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Blood, 15 August 2002, Vol. 100, No. 4, pp. 1511-1511
CORRESPONDENCE
To the editor:
Acidic and neutral sialidase in the erythrocytes of
patients with Type 2 diabetes: influence on erythrocyte
lifespan
Venerando et al reported an increased quantity of sialic
acid at the surface of erythrocytes in diabetic patients and associated the increase with decreased activity of neutral sialidase, an enzyme
for which they had previously demonstrated a role in physiologic desialylation of red cells.1 In their discussion they
hypothesized that this excess in sialic acid was responsible for a
shorter life span of erythrocytes in diabetes mellitus. This second assertion is in contradiction with what is commonly known
about phagocytosis of senescent red cells. Indeed, several lines of
evidence support the contrary hypothesis. The mechanism proposed for
this selective recognition and uptake of desialylated red cells is that
the macrophage recognizes the adjacent galactose group, which is
unmasked by desialylation of glycophorin glycans. Several studies
support this hypothesis. First, in vivo studies showed that neuraminidase-treated
erythrocytes are sequestrated more quickly by resident macrophages of
the spleen, liver, and bone marrow.2,3,4 Their life span
is also decreased.2 Second, centrifugation and lectin recognition studies have showed
that older erythrocytes carry less sialic acid residue than younger
ones. Moreover, these erythrocytes can be resialylated in vitro,
suggesting that the rest of the sialic acid-binding group remains
intact. Older red cells can be more resialylated than younger
ones.2 Third, a receptor for galactose residue has been identified at the
surface of peritoneal macrophages that are capable of performing erythrophagocytosis in vitro.2,3,5 Fourth, in vitro studies showed that older erythrocytes are
preferentially by murine peritoneal macrophages, a reaction
that can be inhibited by lactose, which is used as a competitive
inhibitor of galactose recognition.2 To our knowledge no recent data have invalidated this theory.
Thibault Richard, Karim
Zouaoui Boudjeltia, Michaël Piagnerelli, and Michel Vanhaeverbeek
Correspondence: Thibault Richard, ISPPC André
Vésale, Laboratory of experimental medicine, 706, route de
Gozée 6110, Montigny Le Tilleul, Belgium; e-mail: tqr{at}swing.be.
References
1.
Venerando B, Fiorilli A, Tettamanti G.
Presence in human erythrocyte membranes of a novel form of sialidase acting optimally at neutral pH.
Blood.
1997;90:2047-2056[Abstract/Free Full Text].
2.
Bratosin D, Masurier D, Mazurier J, et al.
Cellular and molecular mechanisms of senescent erythrocyte phagocytosis by macrophage: a review.
Biochimie.
1998;80:173-195[Medline]
[Order article via Infotrieve].
3.
Deiss A.
Destruction of erythrocytes. In:
Richard Lee G,Foerster J,Lukens J, et al., eds.
Wintrobe's Clinical Hematology. Baltimore, MD: Williams & Wilkins; 1999:267-299.
4.
Simchon S, Jan KM, Chien S.
Studies on sequestration of neuraminidase-teated red blood cells.
Am J Physiol.
1988;254:H1167-H1171[Medline]
[Order article via Infotrieve].
5.
Traving C, Schauer R.
Structure, function and metabolism of sialiv acids.
Cell Mol Life Sci.
1998;54:1330-1349[CrossRef][Medline]
[Order article via Infotrieve].

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B. Venerando, A. Fiorilli, G. Croci, C. Tringali, G. Goi, L. Mazzanti, G. Curatola, G. Segalini, L. Massaccesi, A. Lombardo, et al.
Acidic and neutral sialidase in the erythrocytes of patients with type 2 diabetes: an answer to comments by Richard et al
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