ArticlePLoS pathogens2010
Mycobacterium tuberculosis eis regulates autophagy, inflammation, and cell death through redox-dependent signaling.
Article in PLoS pathogens, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 194 papers, 1 of them a synthesis that pooled it.
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Who cites it
194 citing papers in PubMed, 1 synthesis or guideline pooled it, 324 citations in OpenAlex.
- Pooled it
- Mitophagy-mediated immune evasion: Shared strategies of pathogens.Redox biology · 2026Review
- Exploiting autophagy-targeting natural compounds for potential antimicrobial actions.Autophagy · 2026Review
- Mycobacterium bovis induces cellular oxidative stress via the host protein SH3PXD2B.BMC veterinary research · 2026Article
- Article
- Key Proteins and Enzymatic Mechanisms Underlying Drug Resistance in Mycobacterium tuberculosis.Advances in experimental medicine and biology · 2026Review
- Immunotherapy for tuberculosis: current landscape, mechanistic insights, and translational perspectives.Frontiers in immunology · 2026Review
- Functional analysis of type VII secretion system links to host immune evasion mechanism inFrontiers in cellular and infection microbiology · 2026Review
- Rv1899c, an HDAC1-ZBTB25-Interacting Protein ofInternational journal of molecular sciences · 2025Article
- Unraveling Epistatic Interactions Between Sites Under Drug-Dependent Selection in the Mycobacterium tuberculosis Genome.Molecular biology and evolution · 2025Article
- Cell death pathways in response toInfection and immunity · 2025Review
- The acetyltransferase CysE modulates virulence and drug resistance of Mycobacterium tuberculosis by interfering with oxidative stress responses.Communications biology · 2025Article
- SMURF2 inhibits autophagic control ofbioRxiv : the preprint server for biology · 2025Article
- Cell Death Mechanisms inPathogens (Basel, Switzerland) · 2025Review
- Suppressing Mycobacterium tuberculosis virulence and drug resistance by targeting Eis protein through computational drug discovery.Molecular diversity · 2025Article
- Mycobacterial PstP impairs host RNA alternative splicing by dephosphorylation of spliceosome RBMX at S189.iMetaOmics · 2025Article
- Dynamic interplay of autophagy and membrane repair during Mycobacterium tuberculosis Infection.PLoS pathogens · 2025Article
- Dysregulation of the JNK signaling pathway in tuberculosis: mechanisms and therapeutic strategies.Frontiers in cellular and infection microbiology · 2025Review
- Autophagy in mycobacterial infections: molecular mechanisms, host-pathogen interactions, and therapeutic opportunities.Frontiers in cellular and infection microbiology · 2025Review
- Resistance phenotypes and genomic features ofFrontiers in cellular and infection microbiology · 2025Article
134 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The "enhanced intracellular survival" (eis) gene of Mycobacterium tuberculosis (Mtb) is involved in the intracellular survival of M. smegmatis. However, its exact effects on host cell function remain elusive. We herein report that Mtb Eis plays essential roles in modulating macrophage autophagy, inflammatory responses, and cell death via a reactive oxygen species (ROS)-dependent pathway. Macrophages infected with an Mtb eis-deletion mutant H37Rv (Mtb-Δeis) displayed markedly increased accumulation of massive autophagic vacuoles and formation of autophagosomes in vitro and in vivo. Infection of macrophages with Mtb-Δeis increased the production of tumor necrosis factor-α and interleukin-6 over the levels produced by infection with wild-type or complemented strains. Elevated ROS generation in macrophages infected with Mtb-Δeis (for which NADPH oxidase and mitochondria were largely responsible) rendered the cells highly sensitive to autophagy activation and cytokine production. Despite considerable activation of autophagy and proinflammatory responses, macrophages infected with Mtb-Δeis underwent caspase-independent cell death. This cell death was significantly inhibited by blockade of autophagy and c-Jun N-terminal kinase-ROS signaling, suggesting that excessive autophagy and oxidative stress are detrimental to cell survival. Finally, artificial over-expression of Eis or pretreatment with recombinant Eis abrogated production of both ROS and proinflammatory cytokines, which depends on the N-acetyltransferase domain of the Eis protein. Collectively, these data indicate that Mtb Eis suppresses host innate immune defenses by modulating autophagy, inflammation, and cell death in a redox-dependent manner.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.