ArticlePloS one2012
The stress-response factor SigH modulates the interaction between Mycobacterium tuberculosis and host phagocytes.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
53 citing papers in PubMed, 70 citations in OpenAlex.
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- Protein-Mediated Virulence in Mycobacterium tuberculosis.Advances in experimental medicine and biology · 2026Review
- Protein Architecture and Composition in Mycobacterium tuberculosis.Advances in experimental medicine and biology · 2026Review
- Development and preclinical evaluation of next-generation ΔsigH-based live candidate vaccines.JCI insight · 2025Article
- Phagosomal RNA sensing through TLR8 controls susceptibility to tuberculosis.Cell reports · 2025Article
- Prevention of tuberculosis in cynomolgus macaques by an attenuated Mycobacterium tuberculosis vaccine candidate.Nature communications · 2025Article
- Driving innovation from discovery to access: Meeting report of the 7Gates open research · 2025Article
- Model systems to studyFrontiers in cellular and infection microbiology · 2025Review
- From pathogenesis to antigens: the key to shaping the future of TB vaccines.Frontiers in immunology · 2024Review
- From immunology to artificial intelligence: revolutionizing latent tuberculosis infection diagnosis with machine learning.Military Medical Research · 2023Review
- Inhibition of indoleamine dioxygenase leads to better control of tuberculosis adjunctive to chemotherapy.JCI insight · 2023Article
- Review
- Comparative Genome Analysis of 19Antibiotics (Basel, Switzerland) · 2022Article
- Peripheral Blood Markers Correlate with the Progression of Active Tuberculosis Relative to Latent Control ofPathogens (Basel, Switzerland) · 2022Article
- In-depth systems biological evaluation of bovine alveolar macrophages suggests novel insights into molecular mechanisms underlyingFrontiers in microbiology · 2022Article
- Dormancy: There and Back Again.Molecular biology · 2022Article
- Advancing Adjuvants forFrontiers in immunology · 2021Review
- RNA-Seq Transcriptome Analysis of Peripheral Blood From Cattle Infected WithFrontiers in veterinary science · 2021Article
- Infections of the lung: a predictive, preventive and personalized perspective through the lens of evolution, the emergence of SARS-CoV-2 and its pathogenesis.The EPMA journal · 2020Review
- Intelligent Mechanisms of Macrophage Apoptosis Subversion byPathogens (Basel, Switzerland) · 2020Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
The Mycobacterium tuberculosis stress response factor SigH plays a crucial role in modulating the pathogen's response to heat, oxidative-stress, envelope damage and hypoxia. We hypothesized that the lack of this key stress response factor would alter the interaction between the pathogen and its host cells. We compared the interaction of Mtb, Mtb:Δ-sigH and a strain where the mutation had been genetically complemented (Mtb: Δ-sigH:CO) with primary rhesus macaque bone marrow derived macrophages (Rh-BMDMs). The expression of numerous inducible and homeostatic (CCL) β-chemokines and several apoptotic markers was induced to higher levels in the cells infected with Mtb:Δ-sigH, relative to Mtb or the complemented strain. The differential expression of these genes manifested into functional differences in chemotaxis and apoptosis in cells infected with these two strains. The mutant strain also exhibited reduced late-stage survival in Rh-BMDMs. We hypothesize that the product of one or more SigH-dependent genes may modulate the innate interaction of Mtb with host cells, effectively reducing the chemokine-mediated recruitment of immune effector cells, apoptosis of infected monocytes and enhancing the long-term survival and replication of the pathogen in this milieu The significantly higher induction of Prostaglandin Synthetase 2 (PTGS2 or COX2) in Rh-BMDMs infected with Mtb relative to Mtb: Δ-sigH may explain reduced apoptosis in Mtb-infected cells, as PTGS2 is known to inhibit p53-dependent apoptosis.The SigH-regulon modulates the innate interaction of Mtb with host phagocytes, perhaps as part of a strategy to limit its clearance and prolong its survival. The SigH regulon appears to be required to modulate innate immune responses directed against Mtb.
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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.