Adenosine derived from Staphylococcus aureus-engulfed macrophages functions as a potent stimulant for the induction of inflammatory cytokines in mast cells

Jie, Ying; Kim, Chan Hee; Ryu, Kyoung Hwa; Kim, Min Su; So, Young; Lee, Kong Joo; Garred, Peter; Lee, Bok Luel

doi:10.5483/bmbrep.2011.44.5.335

Cited by 4 publications

(4 citation statements)

References 19 publications

(16 reference statements)

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“…It has been shown that mast cells produce certain cytokines, e.g. TNF‐ α and IL‐6, in response to S. aureus . Here we extend these findings by unbiased technology and show that peritoneal mast cells also up‐regulate a number of additional pro‐inflammatory compounds when encountering S. aureus , including IL‐3, IL‐13, Oncostatin M, Lif, and chemokines Ccl3, Ccl7 and Cxcl2.…”

Section: Discussionsupporting

confidence: 75%

Mast cells are activated by Staphylococcus aureus in vitro but do not influence the outcome of intraperitoneal S. aureus infection in vivo

et al. 2014

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SummaryStaphylococcus aureus is a major pathogen that can cause a broad spectrum of serious infections including skin infections, pneumonia and sepsis. Peritoneal mast cells have been implicated in the host response towards various bacterial insults and to provide mechanistic insight into the role of mast cells in intraperitoneal bacterial infection we here studied the global effects of S. aureus on mast cell gene expression. After co-culture of peritoneal mast cells with live S. aureus we found by gene array analysis that they up-regulate a number of genes. Many of these corresponded to pro-inflammatory cytokines, including interleukin-3, interleukin-13 and tumour necrosis factor-a. The cytokine induction in response to S. aureus was confirmed by ELISA. To study the role of peritoneal mast cells during in vivo infection with S. aureus we used newly developed Mcpt5-Cre + 3 R-DTA mice in which mast cell deficiency is independent of c-Kit. This is in contrast to previous studies in which an impact of mast cells on bacterial infection has been proposed based on the use of mice whose mast cell deficiency is a consequence of defective c-Kit signalling. Staphylococcus aureus was injected intraperitoneally into mast-cell-deficient Mcpt5-Cre + 3 R-DTA mice using littermate mast-cellsufficient mice as controls. We did not observe any difference between mast-cell-deficient and control mice with regard to weight loss, bacterial clearance, inflammation or cytokine production. We conclude that, despite peritoneal mast cells being activated by S. aureus in vitro, they do not influence the in vivo manifestations of intraperitoneal S. aureus infection.

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Section: Discussionsupporting

confidence: 75%

Mast cells are activated by Staphylococcus aureus in vitro but do not influence the outcome of intraperitoneal S. aureus infection in vivo

et al. 2014

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“…One factor produced in response to microbial infection that prevents airway hyperresponsiveness is adenosine. Moreover, bacteria or macrophages that have engulfed bacteria were found to release adenosine, which influenced cytokine release from mast cells (33). We speculate that adenosine produced by bacteria or by macrophages engulfing bacteria also influences allergen sensitization by effects on APCs.…”

Section: Myeloid Cells As Targets Ofmentioning

confidence: 94%

Adenosine influences myeloid cells to inhibit aeroallergen sensitization

Pei

Linden

2016

American Journal of Physiology-Lung Cellular and Molecular Phys

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Agonists of adenosine A2A receptors (A2ARs) suppress the activation of most immune cells and reduce acute inflammatory responses. Asthma is characterized by sensitization in response to initial allergen exposure and by airway hyperreactivity in response to allergen rechallenge. We sought to determine if A2AR activation with CGS-21680 (CGS) is more effective when CGS is administered during sensitization or rechallenge. C57BL/6 wild-type mice and Adora2a(f/f)LysMCre(+/-) mice, which lack A2ARs on myeloid cells, were sensitized with intranasal ovalbumin (OVA) and LPS. Airway sensitization was characterized by a rapid increase in numbers of IL-6(+) and IL-12(+) macrophages and dendritic cells in lungs. A2AR activation with CGS (0.1 μg·kg(-1)·min(-1) sc) only during sensitization reduced numbers of IL-6(+) and IL-12(+) myeloid cells in the lungs and reversed the effects of OVA rechallenge to increase airway hyperresponsiveness to methacholine. CGS treatment during sensitization also reduced the expansion of lung T helper (Th1 and Th17) cells and increased expansion of regulatory T cells in response to OVA rechallenge. Most of the effects of CGS administered during sensitization were eliminated by myeloid-selective A2AR deletion. Administration of CGS only during OVA rechallenge failed to reduce airway hyperresponsiveness. We conclude that myeloid cells are key targets of adenosine during sensitization and indirectly modify T cell polarization. The results suggest that a clinically useful strategy might be to use A2AR agonists to inhibit sensitization to new aeroallergens. We speculate that adenosine production by macrophages engulfing bacteria contributes to the curious suppression of sensitization in response to early-life infections.

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“…Mouse bone marrow stem cell-derived mast cells (mBMMCs) were prepared and cultured as previously described (29,30). Briefly, mouse bone marrow stem cells were isolated from the femur and tibia of 6∼8-week-old mice, and cultured to a final density of 1 × 10 6 cells/ml in Iscove’s modified Dulbecco’s medium (IMDM) (Gibco) supplemented with L-glutamine (2 mM, Sigma), heat inactivated fetal calf serum (10%, Gibco), penicillin (100 IU/ml, Sigma), streptomycin (100 μg/ml, Sigma), murine stem cell factor (SCF) (30 ng/ml, Peprotech), and IL-3 (30 ng/ml, Peprotech) at 37℃, in 5% (v/v) CO 2 air with 95% humidity.…”

Section: Methodsmentioning

confidence: 99%

Mouse mannose-binding lectin-A and ficolin-A inhibit lipopolysaccharide-mediated pro-inflammatory responses on mast cells

Jie¹,

Kang²,

Kim³

et al. 2013

BMB Reports

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It is unknown how soluble pattern-recognition receptors in blood, such as mannose-binding lectin (MBL) and ficolins, modulate mast cell-mediated inflammatory responses. We investigate how mouse MBL-A or ficolin-A regulate mouse bone marrow-derived mast cells (mBMMCs)-derived inflammatory response against bacterial lipopolysaccharide (LPS) stimulation. LPS-mediated pro-inflammatory cytokine productions on mBMMCs obtained from Toll-like receptor4 (TLR4)-deficient mice, TLR2-defficient mice, and their wildtype, were specifically attenuated by the addition of either mouse MBL-A or ficolin-A in a dose-dependent manner. However, the inhibitory effects by mouse MBL-A or ficolin-A were restored by the addition of mannose or N-acetylglucosamine, respectively. These results suggest that mouse MBL-A and ficolin-A bind to LPS via its carbohydrate-recognition domain and fibrinogen-like domain, respectively, whereby cytokine production by LPSmediated TLR4 in mBMMCs appears to be down-regulated, indicating that mouse MBL and ficolin may have an inhibitory function toward mouse TLR4-mediated excessive inflammation on the mast cells. [BMB Reports 2013; 46(7): 376-381]

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Adenosine derived from Staphylococcus aureus-engulfed macrophages functions as a potent stimulant for the induction of inflammatory cytokines in mast cells

Cited by 4 publications

References 19 publications

Mast cells are activated by Staphylococcus aureus in vitro but do not influence the outcome of intraperitoneal S. aureus infection in vivo

Mast cells are activated by Staphylococcus aureus in vitro but do not influence the outcome of intraperitoneal S. aureus infection in vivo

Adenosine influences myeloid cells to inhibit aeroallergen sensitization

Mouse mannose-binding lectin-A and ficolin-A inhibit lipopolysaccharide-mediated pro-inflammatory responses on mast cells

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