The Role of Non-Phagocytic Cells in Mycobacterial Infections

Garcı́a-Pérez, Blanca Estela; Castrejón-Jiménez, Nayeli Shantal; Luna-Herrera, Julieta

doi:10.5772/30335

Cited by 8 publications

(16 citation statements)

References 145 publications

(96 reference statements)

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“…ATIIs also express cell surface co-stimulatory molecules that coordinate antigen presentation to CD4 + T cells [6;32]. These factors can be induced by TNF [20] and include ICAM/CD54, co-stimulatory molecule/signal for T cell activation CD80 (or B7–1), lymphocyte function-associated antigen 3 (LFA-3 or CD58), and vascular cell adhesion molecule (or CD106) [6].…”

Section: Ats Role In Initiating Adaptive Immunitymentioning

confidence: 99%

“…These factors can be induced by TNF [20] and include ICAM/CD54, co-stimulatory molecule/signal for T cell activation CD80 (or B7–1), lymphocyte function-associated antigen 3 (LFA-3 or CD58), and vascular cell adhesion molecule (or CD106) [6]. Published studies have shown differences in the expression levels of MHC-I, MHC–II and co-stimulatory molecules in primary cells, cell lines and between species [32;34].…”

Section: Ats Role In Initiating Adaptive Immunitymentioning

confidence: 99%

“…During the initial infection following direct deposition in the alveolus, ATIIs internalize M.tb via macropinocytosis [6;16;38] in both a receptor-mediated and actin-dependent manner. The process of bacterial uptake is highly coordinated and involves membrane ruffling, microtubule and microfilament polymerization and subsequent signal transduction, bacterial entry and innate immune activation [6].…”

Section: Mtb Binding and Invasion Of The Alveolar Epitheliummentioning

confidence: 99%

“…Early infection is founded on the principal that upon lung deposition M.tb is phagocytized by alveolar macrophages (AMs) [4] and dendritic cells (DCs) [3]; however, the human lung is comprised of approximately 40 host cell types [5] and how many of these cell populations may become infected is still unknown. In this regard, recent studies have demonstrated that bacterial recognition and uptake can occur via alveolar epithelial cells (ATs), non-professional phagocytic cells that line the alveolar tissue [6]. In order to understand the role of ATs during infection, it is necessary to first define the interaction between ATs and M.tb , as well as the subsequent crosstalk between M.tb infected ATs and other host cells at different stages of the infection.…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Alveolar Epithelial Cells in Mycobacterium tuberculosis Infection: Active Players or Innocent Bystanders?

Scordo

Knoell²,

Torrelles

2015

J Innate Immun

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Tuberculosis (TB) is a disease that kills one person every 18 s. TB remains a global threat due to the emergence of drug-resistant Mycobacterium tuberculosis (M.tb) strains and the lack of an efficient vaccine. The ability of M.tb to persist in latency, evade recognition following seroconversion, and establish resistance in vulnerable populations warrants closer examination. Past and current research has primarily focused on examination of the role of alveolar macrophages and dendritic cells during M.tb infection, which are critical in the establishment of the host response during infection. However, emerging evidence indicates that the alveolar epithelium is a harbor for M.tb and critical during progression to active disease. Here we evaluate the relatively unexplored role of the alveolar epithelium as a reservoir and also its capacity to secrete soluble mediators upon M.tb exposure, which influence the extent of infection. We further discuss how the M.tb-alveolar epithelium interaction instigates cell-to-cell crosstalk that regulates the immune balance between a proinflammatory and an immunoregulatory state, thereby prohibiting or allowing the establishment of infection. We propose that consideration of alveolar epithelia provides a more comprehensive understanding of the lung environment in vivo in the context of host defense against M.tb.

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Section: Ats Role In Initiating Adaptive Immunitymentioning

confidence: 99%

Section: Ats Role In Initiating Adaptive Immunitymentioning

confidence: 99%

Section: Mtb Binding and Invasion Of The Alveolar Epitheliummentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Alveolar Epithelial Cells in Mycobacterium tuberculosis Infection: Active Players or Innocent Bystanders?

Scordo

Knoell²,

Torrelles

2015

J Innate Immun

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“…This invasive bacterium actively induces its own uptake by macropinocytosis to enter normally non-phagocytic cells such as AECs [15] . Until now, Toll-like receptor (TLR)2, TLR4 and C-type lectins have been implicated in mycobacteria-induced epithelial signalling and uptake [16,17] . It has also been observed that mycobacteria manipulate epithelial production of the cytokine CXCL8 through the inhibitory G-protein-coupled receptor (GPCR) kinase 2 [18] .…”

Section: Mycobacteria Manipulate G-proteincoupled Receptors To Increamentioning

confidence: 99%

Mycobacteria Manipulate G-Protein-Coupled Receptors to Increase Mucosal Rac1 Expression in the Lungs

Alaridah¹,

Lutay²,

Tenland³

et al. 2016

J Innate Immun

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Mycobacterium bovis bacille Calmette-Guérin (BCG) is currently the only approved vaccine against tuberculosis (TB). BCG mimics M. tuberculosis (Mtb) in its persistence in the body and is used as a benchmark to compare new vaccine candidates. BCG was originally designed for mucosal vaccination, but comprehensive knowledge about its interaction with epithelium is currently lacking. We used primary airway epithelial cells (AECs) and a murine model to investigate the initial events of mucosal BCG interactions. Furthermore, we analysed the impact of the G-protein-coupled receptors (GPCRs), CXCR1 and CXCR2, in this process, as these receptors were previously shown to be important during TB infection. BCG infection of AECs induced GPCR-dependent Rac1 up-regulation, resulting in actin redistribution. Thealtered distribution of the actin cytoskeleton involved the MAPK signalling pathway. Blocking of the CXCR1 or CXCR2 prior to infection decreased Rac1 expression, and increased epithelial transcriptional activity and epithelial cytokine production. BCG infection did not result in epithelial cell death as measured by p53 phosphorylation and annexin. This study demonstrated that BCG infection of AECs manipulated the GPCRs to suppress epithelial signalling pathways. Future vaccine strategies could thus be improved by targeting GPCRs.

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Comparative study of interruption of signaling pathways in lung epithelial cell by two different Mycobacterium tuberculosis lineages

Hadifar

Behrouzi

Fateh

et al. 2018

Journal Cellular Physiology

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Alveolar epithelial cell (AEC) provides a replication niche for Mycobacterium tuberculosis. Based on the role of AEC in M. tuberculosis pathogenesis and existence of genetic diversity within this bacterium, we investigated interactions between AEC II and two different M. tuberculosis lineages. We have compared the transcriptome and cytokines/chemokines levels of A549 infected by M. tuberculosis lineage three and four using qRT-PCR and ELISA arrays, respectively. We showed different M. tuberculosis strains induced changes in different effectors that involved in TLRs and NF-κB signaling pathways. We observed different reaction of the studied lineages specifically in pathogenesis, immune evasion mechanism, IL-12/IFN-γ axis, and autophagy. Similar behavior was detected in regarding to apoptosis, necroptosis, anti-inflammatory responses, and canonical inflammasome. Our findings contribute to elucidate more details in pathogenesis, immune evasion strategies, novel target and druggable pathway for therapeutic intervention, and host directed therapy in tuberculosis infection. Also, different M. tuberculosis lineages-dependent host-pathogen interactions suggested using only one strain for this kind of research will be controversial.

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The Role of Non-Phagocytic Cells in Mycobacterial Infections

Cited by 8 publications

References 145 publications

Alveolar Epithelial Cells in <b><i>Mycobacterium tuberculosis</i></b> Infection: Active Players or Innocent Bystanders?

Alveolar Epithelial Cells in <b><i>Mycobacterium tuberculosis</i></b> Infection: Active Players or Innocent Bystanders?

Mycobacteria Manipulate G-Protein-Coupled Receptors to Increase Mucosal Rac1 Expression in the Lungs

Comparative study of interruption of signaling pathways in lung epithelial cell by two different Mycobacterium tuberculosis lineages

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