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

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; Dhiraj Kumar; Gobardhan Das; Asif Mohmmed; Pawan Malhotra; Anand Ranganathan

doi:10.1038/ncomms7049

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

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, Dhiraj Kumar, Gobardhan Das, Asif Mohmmed, Pawan Malhotra, Anand Ranganathan

Research output: Contribution to journal › Article › peer-review

43 Scopus citations

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.

Original language	English (US)
Article number	6049
Journal	Nature Communications
Volume	6
DOIs	https://doi.org/10.1038/ncomms7049
State	Published - Jan 2015

ASJC Scopus subject areas

Chemistry(all)
Biochemistry, Genetics and Molecular Biology(all)
Physics and Astronomy(all)

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Bhalla, K., Chugh, M., Mehrotra, S., Rathore, S., Tousif, S., Dwivedi, V. P., Prakash, P., Samuchiwal, S. K., Kumar, S., Singh, D. K., Ghanwat, S., Kumar, D., Das, G., Mohmmed, A., Malhotra, P., & Ranganathan, A. (2015). Host ICAMs play a role in cell invasion by Mycobacterium tuberculosis and Plasmodium falciparum. Nature Communications, 6, Article 6049. https://doi.org/10.1038/ncomms7049

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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.",

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AU - Bhalla, Kuhulika

AU - Chugh, Monika

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AU - Tousif, Sultan

AU - Dwivedi, Ved Prakash

AU - Prakash, Prem

AU - Samuchiwal, Sachin Kumar

AU - Kumar, Sushil

AU - Singh, Dhiraj Kumar

AU - Ghanwat, Swapnil

AU - Kumar, Dhiraj

AU - Das, Gobardhan

AU - Mohmmed, Asif

AU - Malhotra, Pawan

AU - Ranganathan, Anand

PY - 2015/1

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

Abstract

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