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Miltefosine effectively modulates the cytokine milieu in Indian post kala-azar dermal leishmaniasis.
J Infect Dis. 2011 Nov; 204(9):1427-36.JI

Abstract

BACKGROUND

The increasing incidence of unresponsiveness to antimonials in leishmaniasis prompted the use of newer drugs such as miltefosine. Miltefosine influences macrophage effector functions, but its effect on patients with post kala-azar dermal leishmaniasis (PKDL) has not been evaluated.

METHODOLOGY

The immunomodulatory activity of miltefosine was evaluated in patients with PKDL by studying the expression of activation markers (CD14 and CD16) and costimulatory molecules (CD80 and CD86) on circulating monocytes, levels of pro-inflammatory cytokines (tumor necrosis factor α, interleukin 6, interleukin 1β, and interleukin 8) and anti-inflammatory cytokines (interleukin 10, transforming growth factor β, interleukin 4, and interleukin 13) in serum and peripheral blood mononuclear cell culture supernatants, and serum nitrite and arginase activity.

RESULTS

Miltefosine on circulating monocytes upregulated expression of CD16 and CD86 and reduced that of CD14. Miltefosine also induced a significant increase in circulating levels of pro-inflammatory cytokines with a concomitant decrease in anti-inflammatory cytokines. Its macrophage activating potential was evidenced by its ability to decrease serum arginase activity and increase serum nitrite.

CONCLUSIONS

Miltefosine increased the proportion of monocytes that have a pro-inflammatory phenotype, which was accompanied by an enhanced secretion of pro-inflammatory cytokines and increased levels of serum nitrite. The decrease in anti-inflammatory cytokine levels and serum arginase activity collectively indicated that miltefosine triggered a robust T-helper 1 response that facilitated parasite elimination.

Authors+Show Affiliations

Department of Pharmacology, Institute of Post Graduate Medical Education and Research, India.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

21933878

Citation

Mukhopadhyay, Debanjan, et al. "Miltefosine Effectively Modulates the Cytokine Milieu in Indian Post Kala-azar Dermal Leishmaniasis." The Journal of Infectious Diseases, vol. 204, no. 9, 2011, pp. 1427-36.
Mukhopadhyay D, Das NK, Roy S, et al. Miltefosine effectively modulates the cytokine milieu in Indian post kala-azar dermal leishmaniasis. J Infect Dis. 2011;204(9):1427-36.
Mukhopadhyay, D., Das, N. K., Roy, S., Kundu, S., Barbhuiya, J. N., & Chatterjee, M. (2011). Miltefosine effectively modulates the cytokine milieu in Indian post kala-azar dermal leishmaniasis. The Journal of Infectious Diseases, 204(9), 1427-36. https://doi.org/10.1093/infdis/jir551
Mukhopadhyay D, et al. Miltefosine Effectively Modulates the Cytokine Milieu in Indian Post Kala-azar Dermal Leishmaniasis. J Infect Dis. 2011;204(9):1427-36. PubMed PMID: 21933878.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Miltefosine effectively modulates the cytokine milieu in Indian post kala-azar dermal leishmaniasis. AU - Mukhopadhyay,Debanjan, AU - Das,Nilay Kanti, AU - Roy,Susmita, AU - Kundu,Sunanda, AU - Barbhuiya,J N, AU - Chatterjee,Mitali, Y1 - 2011/09/20/ PY - 2011/9/22/entrez PY - 2011/9/22/pubmed PY - 2011/12/13/medline SP - 1427 EP - 36 JF - The Journal of infectious diseases JO - J Infect Dis VL - 204 IS - 9 N2 - BACKGROUND: The increasing incidence of unresponsiveness to antimonials in leishmaniasis prompted the use of newer drugs such as miltefosine. Miltefosine influences macrophage effector functions, but its effect on patients with post kala-azar dermal leishmaniasis (PKDL) has not been evaluated. METHODOLOGY: The immunomodulatory activity of miltefosine was evaluated in patients with PKDL by studying the expression of activation markers (CD14 and CD16) and costimulatory molecules (CD80 and CD86) on circulating monocytes, levels of pro-inflammatory cytokines (tumor necrosis factor α, interleukin 6, interleukin 1β, and interleukin 8) and anti-inflammatory cytokines (interleukin 10, transforming growth factor β, interleukin 4, and interleukin 13) in serum and peripheral blood mononuclear cell culture supernatants, and serum nitrite and arginase activity. RESULTS: Miltefosine on circulating monocytes upregulated expression of CD16 and CD86 and reduced that of CD14. Miltefosine also induced a significant increase in circulating levels of pro-inflammatory cytokines with a concomitant decrease in anti-inflammatory cytokines. Its macrophage activating potential was evidenced by its ability to decrease serum arginase activity and increase serum nitrite. CONCLUSIONS: Miltefosine increased the proportion of monocytes that have a pro-inflammatory phenotype, which was accompanied by an enhanced secretion of pro-inflammatory cytokines and increased levels of serum nitrite. The decrease in anti-inflammatory cytokine levels and serum arginase activity collectively indicated that miltefosine triggered a robust T-helper 1 response that facilitated parasite elimination. SN - 1537-6613 UR - https://www.unboundmedicine.com/medline/citation/21933878/Miltefosine_effectively_modulates_the_cytokine_milieu_in_Indian_post_kala_azar_dermal_leishmaniasis_ L2 - https://academic.oup.com/jid/article-lookup/doi/10.1093/infdis/jir551 DB - PRIME DP - Unbound Medicine ER -