Metallothionein mediates leukocyte chemotaxis

Yin, Xianzhen; Knecht, David A.; Lynes, Michael A.

doi:10.1186/1471-2172-6-21

Cited by 82 publications

(42 citation statements)

References 65 publications

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“…These findings complement earlier work by Lynes’ group, which showed that MT was able to act in a chemokine-like manner and to influence the migration of leukocytes (Yin et al 2005). These actions are additional to the well-characterised ability of intracellular MT to protect cells against toxic levels of heavy metal and against a broad range of agents, which induce oxidative stress.…”

Section: Endogenous Neuroprotective Molecules (Akw Gjg)supporting

confidence: 91%

New Strategies in Neuroprotection and Neurorepair

et al. 2011

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There are currently few clinical strategies in place, which provide effective neuroprotection and repair, despite an intense international effort over the past decades. One possible explanation for this is that a deeper understanding is required of how endogenous mechanisms act to confer neuroprotection. This mini-review reports the proceedings of a recent workshop “Neuroprotection and Neurorepair: New Strategies” (Iguazu Falls, Misiones, Argentina, April 11–13, 2011, Satellite Symposium of the V Neurotoxicity Society Meeting, 2011) in which four areas of active research were identified to have the potential to generate new insights into this field. Topics discussed were i) metallothionein and other multipotent neuroprotective molecules; ii) oxidative stress and their signal mediated pathways in neuroregeneration; iii) neurotoxins in glial cells, and iv) drugs of abuse with neuroprotective effects.

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Section: Endogenous Neuroprotective Molecules (Akw Gjg)supporting

confidence: 91%

New Strategies in Neuroprotection and Neurorepair

et al. 2011

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“…RALGDS was reported in SLE PBMCs whereas MT2A and GRB2 were observed to be upregulated in lupus T cells [78, 79]. MT2A has been reported to play crucial role in leukocyte chemotaxis [80]. …”

Section: Discussionmentioning

confidence: 99%

RNA-seq Analysis Reveals Unique Transcriptome Signatures in Systemic Lupus Erythematosus Patients with Distinct Autoantibody Specificities

et al. 2016

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Systemic lupus erythematosus (SLE) patients exhibit immense heterogeneity which is challenging from the diagnostic perspective. Emerging high throughput sequencing technologies have been proved to be a useful platform to understand the complex and dynamic disease processes. SLE patients categorised based on autoantibody specificities are reported to have differential immuno-regulatory mechanisms. Therefore, we performed RNA-seq analysis to identify transcriptomics of SLE patients with distinguished autoantibody specificities. The SLE patients were segregated into three subsets based on the type of autoantibodies present in their sera (anti-dsDNA+ group with anti-dsDNA autoantibody alone; anti-ENA+ group having autoantibodies against extractable nuclear antigens (ENA) only, and anti-dsDNA+ENA+ group having autoantibodies to both dsDNA and ENA). Global transcriptome profiling for each SLE patients subsets was performed using Illumina® Hiseq-2000 platform. The biological relevance of dysregulated transcripts in each SLE subsets was assessed by ingenuity pathway analysis (IPA) software. We observed that dysregulation in the transcriptome expression pattern was clearly distinct in each SLE patients subsets. IPA analysis of transcripts uniquely expressed in different SLE groups revealed specific biological pathways to be affected in each SLE subsets. Multiple cytokine signaling pathways were specifically dysregulated in anti-dsDNA+ patients whereas Interferon signaling was predominantly dysregulated in anti-ENA+ patients. In anti-dsDNA+ENA+ patients regulation of actin based motility by Rho pathway was significantly affected. The granulocyte gene signature was a common feature to all SLE subsets; however, anti-dsDNA+ group showed relatively predominant expression of these genes. Dysregulation of Plasma cell related transcripts were higher in anti-dsDNA+ and anti-ENA+ patients as compared to anti-dsDNA+ ENA+. Association of specific canonical pathways with the uniquely expressed transcripts in each SLE subgroup indicates that specific immunological disease mechanisms are operative in distinct SLE patients’ subsets. This ‘sub-grouping’ approach could further be useful for clinical evaluation of SLE patients and devising targeted therapeutics.

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“…Indeed, defects in neutrophil recruitment or function, such as neutropenia, leukocyte adhesion deficiency (LAD), and Chediak-Higashi syndrome, strongly predispose the affected individuals to periodontitis (25). Directional movement, or chemotaxis, of neutrophils toward sites of injury and inflammation occurs by sensing and deciphering a chemoattractant gradient (26)(27)(28)(29)(30). Neutrophils are able to respond to signals from both intermediary chemoattractants (such as interleukin-8 ), which are encountered upon travel to sites of infection and inflammation, and from end-target cellular chemoattractants (such as formylated bacterial peptides, like fMLF), operating at the site of infection (28,30,31).…”

mentioning

confidence: 99%

Filifactor alocis Promotes Neutrophil Degranulation and Chemotactic Activity

et al. 2016

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Filifactor alocis is a recently recognized periodontal pathogen; however, little is known regarding its interactions with the immune system. As the first-responder phagocytic cells, neutrophils are recruited in large numbers to the periodontal pocket, where they play a crucial role in the innate defense of the periodontium. Thus, in order to colonize, successful periodontal pathogens must devise means to interfere with neutrophil chemotaxis and activation. In this study, we assessed major neutrophil functions, including degranulation and cell migration, associated with the p38 mitogen-activated protein kinase (MAPK) signaling pathway upon challenge with F. alocis. Under conditions lacking a chemotactic gradient, F. alocischallenged neutrophils had increased migration compared to uninfected cells, indicating that F. alocis increases chemokinesis in human neutrophils. In addition, neutrophil chemotaxis induced by interleukin-8 was significantly enhanced when cells were challenged with F. alocis, compared to noninfected cells. Similar to live bacteria, heat-killed F. alocis induced both random and directed migration of human neutrophils. The interaction of F. alocis with Toll-like receptor 2 induced granule exocytosis along with a transient ERK1/2 and sustained p38 MAPK activation. Moreover, F. alocis-induced secretory vesicle and specific granule exocytosis were p38 MAPK dependent. Blocking neutrophil degranulation with TAT-SNAP23 fusion protein significantly reduced the chemotactic and random migration induced by F. alocis. Therefore, we propose that induction of random migration by F. alocis will prolong neutrophil traffic time in the gingival tissue, and subsequent degranulation will contribute to tissue damage.

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Metallothionein mediates leukocyte chemotaxis

Cited by 82 publications

References 65 publications

New Strategies in Neuroprotection and Neurorepair

New Strategies in Neuroprotection and Neurorepair

RNA-seq Analysis Reveals Unique Transcriptome Signatures in Systemic Lupus Erythematosus Patients with Distinct Autoantibody Specificities

Filifactor alocis Promotes Neutrophil Degranulation and Chemotactic Activity

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