Musumeci Maria
Not Available
Simpore Jacques
Not Available
Barone Rita
Not Available
Angius Andrea
Not Available
Malaguarnera Lucia
Not Available
Musumeci Salvatore
Not Available
ABSTRACT
This study describe the levels of plasma Chitotriosidase (CHIT) activity in 62 African children with severe and uncomplicated Plasmodium falciparum malaria with respect to 140 healthy African children. Medially all children with acute malaria showed plasma CHIT activity levels higher than healthy control subjects (140 nmol/mL/h, range 13-521, versus 72 nmol/mL/h, range 14-150, p<0.0001). Although the distribution curve of plasma CHIT activity showed a bimodal behavior, both children with severe malaria (n=22) and with uncomplicated malaria (n=40) showed elevated levels of plasma CHIT activity (median 138 nmol/mL/h, range 13-521 and median 151 nmol/mL/h, range 13-491, respectively). The difference between the two groups was not significant. On the contrary a significant correlation was found between plasma CHIT activity and serum ferritin only in children with uncomplicated malaria, but not in children with severe malaria. Since it is generally accepted that P. falciparum infection is mediated by the immune system, only a synchronic macrophage response guarantees the favourable outcome of this infection. We do not know how the expression of the CHIT gene is regulated, but the lack of correlation between plasma CHIT activity and serum ferritin in African children with severe P. falciparum malaria suggests in a failure of the synchronic macrophage response an important determinant of disease outcome.
PDF References Citation
How to cite this article
Musumeci Maria, Simpore Jacques, Barone Rita, Angius Andrea, Malaguarnera Lucia and Musumeci Salvatore, 2005. Synchronic Macrophage Response and Plasmodium falciparum Malaria. Pakistan Journal of Biological Sciences, 8: 954-958.
DOI: 10.3923/pjbs.2005.954.958
URL: https://scialert.net/abstract/?doi=pjbs.2005.954.958
DOI: 10.3923/pjbs.2005.954.958
URL: https://scialert.net/abstract/?doi=pjbs.2005.954.958
REFERENCES
- Eiberg, H. and W.R. Den-Tandt, 1997. Assignment of human plasma methylumbelliferyl-tetra-N-acetylchitotetraoside hydrolase or chitinase to chromosome 1q by a linkage study. Hum. Genet., 101: 205-207.
CrossRefDirect Link - Boot, R.G., G.H. Rankema, M. Verhoek, A. Strijland and J. Bliek et al., 1998. The human chitotriosidase gene. Nature of inherited enzyme deficiency. J. Biol. Chem., 273: 25680-25685.
PubMedDirect Link - Barone, R., J. Simpore, L. Malaguarnera, S. Pignatelli and S. Musumeci, 2003. Plasma chitotriosidase activity in acute Plasmodium falciparum malaria. Clin. Chim. Acta, 331: 79-85.
CrossRefDirect Link - Barone, R., F. Di Gregorio, M.A. Romeo, G. Schiliro and L. Pavone, 1999. Plasma chitotriosidase activity in patients with β-thalassemia. Blood Cells Mol. Dis., 15: 1-8.
Direct Link - Korolenko, T.A., S.Y. Zhanaeva, O.V. Falameeva, V.I. Kaledin, E.E. Filyushina, I.I. Buzueva and G.A. Paul, 2000. Chitotriosidase as a marker of macrophage stimulation. Bull. Exp. Biol. Med., 130: 948-950.
PubMedDirect Link - Hollak, C.E., S. van Weely, M.H.J. van Oers and J.M. Aerts, 1994. Marked elevation of plasma chitotriosidase activity. A novel hallmark of gaucher disease. J. Clin. Invest., 93: 1288-1292.
CrossRefPubMedDirect Link - Lambotte, O., P. Cacoub, N. Costedoat, G. Le Moel, Z. Amoura and J.C. Piette, 2003. High ferritin and low glycosylated ferritin may also be a marker of excessive macrophage activation. J. Rheumatol., 30: 1027-1028.
Direct Link - Barone, R., L. Malaguarnera, A. Angius and S. Musumeci, 2002. Plasma chitotriosidase activity in patients with β-thalassemia. Am. J. Hematol., 71: 7-10.
Direct Link - Malaguarnera, L., M. Musumeci, F. Licata, M. Di Rosa, A. Messina and S. Musumeci, 2004. Prolactin induces chitotriosidase gene expression in human monocyte-derived macrophages. Immunol. Lett., 94: 57-63.
CrossRefDirect Link - Malaguarnera, L., R.M. Imbesi, S. Pignatelli, J. Simpore, M. Malaguarnera and S. Musumeci, 2002. Increased levels of interleukin-12 in Plasmodium falciparum malaria: Correlation with the severity of disease. Parasite Immunol., 24: 387-389.
PubMedDirect Link - Musumeci, M., L. Malaguarnera, J. Simpore, A. Messina and S. Musumeci, 2003. Modulation of immune response in Plasmodium falciparum malaria: Role of IL-12, IL-18 and TGF-β. Cytokine, 21: 172-178.
CrossRefDirect Link - Lauw, F.N., A.A. Te Velde, P.E. Dekkers, P. Speelman and J.M. Aerts et al., 1999. Activation of mononuclear cells by interleukin-12: An in vivo study in chimpanzees. J. Clin. Immunol., 19: 231-238.
PubMedDirect Link - Choi, E.H., P.A. Zimmerman, C.B. Foster, S. Zhu, V. Kumaraswami, T.B. Nutman and S.J. Chanock, 2001. Genetic polymorphisms in molecules of innate immunity and susceptibility to infection with Wuchereria bancrofti in South India. Genes Immunity, 2: 248-253.
PubMedDirect Link - Modiano, D., A. Sirima, A. Sawadogo, L. Sanou, J. Pare, A. Konate and F. Pagnoni, 1998. Severe malaria in Burkina Faso: Influence of age and transmission level on clinical presentation. Am. J. Trop. Med. Hyg., 59: 539-542.
PubMed