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Host ICAMs play a role in cell invasion by Mycobacterium tuberculosis and Plasmodium falciparum

Author

Listed:
  • Kuhulika Bhalla

    (Recombinant Gene Products Group, International Centre for Genetic Engineering and Biotechnology, ICGEB)

  • Monika Chugh

    (Malaria Group, International Centre for Genetic Engineering and Biotechnology, ICGEB)

  • Sonali Mehrotra

    (Malaria Group, International Centre for Genetic Engineering and Biotechnology, ICGEB)

  • Sumit Rathore

    (All India Institute of Medical Sciences)

  • Sultan Tousif

    (Immunology Group, International Centre for Genetic Engineering and Biotechnology, ICGEB)

  • Ved Prakash Dwivedi

    (Immunology Group, International Centre for Genetic Engineering and Biotechnology, ICGEB)

  • Prem Prakash

    (Recombinant Gene Products Group, International Centre for Genetic Engineering and Biotechnology, ICGEB)

  • Sachin Kumar Samuchiwal

    (Recombinant Gene Products Group, International Centre for Genetic Engineering and Biotechnology, ICGEB)

  • Sushil Kumar

    (Recombinant Gene Products Group, International Centre for Genetic Engineering and Biotechnology, ICGEB)

  • Dhiraj Kumar Singh

    (Recombinant Gene Products Group, International Centre for Genetic Engineering and Biotechnology, ICGEB)

  • Swapnil Ghanwat

    (Immunology Group, International Centre for Genetic Engineering and Biotechnology, ICGEB)

  • Dhiraj Kumar

    (Immunology Group, International Centre for Genetic Engineering and Biotechnology, ICGEB)

  • Gobardhan Das

    (Immunology Group, International Centre for Genetic Engineering and Biotechnology, ICGEB)

  • Asif Mohmmed

    (Malaria Group, International Centre for Genetic Engineering and Biotechnology, ICGEB)

  • Pawan Malhotra

    (Malaria Group, International Centre for Genetic Engineering and Biotechnology, ICGEB)

  • Anand Ranganathan

    (Recombinant Gene Products Group, International Centre for Genetic Engineering and Biotechnology, ICGEB)

Abstract

Intercellular adhesion molecules (ICAMs) belong to the immunoglobulin superfamily and participate in diverse cellular processes including host–pathogen interactions. ICAM-1 is expressed on various cell types including macrophages, whereas ICAM-4 is restricted to red blood cells. Here we report the identification of an 11-kDa synthetic protein, M5, that binds to human ICAM-1 and ICAM-4, as shown by in vitro interaction studies, surface plasmon resonance and immunolocalization. M5 greatly inhibits the invasion of macrophages and erythrocytes by Mycobacterium tuberculosis and Plasmodium falciparum, respectively. Pharmacological and siRNA-mediated inhibition of ICAM-1 expression also results in reduced M. tuberculosis invasion of macrophages. ICAM-4 binds to P. falciparum merozoites, and the addition of recombinant ICAM-4 to parasite cultures blocks invasion of erythrocytes by newly released merozoites. Our results indicate that ICAM-1 and ICAM-4 play roles in host cell invasion by M. tuberculosis and P. falciparum, respectively, either as receptors or as crucial accessory molecules.

Suggested Citation

  • Kuhulika Bhalla & Monika Chugh & Sonali Mehrotra & Sumit Rathore & Sultan Tousif & Ved Prakash Dwivedi & Prem Prakash & Sachin Kumar Samuchiwal & Sushil Kumar & Dhiraj Kumar Singh & Swapnil Ghanwat & , 2015. "Host ICAMs play a role in cell invasion by Mycobacterium tuberculosis and Plasmodium falciparum," Nature Communications, Nature, vol. 6(1), pages 1-13, May.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms7049
    DOI: 10.1038/ncomms7049
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