Supplement 688
The 62nd National Congress of the Italian Physiological Society
9/25/2011-9/27/2011
Sorrento, Italy


PHAGOCYTOSIS ROLE ON APOPTOSIS IN IMMUNOSENESCENCE: ANALYSIS BY SPACE BIOTECHNOLOGIES
Abstract number: P30

SABA1 A, SPANO1 A, MANUNTA2 A, GANADU2 M, CRESCIO1 C, SCIOLA1 L, PIPPIA1 P

1Dept Physiological, Biochemical and Cellular Sciences, Univ., Sassari, Italy
2Nephrology and Dialysis Unit, A. Segni Hospital, Ozieri (SS), Italy

Several space biology studies demonstrated that microgravity affects human immune system. Strong analogies between these effects and immunosenescence were observed. In fact, T cells proliferation and IL-2 production decrease, whereas circulating levels of pro-inflammatory cytokine (IL-6, TNF-a, IL-1b) and apoptosis increase. This is a paradox currently still unclear because the most remarkable apoptotic feature is to preserve the normal tissue homeostasis without inflammation. Considering that an inefficient phagocytosis can underlie inflammatory events, in vivo and in vitro experiments in simulated microgravity conditions were carried out to evaluate the phagocytosis capability in macrophages and apoptotic T lymphocytes co-cultured for 2h. We also analyzed the phagocytosis capability from elderly people. Microscopy analysis of phagocyted cells was carried out after DAPI/phalloidin fluorochromization. A reduced phagocytic capability as well as a preferential phagocytosis of late stages of apoptosis have been observed in microgravity conditions and in the 54% of the 70 years people identified as a critical age range. Since both surface molecules and extracellular factors play a role in the removal of apoptotic cells, CD18 and thrombospondin involvement were evaluated. The defective clearance of apoptosis is associated with autoimmunity and inflammation, therefore the evaluation of autoimmune profile of young and elderly people is in progress. This research was supported by Fondazione Banco di Sardegna, Sassari.

To cite this abstract, please use the following information:
Acta Physiologica 2011; Volume 203, Supplement 688 :P30

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