Biofilm Formation and Toll-Like Receptor 2, Toll-Like Receptor 4, and NF-kappaB Expression in Sinus Tissues of Patients with Chronic Rhinosinusitis

Sun, Yan; Zhou, Bing; Wang, Chengshuo; Huang, Qian; Zhang, Qi; Han, Yehua; Dai, Wei; Fan, Erzhong; Liu, Ying

doi:10.2500/ajra.2012.26.3718

Cited by 49 publications

(47 citation statements)

References 35 publications

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“…In addition, TLR2 participates in the immune response to Mycoplasma pneumonia (7), Chlamydophila pneumonia (8), and Staphylococcus aureus (SA) (9), and it has been shown that these TLR2 ligandexpressing pathogens are associated with acute exacerbations of asthma (10). Expression of TLR2 was shown to be up-regulated in asthmatic epithelial cells and in nasal epithelial cells from patients with chronic rhinosinusitis (CRS) (11)(12)(13).…”

Section: Clinical Relevancementioning

confidence: 99%

Involvement of Toll-Like Receptor 2 and Epidermal Growth Factor Receptor Signaling in Epithelial Expression of Airway Remodeling Factors

Homma

Kato

Sakashita

et al. 2015

Am J Respir Cell Mol Biol

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Staphylococcus aureus (SA) colonization and infection is common, and may promote allergic or inflammatory airway diseases, such as asthma, cystic fibrosis, and chronic rhinosinusitis by interacting with airway epithelial cells. Airway epithelial cells not only comprise a physical barrier, but also play key roles in immune, inflammatory, repair, and remodeling responses upon encounters with pathogens. To elucidate the impact of SA on epithelial-mediated remodeling of allergic airways, we tested the hypothesis that SA can enhance the remodeling process. Normal human bronchial epithelial (NHBE) cells were stimulated with heat-killed SA (HKSA) or transforming growth factor (TGF) a. Cell extracts were collected to measure mRNA (real-time RT-PCR) and signaling molecules (Western blot); supernatants were collected to measure protein (ELISA) after 24 hours of stimulation. Epidermal growth factor receptor (EGFR) signaling inhibition experiments were performed using a specific EGFR kinase inhibitor (AG1478) and TGF-a was blocked with an anti-TGF-a antibody. HKSA induced both mRNA and protein for TGF-a and matrix metalloproteinase (MMP) 1 from NHBE cells by a Toll-like receptor 2-dependent mechanism. Recombinant human TGF-a also induced mRNA and protein for MMP-1 from NHBE cells; anti-TGF-a antibody inhibited HKSA-induced MMP-1, suggesting that endogenous TGF-a mediates the MMP-1 induction by HKSA. HKSA-induced MMP-1 expression was suppressed when a specific EGFR kinase inhibitor was added, suggesting that EGFR signaling was mediating the HKSA-induced MMP-1 release. Exposure or colonization by SA in the airway may enhance the remodeling of tissue through a TGF-a-dependent induction of MMP-1 expression, and may thereby promote remodeling in airway diseases in which SA is implicated, such as asthma and chronic rhinosinusitis.

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Section: Clinical Relevancementioning

confidence: 99%

Involvement of Toll-Like Receptor 2 and Epidermal Growth Factor Receptor Signaling in Epithelial Expression of Airway Remodeling Factors

Homma

Kato

Sakashita

et al. 2015

Am J Respir Cell Mol Biol

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“…больных [1]. Повышенная экспрессия мРНК TLR2 при ХРС, диагностированном на основании анамнестических, эндоскопических и рентгенологических (уровень воздух-жидкость) критериев, встречается в литера-туре чаще [3,5,[13][14][15], чем пониженная [7] или не-значимые различия ХРС и контроля [6,11,16].…”

Section: результаты и обсуждениеunclassified

“…В исследованиях в качестве контроля использу-ют нижние носовые раковины [3,4,[11][12][13], браш-биопсии той же области слизистой оболочки носа здоровых добровольцев [1,14,15], образцы слизи-стой оболочки резецированных крючковидных от-ростков и передней решетчатой пазухи пациентов с невоспалительными заболеваниями, подвергнутых эндоскопическому хирургическому вмешательству на пазухах [2,[5][6][7]. Часть имеющихся работ выпол-нена на эпителиальных клетках носа [14,15], в боль-шинстве случаев исследована цельная ткань (гомо-генаты слизистой оболочки) [1-7, 11-13, 16].…”

Section: результаты и обсуждениеunclassified

“…[1,3,5,7,11,12,16], иногда даже подлежащей над-костницы и кости [2,6]. Смешанные образцы ткани содержали эпителий, фибробласты, иммунные и воспалительные клетки, поэтому клеточный источ-ник измеренной мРНК не установлен.…”

Section: результаты и обсуждениеunclassified

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Toll-like receptor 2 gene expression in the nasal and sinonasal mucosa

Tyrnova¹,

Алешина²,

Yanov³

et al. 2016

Ross. rinol.

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“…There is a broad consensus that chronic infections are caused by the formation of bacterial biofilms (Prabhakara et al, 2011b;Moutsopoulos et al, 2012;Peyyala et al, 2012;Cantero et al, 2013a). There have been a few reports on immune responses caused by bacterial biofilm infections (Sun et al, 2012;Granslo et al, 2013), and some reports have shown that bacterial biofilm infection stimulates T helper 17 (Th17) cell proliferation and interleukin 17 (IL-17) expression (Ohlrich et al, 2009;Prabhakara et al, 2011a;Snowden et al, 2012;Cheng et al, 2014), while some reports have shown that biofilms do not cause a significant immune response (Wood et al, 2012). In view of this, the purpose of this study was to examine the relationship between the ability for biofilm formation and Th17 cells.…”

Section: Introductionmentioning

confidence: 99%

Stimulation of bacterial biofilms on Th17 immune cells

Gq¹,

Wang²,

Hl³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. We investigated the role of bacterial biofilms in stimulating T helper 17 (Th17) cells in infected organisms. The formation of bacterial biofilms isolated from clinical lavage fluid samples was measured. Th17 cells and interleukin 17 (IL-17) levels in the peripheral blood of healthy individuals, people infected by biofilm bacteria, people infected by nonbiofilm bacteria, and in the lavage fluid from people infected by bacteria were determined. Differences in those data were tested using the SPSS 17.0 statistical software. Th17 cells and IL-17 levels in the peripheral blood of biofilm bacteria-infected people, non-biofilm bacteria-infected people, and healthy controls were 0.59 ± 0.18% and 108.8 ± 20.5 pg/ mL; 0.58 ± 0.18% and 100.1 ± 20.7 pg/mL; and 0.55 ± 0.17% and 100.0 ± 21.4 pg/mL, respectively; there were no statistically significant differences (P > 0.05). Th17 cells and IL-17 levels in the lavage fluid of biofilm bacteria-infected people and non-biofilm bacteria-infected people were 1.37 ± 0.34% and 157.4 ± 30.8 pg/mL; and 1.11 ± 0.21% and 136.2 ± 24.3 mg/mL, respectively; the differences were statistically significant (P < 0.05). Bacterial biofilms can increase the expression levels of Th17 cells and IL-17 in local infections; this may be the mechanism by which chronic injuries are caused by biofilm infections.

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Biofilm Formation and Toll-Like Receptor 2, Toll-Like Receptor 4, and NF-kappaB Expression in Sinus Tissues of Patients with Chronic Rhinosinusitis

Abstract: Our data indicated that bacterial biofilms were associated with higher levels of TLR2 and NF-kappaB in the majority of sinus tissues from patients with CRS.

Cited by 49 publications

References 35 publications

Involvement of Toll-Like Receptor 2 and Epidermal Growth Factor Receptor Signaling in Epithelial Expression of Airway Remodeling Factors

Involvement of Toll-Like Receptor 2 and Epidermal Growth Factor Receptor Signaling in Epithelial Expression of Airway Remodeling Factors

Toll-like receptor 2 gene expression in the nasal and sinonasal mucosa

Stimulation of bacterial biofilms on Th17 immune cells

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