ArticleBMC infectious diseases2014
Outbreaks of Mycobacterium tuberculosis MDR strains differentially induce neutrophil respiratory burst involving lipid rafts, p38 MAPK and Syk.
Article in BMC infectious diseases, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 26 citations in OpenAlex.
- MAPK signaling pathways in host immune regulation during Mycobacterium tuberculosis infection.Frontiers in immunology · 2026Review
- Variants of human DECTIN-1 rs16910526 are linked to differential reactive oxygen species production and susceptibility to tuberculosis.Journal of biomedical science · 2024Article
- Early innate cell interactions withFrontiers in immunology · 2023Review
- Article
- Dose-dependent effects of perfluorocarbon-based blood substitute on cardiac function in myocardial ischemia-reperfusion injury.Molecular and cellular biochemistry · 2022Article
- Emerging advances in identifying signal transmission molecules involved in the interaction betweenFrontiers in cellular and infection microbiology · 2022Review
- Crystal structure of the TreS:Pep2 complex, initiating α-glucan synthesis in the GlgE pathway of mycobacteria.The Journal of biological chemistry · 2019Article
- Luteolin Partially Inhibits LFA-1 Expression in Neutrophils Through the ERK Pathway.Inflammation · 2019Article
- Article
- Immunological consequences of strain variation within the Mycobacterium tuberculosis complex.European journal of immunology · 2017Review
- Genetic-and-Epigenetic Interspecies Networks for Cross-Talk Mechanisms in Human Macrophages and Dendritic Cells during MTB Infection.Frontiers in cellular and infection microbiology · 2016Article
- Immunological mechanisms contributing to the double burden of diabetes and intracellular bacterial infections.Immunology · 2015Review
- Nontuberculous mycobacterial osteomyelitis.Infectious diseases (London, England) · 2015Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNeutrophils (PMN) are the first cells to infiltrate the lung after infection, and they play a significant protective role in the elimination of pathogen, by releasing preformed oxidants and proteolytic enzymes from granules and generating ROS, thus limiting inflammation by succumbing to apoptosis. In a previous study, we found marked differences in ROS-induced apoptosis between two Mycobacterium tuberculosis (Mtb) strains, M and Ra, representative of widespread Mtb families in South America, i.e. Haarlem and Latin-American Mediterranean (LAM), being strain M able to generate further drug resistance and to disseminate aggressively.
methodsIn this study we evaluate the nature of bacteria-PMN interaction by assessing ROS production, apoptosis, lipid raft coalescence, and phagocytosis induced by Mtb strains.
resultsDectin-1 and TLR2 participate in Mtb-induced ROS generation and apoptosis in PMN involving p38 MAPK and Syk activation with the participation of a TLR2-dependent coalescence of lipid rafts. Further, ROS production occurs during the phagocytosis of non-opsonized bacteria and involves α-glucans on the capsule. In contrast, strain M lacks the ability to induce ROS because of: 1) a reduced phagocytosis and 2) a failure in coalescence of lipid raft.
conclusionsThe differences in wall composition could explain the success of some strains which stay unnoticed by the host through inhibition of apoptosis and ROS but making possible its replication inside PMN as a potential evasion mechanism. Innate immune responses elicited by Mtb strain-to-strain variations need to be considered in TB vaccine development.
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