The Effects of Staphylococci on the Degranulation of Human Mast Cell-1

In-Taek Jang; Miso Yang; Eun-Kyeong Jo; Hwa-Jung Kim; Jeong-Kyu Park

doi:10.4167/jbv.2017.47.3.132

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Jang, Yang, Jo, Kim, and Park: The Effects of Staphylococci on the Degranulation of Human Mast Cell-1

Original Article

J Bacteriol Virol 2017;47(3):132-138.

Published online: 9 February 2017

DOI: https://doi.org/10.4167/jbv.2017.47.3.132

The Effects of Staphylococci on the Degranulation of Human Mast Cell-1

In-Taek Jang^1,², Miso Yang¹, Eun-Kyeong Jo¹, Hwa-Jung Kim¹, Jeong-Kyu Park^1,^∗

¹Department of Microbiology and Cancer Research Institute, Daejeon, Korea

²Department of Medical Science, School of Medicine, Chungnam National University, Daejeon, Korea

^∗Corresponding author: Jeong-Kyu Park, M.D., Ph.D. Department of Microbiology, School of Medicine, Chungnam National University, Daejeon 35015, Korea. Phone: +82-42-580-8244, Fax: +82-42-585-3686, e-mail: jekpark@cnu.ac.kr

^∗∗ This work was supported by research fund of Chungnam National University.

Received 3 July 20172 August 2017 Accepted 14 August 2017

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Atopic dermatitis (AD) is characterized by disturbances in epidermal barrier functions and the hyperactive immune response. Staphylococcus aureus (S. aureus) can be cultured from 90% of AD skin lesions and can exacerbate or contribute to the persistent skin inflammation in AD by secreting toxins with superantigenic properties. Superantigens can induce mast cell (MC) degranulation after penetrating the epidermal barrier. The role of MCs in AD is suggested by the increase in the MC number and MC activation. MCs are activated for degranulation and mediator release by allergens that cross-link IgE molecules or by microbial products. Therefore, MCs may be critically involved in the pathogenesis of AD. However, the understanding mechanisms of MC degranulation by S. aureus in relation to AD have still not been fully elucidated. In this study, we found that live S. aureus or methicillin-resistant S. aureus (MRSA) but not heat-killed bacteria induced MC degranulation. The heat-treatment partially inhibited MC degranulation by conditioned media (CM) of S. aureus or MRSA. The calcium chelator ethylene glycol tetraacetic acid (EGTA) did not block MC degranulation induced by live S. aureus or MRSA, but EGTA-treatment partially inhibited MC degranulation by CM from S. aureus or MRSA. These results suggest that live S. aureus and MRSA can degranulate MCs via direct interaction which may be important role in AD.

Keywords: Staphylococci, Mast cell, β-hexosaminidase, Atopic dermatitis

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Figure 1.

MRSA induces HMC-1 degranulation. β-hexosa-minidase activity (%) was determined from HMC-1 cultured with MRSA (MOI = 100) for indicated time (minutes). Data represent means ± s.d. of triplicate independent experiments.

Figure 2.

The conditioned media from MRSA induces HMC-1 degranulation. β-hexosaminidase activity (%) was determined from HMC-1 stimulated with different concentrations of conditioned media of MRSA. Data represent means ± s.d. of triplicate independent experiments. ∗⦤0.05.

Figure 3.

Differences in HMC-1 degranulations between live and heat-killed Staphylococci. β-hexosaminidase activity (%) was determined from HMC-1 stimulated with heat-killed S. epidermidis (SE), S. aureus (SA) or MRSA, and heat-killed bacteria-induced β-hexosaminidase activity (%) was compared with that of live SE, SA or MRSA. Data represent means ± s.d. of triplicate independent experiments. ∗∗∗⦤0.001. ns, no significance.

Figure 4.

Differences in HMC-1 degranulations between conditioned media and heat-inactivated conditioned media from Staphylococci. β-hexosaminidase activity (%) was determined from HMC-1 stimulated with conditioned media (CM) from S. epidermidis (SE), S. aureus (SA) or MRSA, and conditioned media-induced β-hexosaminidase activity (%) was compared with that of heat-inactivated conditioned media (CM). Data represent means ± s.d. of triplicate independent experiments. ∗⦤0.05, ∗∗⦤0.01, ∗∗∗⦤0.001. ns, no significance.

Figure 5.

Differences in HMC-1 degranulations between EGTA pretreated HMC-1 and non-EGTA pretreated HMC-1 induced by Staphylococci. HMC-1 was either pretreated with EGTA or not, and β-hexosaminidase activity (%) induced by S. epidermidis (SE), S. aureus (SA) or MRSA was determined. Data represent means ± s.d. of triplicate independent experiments. ∗∗⦤0.01. ns, no significance.

Figure 6.

Differences in HMC-1 degranulations between EGTA pretreated HMC-1 and non-EGTA pretreated HMC-1 induced by conditioned media (CM) from Staphylococci. HMC-1 was either pretreated with EGTA or not, and β-hexosaminidase activity (%) induced by conditioned media (CM) from S. epidermidis (SE), S. aureus (SA) or MRSA was determined. Data represent means ± s.d. of triplicate independent experiments. ∗∗⦤0.01. ns, no significance.

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