scholarly journals Mast Cells in the Skin: Defenders of Integrity or Offenders in Inflammation?

2021 ◽  
Vol 22 (9) ◽  
pp. 4589
Author(s):  
Martin Voss ◽  
Johanna Kotrba ◽  
Evelyn Gaffal ◽  
Konstantinos Katsoulis-Dimitriou ◽  
Anne Dudeck
Keyword(s):  
Mast Cells ◽  
Defense Mechanisms ◽  
Secretory Granules ◽  
Skin Barrier ◽  
Skin Inflammation ◽  
Disease Exacerbation ◽  
Immune Effector ◽  
Effector Cells ◽  
Proinflammatory Mediators ◽  
Chronic Skin

Mast cells (MCs) are best-known as key effector cells of immediate-type allergic reactions that may even culminate in life-threatening anaphylactic shock syndromes. However, strategically positioned at the host–environment interfaces and equipped with a plethora of receptors, MCs also play an important role in the first-line defense against pathogens. Their main characteristic, the huge amount of preformed proinflammatory mediators embedded in secretory granules, allows for a rapid response and initiation of further immune effector cell recruitment. The same mechanism, however, may account for detrimental overshooting responses. MCs are not only detrimental in MC-driven diseases but also responsible for disease exacerbation in other inflammatory disorders. Focusing on the skin as the largest immune organ, we herein review both beneficial and detrimental functions of skin MCs, from skin barrier integrity via host defense mechanisms to MC-driven inflammatory skin disorders. Moreover, we emphasize the importance of IgE-independent pathways of MC activation and their role in sustained chronic skin inflammation and disease exacerbation.

scholarly journals Mast Cells in the Skin: Defenders of Integrity or Offenders in Inflammation?

2021 ◽  
Author(s):  
Martin Voss ◽  
Johanna Kotrba ◽  
Evelyn Gaffal ◽  
Konstantinos Katsoulis-Dimitriou ◽  
Anne Dudeck
Keyword(s):  
Mast Cells ◽  
Defense Mechanisms ◽  
Secretory Granules ◽  
Skin Barrier ◽  
Skin Inflammation ◽  
Disease Exacerbation ◽  
Immune Effector ◽  
Effector Cells ◽  
Life Threatening ◽  
Chronic Skin

Mast cells (MCs) are best known as key effector cells of immediate type allergic reactions that may even culminate in life-threatening anaphylactic shock syndromes. However, strategically positioned at host-environment interfaces and equipped with a plethora of receptors, MCs also play an important role in the first line defense against pathogens. Their main characteristic, the huge amount of preformed pro-inflammatory mediators embedded in secretory granules, allow for a rapid response and initiation of further immune effector cell recruitment. The same mechanism, however, may account for detrimental overshooting responses. MCs are not only detrimental in MC-driven diseases, but also responsible for disease exacerbation in other inflammatory disorders. Focusing on the skin as the largest immune organ, we herein review both beneficial and detrimental functions of skin MCs all the way from skin barrier integrity via host defense mechanisms to MC-driven inflammatory skin disorders. Moreover, we emphasize the importance of IgE-independent pathways of MC activation and their role in sustained chronic skin inflammation and disease exacerbation.

scholarly journals Comparison of the Inhibitory Activities of 5,6-Dihydroergosterol Glycoside α- and β-Anomers on Skin Inflammation

Molecules ◽  
2019 ◽  
Vol 24 (2) ◽  
pp. 371 ◽  
Author(s):  
Tae Kim ◽  
Young Cho ◽  
HoonGyu Park ◽  
Tae Lee ◽  
Hakwon Kim
Keyword(s):  
Protein Expression ◽  
Inflammatory Diseases ◽  
Skin Barrier ◽  
Skin Inflammation ◽  
New Drugs ◽  
Inflammatory Biomarker ◽  
Cytokines And Chemokines ◽  
Inflammatory Stimuli ◽  
Mrna And Protein Expression ◽  
Chronic Skin

Chronic skin inflammatory diseases, such as atopic dermatitis, are associated with a dysfunctional skin barrier due to an increase in various inflammatory stimuli, for instance inflammatory cytokines and chemokines. In particular, CCL17 and CCL22 expression is increased in patients with chronic skin inflammation. In this study, we synthesized several α- and β-anomers of dihydroergosterol (DHE)-glycosides and assessed their effects on CCL17 and CCL22 expression. We confirmed that the β-anomers of DHE-glycosides were superior to α-anomers of DHE-glycosides in inhibiting CCL17 and CCL22 mRNA and protein expression. In addition, we determined that DHE-glycoside β-anomers showed strong inhibitory activity towards pro-inflammatory cytokine mRNA and protein expression, including that of TNF-α, IL-6, and IL-1β- in stimulated HaCaT cells. These results imply that DHE-glycoside α- and β-anomers should be separated during synthesis of drugs for chronic skin inflammation. Our results also suggest that β-anomers of DHE-glycosides may play an important role as new drugs for chronic skin inflammation because of their ability to inhibit the skin inflammatory biomarker proteins CCL17 and CCL22.

scholarly journals Bacterial skin colonization and infections in patients with atopic dermatitis

2012 ◽  
Vol 87 (5) ◽  
pp. 729-734 ◽  
Author(s):  
Vanessa Petry ◽  
Giancarlo Resende Bessa ◽  
Claudia Schermann Poziomczyck ◽  
Caio Fernando de Oliveira ◽  
Magda Blessmann Weber ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
Bacterial Resistance ◽  
Antimicrobial Agents ◽  
Secondary Infection ◽  
Skin Barrier ◽  
Skin Inflammation ◽  
Skin Surface ◽  
Number Of Children ◽  
Chronic Skin ◽  
Systemic Antibiotics

Atopic Dermatitis is a chronic inflammatory skin disease that affects a large number of children and adults. The disease results from an interaction between genetic predisposition, host environment, skin barrier defects, and immunological factors. A major aggravating factor associated with Atopic Dermatitis is the presence of microorganisms on the patient's skin surface. Staphylococcus aureus and Streptococcus pyogenes, for instance, can exacerbate chronic skin inflammation. As a result, antimicrobials have often been prescribed to control the acute phase of the disease. However, increased bacterial resistance to antimicrobial agents has made it difficult for dermatologists to prescribe appropriate medication. In the presence of disseminated dermatitis with secondary infection, systemic antibiotics need to be prescribed; however, treatment should be individualized, in an attempt to find the most effective antibiotic with fewer side effects. Also, the medication should be used for as short as possible in order to minimize bacterial resistance.

scholarly journals Immunological Aspects ofCandidaandAspergillusSystemic Fungal Infections

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Christoph Mueller-Loebnitz ◽  
Helmut Ostermann ◽  
Anke Franzke ◽  
Juergen Loeffler ◽  
Lutz Uharek ◽  
...  
Keyword(s):  
High Risk ◽  
Defense Mechanisms ◽  
Fungal Infections ◽  
Current Knowledge ◽  
Immunosuppressive Drugs ◽  
Immune Defense ◽  
Immunological Mechanism ◽  
Immune Effector ◽  
Effector Cells ◽  
Risk Patients

Patients with allogeneic stem cell transplantation (SCT) have a high risk of invasive fungal infections (IFIs) even after neutrophil regeneration. Immunological aspects might play a very important role in the IFI development in these patients. Some data are available supporting the identification of high-risk patients with IFI for example patients receiving stem cells from TLR4 haplotype S4 positive donors. Key defense mechanisms against IFI include the activation of neutrophils, the phagocytosis of germinating conidia by dendritic cells, and the fight of the cells of the innate immunity such as monocytes and natural killer cells against germlings and hyphae. Furthermore, immunosuppressive drugs interact with immune effector cells influencing the specific fungal immune defense and antimycotic drugs might interact with immune response. Based on the current knowledge on immunological mechanism inAspergillus fumigatus, the first approaches of an immunotherapy using human T cells are in development. This might be an option for the future of aspergillosis patients having a poor prognosis with conventional treatment.

scholarly journals Cis binding between inhibitory receptors and MHC class I can regulate mast cell activation

2007 ◽  
Vol 204 (4) ◽  
pp. 907-920 ◽  
Author(s):  
Ai Masuda ◽  
Akira Nakamura ◽  
Tsutomu Maeda ◽  
Yuzuru Sakamoto ◽  
Toshiyuki Takai
Keyword(s):  
Mast Cells ◽  
Mhc Class I ◽  
Cell Activation ◽  
Human Leukocyte ◽  
Class I ◽  
Mast Cell Activation ◽  
Inhibitory Receptors ◽  
Immune Effector ◽  
Effector Cells ◽  
In Cis

Allergy is caused by immune effector cells, including mast cells and basophils. Cellular signaling that activates these effector cells is regulated by different inhibitory receptors on their surface. We show that human leukocyte immunoglobulin (Ig)-like receptor (LILR) B2 and its mouse orthologue, paired Ig-like receptor (PIR)–B, constitutively associate to major histocompatibility complex (MHC) class I on the same cell surface (in cis). The IgE-mediated effector responses were augmented in β2-microglobulin (β2m) and PIR-B–deficient mast cells. In addition, the increased cytokine production of β2m-deficient mast cells was not affected by the co-culture with MHC class I–positive mast cells, showing that less cis interaction between PIR-B and MHC class I on mast cells led to the increased cytokine release. Thus, the constitutive cis binding between LILRB2 or PIR-B and MHC class I has an essential role in regulating allergic responses.

Immune effector cells: Mast cells and eosinophils?

2004 ◽  
Vol 37 (S26) ◽  
pp. 42-44
Author(s):  
Shira Fraenkel ◽  
Ilaria Puxeddu ◽  
Francesca Levi-Schaffer
Keyword(s):  
Mast Cells ◽  
Immune Effector ◽  
Effector Cells ◽  
Immune Effector Cells

scholarly journals Mucorales Species and Macrophages

2020 ◽  
Vol 6 (2) ◽  
pp. 94 ◽  
Author(s):  
Francisco E. Nicolás ◽  
Laura Murcia ◽  
Eusebio Navarro ◽  
María Isabel Navarro-Mendoza ◽  
Carlos Pérez-Arques ◽  
...  
Keyword(s):  
Defense Mechanisms ◽  
Genetic Manipulation ◽  
Mucor Circinelloides ◽  
Rnai Pathway ◽  
Invasion Pathways ◽  
Immune Effector ◽  
Effector Cells ◽  
Regulatory Pathways ◽  
Species Specific ◽  
Key Aspects

Mucormycosis is an emerging fungal infection caused by Mucorales with an unacceptable high mortality rate. Mucorales is a complex fungal group, including eleven different genera that can infect humans. This heterogeneity is associated with species-specific invasion pathways and responses to the host defense mechanisms. The host innate immune system plays a major role in preventing Mucorales growth and host invasion. In this system, macrophages are the main immune effector cells in controlling these fungi by rapid and efficient phagocytosis of the spores. However, Mucorales have evolved mechanisms to block phagosomal maturation and species-specific mechanisms to either survive as dormant spores inside the macrophage, as Rhizopus species, or geminate and escape, as Mucor species. Classical fungal models of mucormycosis, mostly Rhizopus, have made important contributions to elucidate key aspects of the interaction between Mucorales and macrophages, but they lack robust tools for genetic manipulation. The recent introduction of the genetically tractable Mucor circinelloides as a model of mucormycosis offers the possibility to analyze gene function. This has allowed the identification of regulatory pathways that control the fungal response to phagocytosis, including a non-canonical RNAi pathway (NCRIP) that regulates the expression of most genes regulated by phagocytosis.

scholarly journals The Role of Vasoactive Intestinal Peptide and Mast Cells in the Regulatory Effect of Lactobacillus casei ATCC 393 on Intestinal Mucosal Immune Barrier

2021 ◽  
Vol 12 ◽  
Author(s):  
Xiaofan Song ◽  
Shanyao Pi ◽  
Yueming Gao ◽  
Fengxia Zhou ◽  
Shuqi Yan ◽  
...  
Keyword(s):  
Mast Cells ◽  
Protective Effect ◽  
Vasoactive Intestinal Peptide ◽  
Regulatory Effect ◽  
Barrier Dysfunction ◽  
Immune Effector ◽  
Effector Cells

Vasoactive intestinal peptide (VIP) plays an important role in the neuro-endocrine-immune system. Mast cells (MCs) are important immune effector cells. This study was conducted to investigate the protective effect of L. casei ATCC 393 on Enterotoxigenic Escherichia coli (ETEC) K88-induced intestinal mucosal immune barrier injury and its association with VIP/MC signaling by in vitro experiments in cultures of porcine mucosal mast cells (PMMCs) and in vivo experiments using VIP receptor antagonist (aVIP) drug. The results showed that compared with the ETEC K88 and lipopolysaccharides (LPS)-induced model groups, VIP pretreatment significantly inhibited the activation of MCs and the release of β-hexosaminidase (β-hex), histamine and tryptase. Pretreatment with aVIP abolished the protective effect of L. casei ATCC 393 on ETEC K88-induced intestinal mucosal immune barrier dysfunction in C57BL/6 mice. Also, with the blocking of VIP signal transduction, the ETEC K88 infection increased serum inflammatory cytokines, and the numbers of degranulated MCs in ileum, which were decreased by administration of L. casei ATCC 393. In addition, VIP mediated the regulatory effect of L. casei ATCC 393 on intestinal microbiota in mice. These findings suggested that VIP may mediate the protective effect of L.casei ATCC 393 on intestinal mucosal immune barrier dysfunction via MCs.

scholarly journals Novel Strategies to Target Mast Cells in Disease

2021 ◽  
pp. 1-17
Author(s):  
Aida Paivandy ◽  
Gunnar Pejler
Keyword(s):  
Mast Cell ◽  
Immune System ◽  
Mast Cells ◽  
Cell Growth ◽  
Secretory Granules ◽  
Effector Cells ◽  
Host Protection ◽  
Pathological Conditions ◽  
Allergic Disorders ◽  
Detrimental Impact

Mast cells (MCs) are versatile effector cells of the immune system, characterized by a large content of secretory granules containing a variety of inflammatory mediators. They are implicated in the host protection toward various external insults, but are mostly well known for their detrimental impact on a variety of pathological conditions, including allergic disorders such as asthma and a range of additional disease settings. Based on this, there is currently a large demand for therapeutic regimens that can dampen the detrimental impact of MCs in these respective pathological conditions. This can be accomplished by several strategies, including targeting of individual mediators released by MCs, blockade of receptors for MC-released compounds, inhibition of MC activation, limiting mast cell growth or by inducing mast cell apoptosis. Here, we review the currently available and emerging regimens to interfere with harmful mast cell activities in asthma and other pathological settings and discuss the advantages and limitations of such strategies.

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