Studies on Shigella boydii infection in Caenorhabditis elegans and bioinformatics analysis of immune regulatory protein interactions.

Shigella boydii causes bacillary dysentery or shigellosis and generates a significant burden in the developing nations. S. boydii-mediated infection assays were performed at both physiological and molecular levels using Caenorhabditis elegans as a host. Continuous exposure of worms to S. boydii showed a reduced life span indicating the pathogenicity of Shigella. Quantitative Real-Time PCR analysis was performed to analyze the expression and regulation of host specific candidate-antimicrobial genes (clec-60, clec-87, lys-7), which were expressed significantly during early infection, but weakened during the latter hours. Increased mortality of mutant RB1285 by S. boydii and Shigella flexneri indicated the role of lys-7 during Shigella infection. Protein-protein interactions (PPIs) database was used to analyze the interaction of immune proteins in both C. elegans and humans. In addition, the expression and regulation were revealed about immune genes (clec-61, clec-62, clec-63, F54D5.3 and ZK1320.2), which encode several intermediate immune protein partners (CLEC-61, CLEC-62, CLEC-63, F54D5.3, ZK1320.2, W03D2.6 and THN-2) that interact with LYS-7 and CLEC-60 and were found to play a role in C. elegans immune defense against S. boydii infections. Similarly, the immune genes that are specific to the human defense system, which encode IGHV4-39, A2M, LTF, and CD79A, were predicted to be expressed with LYZ and MBL2, thus indicating their regulation during Shigella infections. Our results using the lowest eukaryotic model system and human database indicated that the major players involved in immunity-related processes appear to be common in cases of Shigella sp. mediated immune responses. This article is part of a Special Issue entitled: Computational Methods for Protein Interaction and Structural Prediction.