Staphylococcus aureus enterotoxin B, protein A, and lipoteichoic acid stimulations in nasal polyps

Patou, Joke; Gevaert, Philippe; Zele, Thibaut Van; Holtappels, Gabriële; Cauwenberge, Paul Van; Bachert, Claus

doi:10.1016/j.jaci.2007.08.059

Cited by 194 publications

(175 citation statements)

References 26 publications

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“…911 SEB also downregulates the anti-inflammatory prostaglandin PGE4 912 in CRSwNP fibroblasts, and induces growth factors and chemokines in nasal epithelial cells. 913 Most importantly, IgE antibodies to enterotoxins (SE-IgE) were associated with significantly higher concentrations of IgG, specifically of the IgG4 subclass, and IgE in NPs.…”

Section: Viiib Crswnp: Comorbid Asthmamentioning

confidence: 98%

International Consensus Statement on Allergy and Rhinology: Rhinosinusitis

Orlandi

Kingdom

Hwang

et al. 2016

Int Forum Allergy Rhinol

559

888

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Background:The body of knowledge regarding rhinosinusitis (RS) continues to expand, with rapid growth in number of publications, yet substantial variability in the quality of those presentations. In an effort to both consolidate and critically appraise this information, rhinologic experts from around the world have produced the International Consensus Statement on Allergy and Rhinology: Rhinosinusitis (ICAR:RS). Methods:Evidence-based reviews with recommendations (EBRRs) were developed for scores of topics, using previously reported methodology. Where existing evidence was insufficient for an EBRR, an evidence-based review (EBR) was produced. The sections were then synthesized and the entire manuscript was then reviewed by all authors for consensus. Results:The resulting ICAR:RS document addresses multiple topics in RS, including acute RS (ARS), chronic RS (CRS) with and without nasal polyps (CRSwNP and CRSsNP), recurrent acute RS (RARS), acute exacerbation of CRS (AE-CRS), and pediatric RS. Conclusion:As a critical review of the RS literature, ICAR:RS provides a thorough review of pathophysiology and evidence-based recommendations for medical and surgical treatment. It also demonstrates the significant gaps in our understanding of the pathophysiology and optimal management of RS. Too o en the foundation upon which these recommendations are based is comprised of lowerlevel evidence. It is our hope that this summary of the evidence in RS will point out where additional research efforts may be directed. C 2016 ARS-AAOA, LLC. Key Words:rhinosinusitis; chronic rhinosinusitis; acute rhinosinusitis; recurrent acute rhinosinusitis; evidence-based medicine; systematic review; endoscopic sinus surgery List of Abbreviations Used

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Section: Viiib Crswnp: Comorbid Asthmamentioning

confidence: 98%

International Consensus Statement on Allergy and Rhinology: Rhinosinusitis

Orlandi

Kingdom

Hwang

et al. 2016

Int Forum Allergy Rhinol

559

888

View full text Add to dashboard Cite

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“…The increase is significantly higher in the former tissue than in the latter, but TGF-b1 is not induced and its expression only decreased in NP tissues. However, the relationship between Staphylococcus aureus, PGs, LTs, and TGF-b1 in NP tissues needs to be further investigated (43)(44)(45).…”

Section: Arachidonic Acid Metabolitesmentioning

confidence: 99%

Transforming growth factor‐beta 1 pathways in inflammatory airway diseases

Yang

Zhang

Feng

et al. 2014

Allergy

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Transforming growth factor-beta 1 (TGF-b1) has been reported being involved in the remodeling and immunosuppression processes of inflammatory airway diseases; understanding the regulation of TGF-b1 is therefore a key to unravel the pathomechanisms of these diseases. This review briefly summarizes the current knowledge on the influencing factors for driving TGF-b1 and its regulatory pathways in inflammatory airway diseases and discusses possible therapeutic approaches to TGF-b1 control. The factors include smoking and oxidative stress, prostaglandins (PGs), leukotrienes (LTs), bradykinin (BK), and microRNAs (miRs). Based on the summary, new innovative treatment strategies may be developed for inflammatory airway diseases with an impaired expression of TGF-b1.The transforming growth factor-beta (TGF-b) superfamily is critically involved in embryonic development, organogenesis, and tissue homeostasis. It acts as multifunctional regulators of cell growth and differentiation and consists of more than 40 members, mainly including TGF-bs, bone morphogenetic proteins (BMPs), growth and differentiation factors (GDFs), activins, and inhibins. Between these superfamily members, there is a complex network of regulatory mechanisms (1, 2).Possessing immunomodulatory and fibrogenic characteristics, TGF-b1 is a pleiotropic and multifunctional cytokine secreted from various types of cells, such as endothelial, epithelial and smooth muscle cells, as well as fibroblasts and most immune system cells.Transforming growth factor-beta 1 regulation is unique because it is targeted to the extracellular matrix as a biologically inactive complex, which consists of a mature 25-kDa polypeptide dimer (TGF-b), a latency-associated protein (LAP), and a latent TGF-b-binding protein (LTBP). Active TGF-b is released from the latent complex that was activated via cleavage by proteases and other molecules. The activated TGF-b then becomes a ligand for TGF-b type I and II receptors, leading to receptor Smad (R-Smad) phosphorylation, which subsequently binds to the common-partner Smad (co-Smad), and becoming Smad complexes. The Smad complexes translocate into the nucleus and combine with several transcription factors, thereby becoming a transcriptional active complex that activates target genes transcription. In Abbreviations AHR, airway hyper-responsiveness; BAMBI, BMP and activin membrane-bound inhibitor; BK, bradykinin; BMP, bone morphogenetic protein; CCL2/MCP-1, chemokine (CC motif) ligand 2/monocyte chemotactic protein-1; COPD, chronic obstructive pulmonary disease; CRS, chronic rhinosinusitis; CysLT, cysteinyl leukotriene; FoxP3, forkhead box P3; LAP, latency-associated protein; LTBP, latent TGF-b-binding protein; miR, microRNA; PG, prostaglandin; RORc, RAR-related orphan receptor C; TGF-b1, transforming growth factor-beta 1.Allergy 69 (2014) 699-707

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“…After the exposure by harmless Ag such as ragweed pollen for sensitization, Ag-specific IgE-bound FcεRI are cross-linked, and then mast cell granules are released (9,10). As well, invasion by harmful microbes or exposure to the components of bacteria (11)(12)(13), hyphae (14), or toxins generated by infecting microbes (15)(16)(17) also lead to mast cell degranulation. As a result, many of the mediators in the granules, including b-hexosaminidase, spread through the tissues, triggering typical allergic reactions for exclusion of harmless Ag or the inflammatory response designed to eliminate harmful substances (9).…”

mentioning

confidence: 99%

Does β-Hexosaminidase Function Only as a Degranulation Indicator in Mast Cells? The Primary Role of β-Hexosaminidase in Mast Cell Granules

Fukuishi

Murakami

Ohno

et al. 2014

The Journal of Immunology

102

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β-Hexosaminidase, which is generally present in the lysosome, is essential for glycoprotein metabolism in the maintenance of cell homeostasis. In mast cells (MCs), large amounts of β-hexosaminidase are present in the granules as opposed to the lysosome, and the biological role of MC β-hexosaminidase has yet to be fully elucidated. Therefore, we investigated the biological role of β-hexosaminidase in MC granules. Bone marrow-derived MCs from C57BL/6 (BL/6-BMMC) or β-hexosaminidase gene–deficient (hexb−/−-BMMC) mice were transplanted into MC-deficient (WBB6F1/J-KitW/KitW-v [W/Wv]) mice to generate MC-reconstituted models. In asthma model experiments, no differences were observed in the symptoms of BL/6, W/Wv, BL/6-BMMC–reconstituted W/Wv, or hexb−/−-BMMC–reconstituted W/Wv mice. In Staphylococcus epidermidis experimental infection model experiments, the severity of symptoms and frequency of death were markedly higher in W/Wv and hexb−/−-BMMC–reconstituted W/Wv mice than in BL/6 and BL/6-BMMC–reconstituted W/Wv mice. The growth of S. epidermidis in an in vitro study was clearly inhibited by addition of BL/6-BMMC lysate, but not by addition of hexb−/−-BMMC lysate. Moreover, suppression of bacterial proliferation was completely recovered when bacteria were incubated with hexb−/−-BMMC lysate plus β-hexosaminidase. Transmission electron microscopy indicated that the cell wall of S. epidermidis was heavily degraded following coincubation of bacteria with BL/6-BMMC lysate, but not following coincubation with hexb−/−-BMMC lysate. These findings strongly suggest that MC granule β-hexosaminidase is crucial for defense against bacterial invasion, but is not involved in the allergic response. Our results also suggest that the bactericidal mechanism of β-hexosaminidase involves degradation of bacterial cell wall peptidoglycan.

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Staphylococcus aureus enterotoxin B, protein A, and lipoteichoic acid stimulations in nasal polyps

Cited by 194 publications

References 26 publications

International Consensus Statement on Allergy and Rhinology: Rhinosinusitis

International Consensus Statement on Allergy and Rhinology: Rhinosinusitis

Transforming growth factor‐beta 1 pathways in inflammatory airway diseases

Does β-Hexosaminidase Function Only as a Degranulation Indicator in Mast Cells? The Primary Role of β-Hexosaminidase in Mast Cell Granules

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