ArticleMucosal immunology2017
Mycobacterium tuberculosis cell wall released fragments by the action of the human lung mucosa modulate macrophages to control infection in an IL-10-dependent manner.
Article in Mucosal immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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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
37 citing papers in PubMed, 49 citations in OpenAlex.
- Phospholipase A2 Isoforms in Lung Immunity and Respiratory Infections: Potential Targets for Next-Generation Therapy.International journal of molecular sciences · 2026Review
- The lipid language of tuberculosis:mBio · 2026Review
- Lung organoids as a human system for Mycobacteria infection modeling and drug testing.The FEBS journal · 2026Review
- Cytotoxic granules and effector molecules from immune cells in tuberculosis: Mechanisms of host defense and therapeutic potential.Virulence · 2025Review
- HIV infection impairs the host response to Mycobacterium tuberculosis infection by altering surfactant protein D function in the human lung alveolar mucosa.Mucosal immunology · 2024Article
- Human alveolar lining fluid from the elderly promotes Mycobacterium tuberculosis intracellular growth and translocation into the cytosol of alveolar epithelial cells.Mucosal immunology · 2024Article
- From pathogenesis to antigens: the key to shaping the future of TB vaccines.Frontiers in immunology · 2024Review
- Challenges in Developing a Controlled Human Tuberculosis Challenge Model.Current topics in microbiology and immunology · 2024Review
- Exposure ofFrontiers in tuberculosis · 2024Article
- Pulmonary Tuberculosis in Children: A Forgotten Disease?Microorganisms · 2023Review
- Allele-dependent interaction of LRRK2 and NOD2 in leprosy.PLoS pathogens · 2023Article
- Resistance and Susceptibility Immune Factors at Play duringPathogens (Basel, Switzerland) · 2022Review
- The Aging Human Lung Mucosa: A Proteomics Study.The journals of gerontology. Series A, Biological sciences and medical sciences · 2022Article
- Tuberculosis in an Aging World.Pathogens (Basel, Switzerland) · 2022Review
- Anti-mycobacterial activity of heat and pH stable high molecular weight protein(s) secreted by a bacterial laboratory contaminant.Microbial cell factories · 2022Article
- Host- and Age-Dependent Transcriptional Changes inInternational journal of molecular sciences · 2022Article
- The Impact of Aging on the Lung Alveolar Environment, Predetermining Susceptibility to Respiratory Infections.Frontiers in aging · 2022Review
- Photoclick Reaction Constructs Glutathione-Responsive Theranostic System for Anti-Tuberculosis.Frontiers in molecular biosciences · 2022Article
- Mycobacteriophages as Potential Therapeutic Agents against Drug-Resistant Tuberculosis.International journal of molecular sciences · 2021Review
- MIR337-3p Enhances Mycobacterial Pathogenicity Involving TLR4/MYD88 and STAT3 Signals, Impairing VDR Antimicrobial Response and Fast-Acting Immunity.Frontiers in immunology · 2021Article
Corrections and comments
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
Abstract
Mycobacterium tuberculosis (M.tb), the causative agent of tuberculosis, is a major public health challenge facing the world. During infection, M.tb is deposited in the lung alveolar space where it comes in contact with the lung mucosa, known as alveolar lining fluid (ALF), an environment that M.tb encounters at different stages of the infection and disease. ALF is abundant in homeostatic and antimicrobial hydrolytic enzymes, also known as hydrolases. Here we demonstrate that ALF hydrolases, at their physiological concentrations and upon contact with M.tb, release M.tb cell envelope fragments into the milieu. These released fragments are bioactive, but non-cytotoxic, regulate the function of macrophages, and thus are capable of modulating the immune response contributing to the control of M.tb infection by human macrophages. Specifically, macrophages exposed to fragments derived from the exposure of M.tb to ALF were able to control the infection primarily by increasing phagosome-lysosome fusion and acidification events. This enhanced control was found to be dependent on fragment-induced interleukin-10 (IL-10) production but also involves the STAT3 signaling pathway in an IL-10-independent manner. Collectively our data indicate that M.tb fragments released upon contact with lung mucosa hydrolases participate in the host immune response to M.tb infection through innate immune modulation.
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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.