Corelationship between Matrix Metalloproteinase 2 and 9 Expression and Severity of Chronic Rhinosinusitis with Nasal Polyposis

Wang, Ling‐Feng; Chien, Chen‐Yu; Chiang, Feng‐Yu; Chai, Chee‐Yin; Tai, Chih-Feng

doi:10.2500/ajra.2012.26.3724

Cited by 33 publications

(30 citation statements)

References 37 publications

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“…No significant correlation has been observed between MMP gene expression and sinonasal computed tomography (CT) scan extension [33]. This confirmed a previous report in which MMP-2 and MMP-9 expression intensity was not correlated with the endoscopic or radiological severity of CRSwNP [34].…”

Section: Metalloproteinasessupporting

confidence: 89%

Remodeling and Repair in Rhinosinusitis

Watelet

Dogné

Mullier

2015

Curr Allergy Asthma Rep

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Remodeling refers to the development of specific but potentially irreversible structural changes in tissue. Caucasian eosinophilic chronic rhinosinusitis (CRS) with polyps associated or not with cystic fibrosis was discriminated by edema from CRS without nasal polyps, characterized by extensive fibrotic fields. However, changes in epithelial and extracellular matrix structures are common findings in all types of chronic inflammatory diseases of upper airways, but rarely specific and highly variable in extend. Recent studies have shown that remodeling in CRS appears to occur in parallel, rather than purely subsequent to inflammation. Furthermore, some preferential remodeling associations can be recognized. Tremendous efforts have been put in research on coagulation factors, cytokines, growth factors, and proteases supporting all phases of upper airway remodeling. The current exploration of other CRS sub-groups and of the particular link with concomitant asthma aims to optimize the classification of CRS and its staging modes and to develop novel therapies.

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Section: Metalloproteinasessupporting

confidence: 89%

Remodeling and Repair in Rhinosinusitis

Watelet

Dogné

Mullier

2015

Curr Allergy Asthma Rep

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“…Fibroblasts also secrete MMPs that may contribute to tissue destruction [13]. Expression levels of MMPs have been found to be elevated in nasal polyp tissues compared to control tissues and play important roles in the formation of nasal polyposis [14], [15]. However, the role of LPS-induced pro-inflammatory cytokines and MMPs in nasal polyp-derived fibroblasts (NPDFs) has not been reported.…”

Section: Introductionmentioning

confidence: 99%

Lipopolysaccharide Induces Pro-Inflammatory Cytokines and MMP Production via TLR4 in Nasal Polyp-Derived Fibroblast and Organ Culture

Cho

Kang

et al. 2014

PLoS ONE

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Nasal polyposis is characterized by persistent inflammation and remodeling in sinonasal mucosa. Toll-like receptors (TLRs) play a role in the innate immune response to microbes in the sinonasal cavity. The aim of this study was to evaluate whether nasal polyp-derived fibroblasts (NPDFs) and organ-cultured nasal polyps can synthesize pro-inflammatory cytokines and matrix metalloproteinases (MMPs) after exposure to lipopolysaccharide (LPS), a TLR4 agonist. NPDFs and organ-cultured nasal polyps were isolated from nasal polyps of 8 patients and exposed to LPS. The mRNA and protein expression levels of TLRs, cytokines, and MMPs were determined using a gene expression microarray, real-time RT-PCR, western blot analysis, enzyme-linked immunosorbent assay, and immunofluorescence staining. The enzymatic activities of MMPs were analyzed using collagen or gelatin zymography. The protein expression level of MMP-1 increased in nasal polyp tissues compared to inferior turbinate tissues. LPS induced mRNA expression of TLR4, IL-6, IL-8, and MMP-1 and activated MAPK signaling in NPDFs. LPS promoted the release of interleukin (IL)-6 through extracellular signal-related kinase (ERK) and IL-8 through ERK and c-Jun N-terminal kinases (JNK). Production of IL-6 and IL-8 was induced by PI3K/Akt signaling in LPS-stimulated NPDFs. LPS increased the transcript and protein expression levels of MMP-1 and induced collagenase activity of MMP-1 via ERK and p38, but did not induce gelatinase activity of MMP-2 and MMP-9. LPS from Rhodobacter sphaeroides (LPS-RS) inhibited the stimulatory effects of LPS in NPDFs as well as in organ culture of nasal polyp. LPS triggers immune response via TLR 4 and activates MAPK and PI3K/Akt signaling pathway, which is involved in remodeling of nasal polyps.

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“…Increased MMP-9 expression has been reported in NPs of patients with recurrent CRSwNP compared with nonrecurrent CRSwNP patients and controls [75]. However, another study reported no significant differences in MMP-9 immunoreactivity between recurrent and nonrecurrent NPs, and MMP-9 immunoreactivity did not either correlate with NP grade and CRSwNP severity [76].…”

Section: Remodeling Factorsmentioning

confidence: 95%

“…and resp. CRSwNP [76] Periostin CRS+AERD (130) Serum ELISA ↑ In patients with high CT score a vs. patients with low CT score [77] Molecules involved in edema VEGF-B…”

Section: Ihqmentioning

confidence: 98%

Clinical and Biological Markers of Difficult-to-Treat Severe Chronic Rhinosinusitis

López-Chacón

Mullol

Pujols

2015

Curr Allergy Asthma Rep

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Chronic rhinosinusitis (CRS) is a chronic inflammatory disease of the upper airways of which two major phenotypes exist, CRS without nasal polyps (CRSsNP) and CRS with nasal polyps (CRSwNP). Some patients with CRS have suboptimal response to current guideline treatments. These patients remain severe and uncontrolled by treatment and have a poor quality of life. It is highly important to identify both clinical and biological markers, so-called biomarkers, in this subset of patients. The presence of nasal polyps and comorbidity with asthma and with aspirin-exacerbated respiratory disease (AERD) are the most common clinical traits that have been associated to difficult-to-treat severe CRS. In addition to clinical traits, numerous biological markers, with known etiopathogenic roles in CRS, have been associated to difficult-to-treat or recalcitrant CRS. This review summarizes the existing knowledge of the clinical and biological markers associated to difficult-to-treat or uncontrolled severe CRS.

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Corelationship between Matrix Metalloproteinase 2 and 9 Expression and Severity of Chronic Rhinosinusitis with Nasal Polyposis

Cited by 33 publications

References 37 publications

Remodeling and Repair in Rhinosinusitis

Remodeling and Repair in Rhinosinusitis

Lipopolysaccharide Induces Pro-Inflammatory Cytokines and MMP Production via TLR4 in Nasal Polyp-Derived Fibroblast and Organ Culture

Clinical and Biological Markers of Difficult-to-Treat Severe Chronic Rhinosinusitis

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