β<sub>2</sub>integrins (CD11/18) are essential for the chemosensory adhesion and migration of polymorphonuclear leukocytes on bacterial cellulose

Kim, Gun Dong; Lee, Seung Eun; Yang, Hana; Park, Hye Rim; Son, Gun Woo; Park, Cheung Seog; Park, Yong Seek

doi:10.1002/jbm.a.35316

Cited by 9 publications

(4 citation statements)

References 33 publications

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“…The phenotypic analysis of peritoneal macrophages showed a high percentage of cells positive for CD11b and CD45, confirming that the peritoneal population analyzed was composed of macrophages. CD11b belongs to the integrin β2 family and plays an important role in the migration of macrophages ( 65 ), while CD45, a protein tyrosine phosphatase expressed on all cells of hematopoietic origin, is associated with the adhesion process ( 66 ). The reduction in the amount of these superficial molecules observed in both the EV Y and control groups may be related to the internalization mechanisms of these molecules in activated macrophages ( 67 ).…”

Section: Discussionmentioning

confidence: 99%

Extracellular Vesicles Shed By Trypanosoma cruzi Potentiate Infection and Elicit Lipid Body Formation and PGE2 Production in Murine Macrophages

et al. 2018

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During the onset of Trypanosoma cruzi infection, an effective immune response is necessary to control parasite replication and ensure host survival. Macrophages have a central role in innate immunity, acting as an important trypanocidal cell and triggering the adaptive immune response through antigen presentation and cytokine production. However, T. cruzi displays immune evasion mechanisms that allow infection and replication in macrophages, favoring its chronic persistence. One potential mechanism is the release of T. cruzi strain Y extracellular vesicle (EV Y), which participate in intracellular communication by carrying functional molecules that signal host cells and can modulate the immune response. The present work aimed to evaluate immune modulation by EV Y in C57BL/6 mice, a prototype resistant to infection by T. cruzi strain Y, and the effects of direct EV Y stimulation of macrophages in vitro. EV Y inoculation in mice prior to T. cruzi infection resulted in increased parasitemia, elevated cardiac parasitism, decreased plasma nitric oxide (NO), reduced NO production by spleen cells, and modulation of cytokine production, with a reduction in TNF-α in plasma and decreased production of TNF-α and IL-6 by spleen cells from infected animals. In vitro assays using bone marrow-derived macrophages showed that stimulation with EV Y prior to infection by T. cruzi increased the parasite internalization rate and release of infective trypomastigotes by these cells. In this same scenario, EV Y induced lipid body formation and prostaglandin E2 (PGE2) production by macrophages even in the absence of T. cruzi. In infected macrophages, EV Y decreased production of PGE2 and cytokines TNF-α and IL-6 24 h after infection. These results suggest that EV Y modulates the host response in favor of the parasite and indicates a role for lipid bodies and PGE2 in immune modulation exerted by EVs.

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Section: Discussionmentioning

confidence: 99%

Extracellular Vesicles Shed By Trypanosoma cruzi Potentiate Infection and Elicit Lipid Body Formation and PGE2 Production in Murine Macrophages

et al. 2018

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“…Then 3 uL of bacteria were stabbed into 0.4 % MH agar and plates were incubated at 42°C under microaerobic conditions for 24 h. From each plate, motility was scored by measuring growth diameter (mm). Assays were repeated at least three times with three technical replicates and the results were averaged (Kim et al, 2015 ).…”

Section: Methodsmentioning

confidence: 99%

The Involvement of the Cas9 Gene in Virulence of Campylobacter jejuni

Shabbir

Tang

et al. 2018

Front. Cell. Infect. Microbiol.

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Campylobacter jejuni is considered as the leading cause of gastroenteritis all over the world. This bacterium has the CRISPR–cas9 system, which is used as a gene editing technique in different organisms. However, its role in bacterial virulence has just been discovered; that discovery, however, is just the tip of the iceberg. The purpose of this study is to find out the relationship between cas9 and virulence both phenotypically and genotypically in C. jejuni NCTC11168. Understanding both aspects of this relationship allows for a much deeper understanding of the mechanism of bacterial pathogenesis. The present study determined virulence in wild and mutant strains by observing biofilm formation, motility, adhesion and invasion, intracellular survivability, and cytotoxin production, followed by the transcriptomic analysis of both strains. The comparative gene expression profile of wild and mutant strains was determined on the basis of De-Seq transcriptomic analysis, which showed that the cas9 gene is involved in enhancing virulence. Differential gene expression analysis revealed that multiple pathways were involved in virulence, regulated by the CRISPR-cas9 system. Our findings help in understanding the potential role of cas9 in regulating the other virulence associated genes in C. jejuni NCTC11168. The findings of this study provide critical information about cas9's potential involvement in enhancing the virulence of C. jejuni, which is a major public health threat.

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“…A previous study suggested that disturbed activation of the Rac-ERK pathway and PI3K is responsible for the aberrant IL-8/CXCL8-induced migration in MDS (14). It has been reported that CD18 plays a critical role regarding fMLF-induced migration (15), and that expression of the CD11b-CD18 complex is decreased in MDS neutrophils (16). When stimulated with fMLF, activation of ERK1/2 and protein kinase B (PKB/Akt) was also attenuated in MDS (17).…”

mentioning

confidence: 98%

Mechanisms of Impaired Neutrophil Migration by MicroRNAs in Myelodysplastic Syndromes

Cao

Shikama

Kimura³

et al. 2017

The Journal of Immunology

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In myelodysplastic syndromes (MDS), functional defects of neutrophils result in high mortality because of infections; however, the molecular basis remains unclear. We recently found that miR-34a and miR-155 were significantly increased in MDS neutrophils. To clarify the effects of the aberrant microRNA expression on neutrophil functions, we introduced miR-34a, miR-155, or control microRNA into neutrophil-like differentiated HL60 cells. Ectopically introduced miR-34a and miR-155 significantly attenuated migration toward chemoattractants fMLF and IL-8, but enhanced degranulation. To clarify the mechanisms for inhibition of migration, we studied the effects of miR-34a and miR-155 on the migration-regulating Rho family members, Cdc42 and Rac1. The introduced miR-34a and miR-155 decreased the fMLF-induced active form of Cdc42 to 29.0 ± 15.9 and 39.7 ± 4.8% of that in the control cells, respectively, although Cdc42 protein levels were not altered. miR-34a decreased a Cdc42-specific guanine nucleotide exchange factor (GEF), dedicator of cytokinesis (DOCK) 8, whereas miR-155 reduced another Cdc42-specific GEF, FYVE, RhoGEF, and PH domain-containing (FGD) 4. The knockdown of DOCK8 and FGD4 by small interfering RNA suppressed Cdc42 activation and fMLF/IL-8-induced migration. miR-155, but not miR-34a, decreased Rac1 protein, and introduction of Rac1 small interfering RNA attenuated Rac1 activation and migration. Neutrophils from patients showed significant attenuation in migration compared with healthy cells, and protein levels of DOCK8, FGD4, and Rac1 were well correlated with migration toward fMLF ( = 0.642, 0.686, and 0.436, respectively) and IL-8 ( = 0.778, 0.659, and 0.606, respectively). Our results indicated that reduction of DOCK8, FGD4, and Rac1 contributes to impaired neutrophil migration in MDS.

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β₂integrins (CD11/18) are essential for the chemosensory adhesion and migration of polymorphonuclear leukocytes on bacterial cellulose

Cited by 9 publications

References 33 publications

Extracellular Vesicles Shed By Trypanosoma cruzi Potentiate Infection and Elicit Lipid Body Formation and PGE2 Production in Murine Macrophages

Extracellular Vesicles Shed By Trypanosoma cruzi Potentiate Infection and Elicit Lipid Body Formation and PGE2 Production in Murine Macrophages

The Involvement of the Cas9 Gene in Virulence of Campylobacter jejuni

Mechanisms of Impaired Neutrophil Migration by MicroRNAs in Myelodysplastic Syndromes

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β2integrins (CD11/18) are essential for the chemosensory adhesion and migration of polymorphonuclear leukocytes on bacterial cellulose

Cited by 9 publications

References 33 publications

Extracellular Vesicles Shed By Trypanosoma cruzi Potentiate Infection and Elicit Lipid Body Formation and PGE2 Production in Murine Macrophages

Extracellular Vesicles Shed By Trypanosoma cruzi Potentiate Infection and Elicit Lipid Body Formation and PGE2 Production in Murine Macrophages

The Involvement of the Cas9 Gene in Virulence of Campylobacter jejuni

Mechanisms of Impaired Neutrophil Migration by MicroRNAs in Myelodysplastic Syndromes

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β₂integrins (CD11/18) are essential for the chemosensory adhesion and migration of polymorphonuclear leukocytes on bacterial cellulose