Intrinsic JNK-MAPK pathway involvement requires daf-16-mediated immune response during Shigella flexneri infection in C. elegans
| Autor: | Krishnaswamy Balamurugan, Shanmugam Marudhupandiyan |
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| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Immunology Microbiology Shigella flexneri Animals Genetically Modified 03 medical and health sciences Immune system Daf-16 Animals Humans Insulin Caenorhabditis elegans Caenorhabditis elegans Proteins Transcription factor Cells Cultured Dysentery Bacillary Innate immune system biology Wild type JNK Mitogen-Activated Protein Kinases Forkhead Transcription Factors Receptor Cross-Talk biology.organism_classification Immunity Innate Crosstalk (biology) Disease Models Animal 030104 developmental biology Mitogen-Activated Protein Kinases Signal Transduction |
| Zdroj: | Immunologic research. 65(3) |
| ISSN: | 1559-0755 |
| Popis: | The c-Jun N-terminal kinase-mitogen-activated protein kinase (JNK-MAPK) pathway assists in modulating signals for growth, survival, and metabolism, thereby coordinating many cellular events during normal and stress conditions. To understand the role of the JNK-MAPK pathway during bacterial infection, an in vivo model organism Caenorhabditis elegans was used. In order to check the involvement of the JNK-MAPK pathway, the survival rate of C. elegans wild type (WT), and JNK-MAPK pathway mutant worms' upon exposure to selective Gram-positive and Gram-negative pathogenic bacteria, was studied. Among the pathogens, Shigella flexneri M9OT was found to efficiently colonize inside the WT and JNK-MAPK pathway mutant worms. qPCR studies had suggested that the above pathway-specific genes kgb-2 and jnk-1 were prominently responsible for the immune response elicited by the host during the M9OT infection. In addition, daf-16, which is a major transcription factor of the insulin/insulin growth factor-1 signaling (IIS) pathway, was also found to be involved during the host response. Crosstalk between IIS and JNK-MAPK pathways has probably been involved in the activation of the host immune system, which consequently leads to lifespan extension. Furthermore, it is also observed that daf-16 activation by JNK-MAPK pathway leads to antimicrobial response, by activating lys-7 expression. These findings suggest that JNK-MAPK is not the sole pathway that enhances the immunity of the host. Nonetheless, the IIS pathway bridges the JNK-MAPK pathway that influences in protecting the host in counter to the M9OT infection. |
| Databáze: | OpenAIRE |
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