Mononuclear phagocyte-mediated antifungal immunity: the role of chemotactic receptors and ligands

Swamydas, Muthulekha; Break, Timothy J.; Lionakis, Michail S.

doi:10.1007/s00018-015-1858-6

Cited by 14 publications

(8 citation statements)

References 134 publications

(195 reference statements)

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“…Dendritic cells, macrophages, and monocytes collectively make up the mononuclear phagocyte arm of the innate immune system. Mononuclear phagocytes readily internalize and kill ingested microbes by ROS-dependent and independent processes [ 131 ]. These cells express innate pattern recognition receptors such as C-Type Lectin Receptors (CLRs) and TLRs that sense fungal pathogens.…”

Section: Hematopoietic Cell-mediated Innate Immunity In mentioning

confidence: 99%

Innate Immunity to Mucosal Candida Infections

Verma

Gaffen

Swidergall

2017

JoF

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Mucosal epithelial tissues are exposed to high numbers of microbes, including commensal fungi, and are able to distinguish between those that are avirulent and those that cause disease. Epithelial cells have evolved multiple mechanisms to defend against colonization and invasion by Candida species. The interplay between mucosal epithelial tissues and immune cells is key for control and clearance of fungal infections. Our understanding of the mucosal innate host defense system has expanded recently with new studies bringing to light the importance of epithelial cell responses, innate T cells, neutrophils, and other phagocytes during Candida infections. Epithelial tissues release cytokines, host defense peptides, and alarmins during Candida invasion that act in concert to limit fungal proliferation and recruit immune effector cells. The innate T cell/IL-17 axis and recruitment of neutrophils are of central importance in controlling mucosal fungal infections. Here, we review current knowledge of the innate immunity at sites of mucosal Candida infection, with a focus on infections caused by C. albicans.

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Section: Hematopoietic Cell-mediated Innate Immunity In mentioning

confidence: 99%

Innate Immunity to Mucosal Candida Infections

Verma

Gaffen

Swidergall

2017

JoF

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“…Polymorphonuclear granulocytes (G) and mononuclear phagocytes: monocytes and macrophages (M) may play a crucial role in the defense against fungal infections. However, fungi and their products may directly or indirectly inhibit their microbiocidal activity [ 1 – 6 ].…”

Section: Introductionmentioning

confidence: 99%

Negative correlation between mycological surfaces pollution in hospital emergency departments and blood monocytes phagocytosis of healthcare workers

Lewicki¹,

Bielawska-Drózd²,

Winnicka³

et al. 2015

cejoi

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The aim of the present study was to find a possible relationship between the presence of yeast and filamentous fungi in hospital emergency departments and the activity levels of blood granulocytes and monocytes in emergency personnel.The study of mycological pollution was conducted in winter; the samples were collected from 10 Warsaw hospitals emergency departments (HE D) and in 10 control locations (office spaces) and included air samples and swabbing of floor and walls. The blood for immunological investigation was taken in spring, from 40 men, 26 to 53 years old, healthcare workers of these departments, who have been working for at least 5 years in their current positions, and from 36 corresponding controls, working in control offices. Evaluation of blood leukocyte subpopulations was done by hematological analyzer and cytometry analysis and monocyte and granulocyte phagocytosis by Phagotest.There were no significant differences in the level of mycological contamination between the test and control places. The qualitative analysis of the surfaces and air samples revealed a prevalence of strains belonging to Aspergillus spp. and Penicillium spp. genus.Statistical analysis revealed the existence of negative correlation between the number of phagocytizing blood monocytes and fungi spores content on floor and wall surfaces in hospital emergency departments (r = –0.3282, p < 0.05 and positive correlation between the number of phagocytizing monocytes in the blood of office workers and fungi pollution of control offices (r = 0.4421, p < 0.01).

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“…Interestingly, SeMet significantly promoted protein expressions of TLR4-mediated NF-κB signaling pathway in bMECs for 4 h, whereas those protein expressions significantly increased in macrophages for 6 h. Perhaps this discrepancy was due to E. coli first invading bMECs and subsequently promoting expression of chemotactic factors. Furthermore, those chemotactic factors recruited, and activated macrophages (Swamydas et al, 2015) that phagocytose pathogenic bacteria (e.g., E. coli) and mount a partial inflammatory response (Feng et al, 2008). In addition, under physiological conditions, NF-κB is present in the cytoplasm as an inactive heterotrimer consisting of p50, p65, and IκB.…”

Section: Discussionmentioning

confidence: 99%

Selenomethionine Suppressed TLR4/NF-κB Pathway by Activating Selenoprotein S to Alleviate ESBL Escherichia coli-Induced Inflammation in Bovine Mammary Epithelial Cells and Macrophages

et al. 2020

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Inflammation is the hallmark of extended-spectrum β-lactamase (ESBL)-producing Escherichia coli-induced bovine mastitis. Organic selenium can activate pivotal proteins in immune responses and regulate the immune system. The present study aimed to investigate whether selenomethionine (SeMet) attenuates ESBL E. coli-induced inflammation in bovine mammary epithelial cells (bMECs) and macrophages. Cells were treated with 0, 5/10, 10/20, 20/40, or 40/60 µM SeMet for 12 h and/or inoculated with ESBL-E. coli [multiplicity of infection (MOI) = 5] for 4/6 h, respectively. We assessed inflammatory responses, including selenoprotein S (SeS), Toll-like receptor 4 (TLR4), Ikappa-B (IκB), phospho-NF-κB p65 (Ser536), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and lactate dehydrogenase (LDH) activities. Treatment with 40/60 µM SeMet promoted cell viability and inhibited LDH activities in both bMECs and macrophages. Inoculation with ESBL-E. coli reduced cell viability, which was attenuated by SeMet treatment in bMECs and macrophages. SeMet increased ESBL E. coli-induced downregulation of SeS and decreased LDH activities, TLR4, IκB, phospho-NF-κB p65 (Ser536), IL-1β, and TNF-α protein expressions in bMECs and macrophages. In addition, knockdown of SeS promoted protein expression of TLR4mediated nuclear factor-kappa (NF-κB) pathway and BAY 11-708 inhibited TNF-α and IL-1β protein levels in bMECs and macrophages after ESBL-E. coli treatment. Moreover, ESBL-E. coli inoculation increased monocyte chemoattractant protein 1 (MCP-1), CC motif ligand 3 (CCL-3), and CCL-5 mRNA expressions in bMECs. In conclusion,

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Mononuclear phagocyte-mediated antifungal immunity: the role of chemotactic receptors and ligands

Cited by 14 publications

References 134 publications

Innate Immunity to Mucosal Candida Infections

Innate Immunity to Mucosal Candida Infections

Negative correlation between mycological surfaces pollution in hospital emergency departments and blood monocytes phagocytosis of healthcare workers

Selenomethionine Suppressed TLR4/NF-κB Pathway by Activating Selenoprotein S to Alleviate ESBL Escherichia coli-Induced Inflammation in Bovine Mammary Epithelial Cells and Macrophages

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