TLR stimulation of human neutrophils lead to increased release of MCP-1, MIP-1α, IL-1β, IL-8 and TNF during tuberculosis

Hilda, J. Nancy; Das, Sulochana D.

doi:10.1016/j.humimm.2015.10.005

Cited by 22 publications

(22 citation statements)

References 16 publications

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“…Neutrophils secrete a wide range of cytokines, chemokines, and enzymes, such as IL-1 β , IL-1 α , TNF- α , CXCL1/KC, CXCL8/IL-8, CCL3/MIP-1 α , CCL4/MIP-1 β , GM-CSF, and metalloproteinases (MMPs) [46–52]. Factors secreted by neutrophils and molecules expressed on their surface underlie neutrophil cross-talk with other immune cells and induce immune cell activation, recruitment to the infectious site, and immune response generation and regulation.…”

Section: Neutrophil Interactions With Other Immune Cellsmentioning

confidence: 99%

Neutrophils in Tuberculosis: Heterogeneity Shapes the Way?

Lyadova

2017

Mediators of Inflammation

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Infection with M. tuberculosis remains one of the most common infections in the world. The outcome of the infection depends on host ability to mount effective protection and balance inflammatory responses. Neutrophils are innate immune cells implicated in both processes. Accordingly, during M. tuberculosis infection, they play a dual role. Particularly, they contribute to the generation of effector T cells, participate in the formation of granuloma, and are directly involved in tissue necrosis, destruction, and infection dissemination. Neutrophils have a high bactericidal potential. However, data on their ability to eliminate M. tuberculosis are controversial, and the results of neutrophil depletion experiments are not uniform. Thus, the overall roles of neutrophils during M. tuberculosis infection and factors that determine these roles are not fully understood. This review analyzes data on neutrophil defensive and pathological functions during tuberculosis and considers hypotheses explaining the dualism of neutrophils during M. tuberculosis infection and tuberculosis disease.

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Section: Neutrophil Interactions With Other Immune Cellsmentioning

confidence: 99%

Neutrophils in Tuberculosis: Heterogeneity Shapes the Way?

Lyadova

2017

Mediators of Inflammation

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“…M. tuberculosis infection triggers TLR signaling and induces NF-κB which mediates the induction of gene expression of pro-inflammatory cytokines such as IL-1β and TNF in neutrophils ( 42 , 131 ). Inflammasomes are multimeric protein complexes and play a key role in the activation of IL-1α, and IL-1β ( 132 ).…”

Section: Neutrophils and The Role Of Cytokines And Chemokines In Inflmentioning

confidence: 99%

Neutrophils: Innate Effectors of TB Resistance?

et al. 2018

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Certain individuals are able to resist Mycobacterium tuberculosis infection despite persistent and intense exposure. These persons do not exhibit adaptive immune priming as measured by tuberculin skin test (TST) and interferon-γ (IFN-γ) release assay (IGRA) responses, nor do they develop active tuberculosis (TB). Genetic investigation of individuals who are able to resist M. tuberculosis infection shows there are likely a combination of genetic variants that contribute to the phenotype. The contribution of the innate immune system and the exact cells involved in this phenotype remain incompletely elucidated. Neutrophils are prominent candidates for possible involvement as primers for microbial clearance. Significant variability is observed in neutrophil gene expression and DNA methylation. Furthermore, inter-individual variability is seen between the mycobactericidal capacities of donor neutrophils. Clearance of M. tuberculosis infection is favored by the mycobactericidal activity of neutrophils, apoptosis, effective clearance of cells by macrophages, and resolution of inflammation. In this review we will discuss the different mechanisms neutrophils utilize to clear M. tuberculosis infection. We discuss the duality between neutrophils' ability to clear infection and how increasing numbers of neutrophils contribute to active TB severity and mortality. Further investigation into the potential role of neutrophils in innate immune-mediated M. tuberculosis infection resistance is warranted since it may reveal clinically important activities for prevention as well as vaccine and treatment development.

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“…THP-1 derived macrophages (M2 differentiated with PMA) Coculture with MCF10A tumor cells Cytokine array, RT-PCR (12) m BMDMs (differentiated in L-cell CM) LPS, IFNγ+LPS RT-PCR (13) RAW264.7 (macrophage cell line) LPS RT-PCR (14) m synovial macrophages (adherent fraction of synovial cells) Tenascin-C, osteopontin RT-PCR (15) m PEMs (adherent fraction) Coculture with MDA-MB 231 tumor cells RT-PCR (16) m PEMs (M2 differentiated with M-CSF) 4T1 cancer-cell-derived GM-CSF Northern blot (17) m microglial cells Fragment of amyloid β-protein Aβ (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35) Northern blot (18) h female reproductive tract DCs (positive selection from endometrium tissue) Human immunodeficiency virus Multiplex assay (19) h DCs (from PBMCs, differentiated with IL-4 and GM-CSF) Dengue virus RT-PCR (20) h DCs (from PBMCs, differentiated with IL-4 and GM-CSF) TLR3, TLR4, and TLR8 agonists ELISA (21) h lung mast cells (isolated by elutriation) rhSCF Northern blot (22) HMC-1 (mast cell line) rhSCF ELISA (22) LAD 2 (mast cell line) Complement factor C3a or C5a ELISA (23) HMC-1 (mast cell line) fMLP (bacterial-derived peptide) RNase protection assay (24) h neutrophils LPS, IFNγ, LPS+IFNγ, IFNγ+TLR2 ligands (LTA or Pam3CSK4), TNFα, TNFα+IFNγ ELISA (25) h neutrophils PMA, LPS, PAM3CSK4 (TLR2 ligand), FSL-1 (bacterial derived TLR2/6 agonist) ELISA (26) RBL-2H3 (rat basophil cell line) fMLP or C3a or C5a ELISA (27) h eosinophils CB+C5a, CB+fMLP, CB+PAF, GM-CSF, Ionomycin, PMA, IL-5+CB+C5a, IL-5+CB+PAF, CB+C5a, IL-5+C5a, IL-5+C5a+CB ELISA (28) This table provides an exemplary overview of the different types of myeloid cells and their ability to secrete CCL2. The stimulant and the readout are provided.…”

Section: Introductionmentioning

confidence: 99%

More Than Just Attractive: How CCL2 Influences Myeloid Cell Behavior Beyond Chemotaxis

2019

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Monocyte chemoattractant protein-1 (MCP-1/CCL2) is renowned for its ability to drive the chemotaxis of myeloid and lymphoid cells. It orchestrates the migration of these cell types both during physiological immune defense and in pathological circumstances, such as autoimmune diseases including rheumatoid arthritis and multiple sclerosis, inflammatory diseases including atherosclerosis, as well as infectious diseases, obesity, diabetes, and various types of cancer. However, new data suggest that the scope of CCL2's functions may extend beyond its original characterization as a chemoattractant. Emerging evidence shows that it can impact leukocyte behavior, influencing adhesion, polarization, effector molecule secretion, autophagy, killing, and survival. The direction of these CCL2-induced responses is context dependent and, in some cases, synergistic with other inflammatory stimuli. The involvement of CCL2 signaling in multiple diseases renders it an interesting therapeutic target, although current targeting strategies have not met early expectations in the clinic. A better understanding of how CCL2 affects immune cells will be pivotal to the improvement of existing therapeutic approaches and the development of new drugs. Here, we provide an overview of the pleiotropic effects of CCL2 signaling on cells of the myeloid lineage, beyond chemotaxis, and highlight how these actions might help to shape immune cell behavior and tumor immunity.

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TLR stimulation of human neutrophils lead to increased release of MCP-1, MIP-1α, IL-1β, IL-8 and TNF during tuberculosis

Cited by 22 publications

References 16 publications

Neutrophils in Tuberculosis: Heterogeneity Shapes the Way?

Neutrophils in Tuberculosis: Heterogeneity Shapes the Way?

Neutrophils: Innate Effectors of TB Resistance?

More Than Just Attractive: How CCL2 Influences Myeloid Cell Behavior Beyond Chemotaxis

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