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 () and Anand Ranganathan ()
Additional contact information
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

Nature Communications, 2015, vol. 6, issue 1, 1-13

Abstract: 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.

Date: 2015
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/ncomms7049 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms7049

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/ncomms7049

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().