Vol 27 No 2 December - The Indian Society for Parasitology

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84 Parasitic infections in travelers JPD : Vol. 27 (2), 2003 Sundar S. 2001. Drug Resistance in Indian visceral leishmaniasis. homosexuals. J Infect Dis; 161:1029-31. Trop Med. Int Health. 6:849-854. Weise HJ. 1976. Tourism and risk of infection. MMW Munch Med Sundar S. 2002. Resurgence of Kala azar in India : Reasons and Wochenschr; 118:1061-8. remedies. JIMSA. 13 : 40-48. Yong TS, Shin HJ, Im Kl, et al. 1992. An imported human case of The medical letter. Drugs for parasitic infections. Chapter 235. In: hookworm infection with worms in the rectum. Feigin RD, Cherry JD. 1998. Textbook of Pediatric Infectious Kisaengchunghak Chapchi; 30: 59-62. th Diseases, 4 ed.; WB Saunders Co., Philadelphia, pp-2707- Zubero Sutibarria Z, Santamaria Jauregui JM, Munoz Sanchez J, 2719. et al. 2000. Tropical" imported diseases: experience of a Thielman NM, Guerrant RL. 1998. Persistent diarrhea in the specialized unit in a general hospital. Rev Clin Esp; 200: returned traveler, Infecr Dis Clin North Am; 12: 489-501. 533-7. Weinke T, Friedrich-Janicke B, Hopp P, et al. 1990. Prevalence and clinical importance of Entamoeba histolytica in two highrisk groups: travelers returning from the tropics and male
Journal of Parasitic Diseases Vol. 27 (2) Dec. 2003, pp. 85-93 Induction of colony-stimulating factors by Leishmania donovani amastigote soluble antigens PRIYA SINGAL AND PRATI PAL SINGH* National Institute of Pharmaceutical Education and Research, S.A.S. Nagar-160 062, India Leishmania donovani amastigote antigens soluble in culture medium (LDAA; 0.01-10 mg/kg), following intravenous injection in BALB/c mice, induced the production of serum colony-stimulating factors (CSFs); 1 mg/kg LDAA induced maximum response (137 ± 18 colonies). In vitro, LDAA (0.01-1 mg/ml) induced mouse macrophages (MØs) to elaborate CSFs in the conditioned medium (CM); 0.1 mg/ml LDAA induced maximum production by peritoneal (73 ± 9 colonies), splenic (69 ± 10 colonies) and bone marrow-derived MØs (77 ± 10 colonies). Both in vivo and in vitro, the CSF production could be observed as early as 6 h, reached maximum by 24 h and then levelled-off to background levels by 72 h. Pre-treatment of LDAA with rabbit anti-LDAA polyclonal antibody significantly (p60%). The colony forming unit-GM counts in the spleen and femur of LDAA-treated mice showed a maximum increase of 2.7- and 2.4-fold, respectively. These data, apparently for the first time, suggest that L. donovani amastigote soluble antigens can induce the production of CSFs. Key Words : Amastigotes, Colony-stimulating factors, Leishmania donovani, Macrophages, Soluble antigens. INTRODUCTION eishmania sp. are dimorphic protozoan parasites Lthat cause a wide range of human diseases called leishmaniases, which include self-healing cutaneous lesions, localized or diffuse mucosal lesions and fatal visceral infections. In the mammalian hosts, the amastigote stages of Leishmania parasite are obligatorily intracellular as they reside and multiply in the phagolysosomal compartments of macrophages (MØs) and dendritic cells (Bogdan and Rollinghoff, 1998). Leishmania donovani, the causative agent of human visceral leishmaniasis (VL), causes VL in BALB/c mice also (Cotterell et al., 2000a). The colony-stimulating factors (CSFs; mol. wt. 18-90 * Corresponding Author kDa) are a group of glycoprotein hormones, which regulate the differentiation and proliferation programme of the committed progenitor cells by binding to their specific surface receptors, in vitro (Metcalf, 1989; Metcalf, 1991); in vivo they stimulate hematopoiesis (Donahue et al., 1986). The lineage specific CSFs i. e. granulocyte (G)-CSF (G-CSF) and MØ (M)-CSF (M-CSF), stimulate G and M colony formation, respectively. GM-CSF, on the other hand, supports the formation of colonies consisting mainly of G, M and eosinophils, whereas multi-CSF (interleukin-3; IL-3) induces colonies containing cells of different lineages. The genes for mouse and human CSFs have been cloned, and large quantities of recombinant CSFs can now be produced (Metcalf, 1991). Structurally, M-CSF is a homodimer, whereas G, GM- and multi-CSFs consist of a single polypeptide chain. The CSFs are active at picomolar
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