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Infection and Immunity, December 2005, p. 8334-8344, Vol. 73, No. 12
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.12.8334-8344.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Regulation of Impaired Protein Kinase C Signaling by Chemokines in Murine Macrophages during Visceral Leishmaniasis

Ranadhir Dey,1 Arup Sarkar,1 Nivedita Majumder,1 Suchandra Bhattacharyya (Majumdar),1 Kaushik Roychoudhury,2 Sandip Bhattacharyya,3 Syamal Roy,2 and Subrata Majumdar1*

Department of Microbiology, Bose Institute, P1/12, C.I.T. Scheme VII-M, Kolkata-700 054, India,1 Division of Immunology, Indian Institute of Chemical Biology, 4, R. S. Mullick Road, Kolkata-700 032, India,2 School of Medicine, Washington University, St. Louis, Missouri3

Received 29 April 2005/ Returned for modification 17 June 2005/ Accepted 23 August 2005

The protein kinase C (PKC) family regulates macrophage function involved in host defense against infection. In the case of Leishmania donovani infection, the impairment of PKC-mediated signaling is one of the crucial events for the establishment of parasite into the macrophages. Earlier reports established that C-C chemokines mediated protection against leishmaniasis via the generation of nitric oxide after 48 h. In this study, we investigated the role of MIP-1{alpha} and MCP-1 in the regulation of impaired PKC activity in the early hours (6 h) of infection. These chemokines restored Ca2+-dependent PKC activity and inhibited Ca2+-independent atypical PKC activity in L. donovani-infected macrophages under both in vivo and in vitro conditions. Pretreatment of macrophages with chemokines induced superoxide anion generation by activating NADPH oxidase components in infected cells. Chemokine administration in vitro induced the migration of infected macrophages and triggered the production of reactive oxygen species. In vivo treatment with chemokines significantly restricted the parasitic burden in livers as well as in spleens. Collectively, these results indicate a novel regulatory role of C-C chemokines in controlling the intracellular growth and multiplication of L. donovani, thereby demonstrating the antileishmanial properties of C-C chemokines in the disease process.

* Corresponding author. Mailing address: Department of Microbiology, Bose Institute, P1/12, C.I.T. Scheme VII-M, Kolkata-700 054, India. Phone: (91) (33) 2337-9416. Fax: (91) (33) 2334-3886. E-mail: subrata{at}boseinst.ernet.in.

Editor: W. A. Petri, Jr.

Infection and Immunity, December 2005, p. 8334-8344, Vol. 73, No. 12
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.12.8334-8344.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Selvapandiyan, A., Dey, R., Nylen, S., Duncan, R., Sacks, D., Nakhasi, H. L. (2009). Intracellular Replication-Deficient Leishmania donovani Induces Long Lasting Protective Immunity against Visceral Leishmaniasis. J. Immunol. 183: 1813-1820 [Abstract] [Full Text]  
  • Dey, R., Majumder, N., Bhattacharjee, S., Majumdar, S. B., Banerjee, R., Ganguly, S., Das, P., Majumdar, S. (2007). Leishmania donovani-Induced Ceramide as the Key Mediator of Akt Dephosphorylation in Murine Macrophages: Role of Protein Kinase C{zeta} and Phosphatase. Infect. Immun. 75: 2136-2142 [Abstract] [Full Text]  


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