Mixed T Helper Cell Signatures In Chronic Rhinosinusitis with and without Polyps

Derycke, Lara; Eyerich, Stefanie; Crombruggen, Koen Van; Pérez-Novo, Claudina; Holtappels, Gabriële; Deruyck, Natalie; Gevaert, Philippe; Bachert, Claus

doi:10.1371/journal.pone.0097581

Cited by 131 publications

(121 citation statements)

References 26 publications

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“…So what, then, is CRSsNP? Although previous studies have suggested that CRSsNP is an adaptive Th1-induced disease process (8)(9)(10), that concept was not confirmed in the current studies. This current investigation is much more extensive than previous work and includes complementary studies simultaneously addressing both tissue and nasal secretions, along with using both proteomics and quantitative transcript expression.…”

contrasting

confidence: 98%

Chronic Rhinosinusitis: More Than Just “Asthma of the Upper Airway”

Borish

2015

Am J Respir Crit Care Med

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contrasting

confidence: 98%

Chronic Rhinosinusitis: More Than Just “Asthma of the Upper Airway”

Borish

2015

Am J Respir Crit Care Med

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“…1 and IFN-g 1 CD4 1 cells in polyps from both groups compared with controls, confirming a recent study from Europe (12). Likewise, they found similar elevations of activated DC subsets (both myeloid DC [mDC] and plasmacytoid DC [pDC]), and these DCs produced equivalent elevated levels of IL-6 and IL12p70 compared with DCs from control tissue.…”

supporting

confidence: 84%

Searching for Distinct Mechanisms in Eosinophilic and Noneosinophilic Airway Inflammation

Kato

Hulse

2014

Am J Respir Crit Care Med

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Finally, they developed a novel triple mTNF knock-in mouse model, in which "triple" refers to the substitution of nonsense nucleotides encoding for three distinct amino acids that are normally required for the Na 1 uptake stimulatory activity of TNF-a, the so-called functional alveolar liquid clearance-stimulatory domain. The authors show that when these triple mTNF knock-in mice were exposed to pneumococcal cholesterol binding pore-forming toxin, a model of pulmonary edema, there was no change in the quantal generation of TNF-a in the bronchoalveolar lavage fluid, but there was reduced ENaC activity, decreased ENaC-a protein expression, and greater lung edema. This finding suggests a physiological role for the lectin-like domain of native TNF-a in alveolar fluid clearance and the resolution of pulmonary edema. Taken together, these basic science results provide new physiological insight into the potential role of the lectin-like domain of TNF-a and support the novel therapeutic use of TIP aerosols in patients with ALI/ARDS and ischemia reperfusion lung injury. n Author disclosures are available with the text of this article at www.atsjournals.org.

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“…The balance in T helper subsets as observed in healthy mucosa is changed in inflamed mucosa. According to flow cytometric analysis of the middle ear in our model, the CD4/CD8 ratio was increased from day 3 to 2 months after inoculation compared to the control group, as Derycke et al (27) reported the CD4/CD8 ratio was increased depending on the severity of inflammation in chronic rhinosinusitis. This result showed that chronic inflammation occurred in the middle ear for a period of 2 months.…”

Section: Discussionmentioning

confidence: 49%

Accumulation of Regulatory T Cells and Chronic Inflammation in the Middle Ear in a Mouse Model of Chronic Otitis Media with Effusion Induced by Combined Eustachian Tube Blockage and Nontypeable Haemophilus influenzae Infection

et al. 2016

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Nontypeable Haemophilus influenzae (NTHi) is associated with chronic otitis media (COM). In this study, we generated a murine model of COM by using eustachian tube (ET) obstruction and NTHi (10 7 CFU) inoculation into the tympanic bulla, and we investigated the relationship between regulatory T cells (Treg) and chronic inflammation in the middle ear. Middle ear effusions (MEEs) and middle ear mucosae (MEM) were collected at days 3 and 14 and at 1 and 2 months after inoculation. Untreated mice served as controls. MEEs were used for bacterial counts and to measure the concentrations of cytokines. MEM were collected for histological evaluation and flow cytometric analysis. Inflammation of the MEM was prolonged throughout this study, and the incidence of NTHi culture-positive MEE was 38% at 2 months after inoculation. The levels of interleukin-1␤ (IL-␤), tumor necrosis factor alpha, IL-10, and transforming growth factor ␤ were increased in the middle ear for up to 2 months after inoculation. CD4؉ CD25 ؉ FoxP3 ؉ Treg accumulated in the middle ear, and the percentage of Treg in the MEM increased for up to 2 months after inoculation. Treg depletion induced a 99.9% reduction of bacterial counts in MEEs and also significantly reduced the ratio of NTHi culture-positive MEE. The levels of these cytokines were also reduced in MEEs. In summary, we developed a murine model of COM, and our findings indicate that Treg confer infectious tolerance to NTHi in the middle ear. Chronic otitis media (COM), including OM with effusion (OME) and recurrent OM, is characterized by clinical evidence of OM and resolution of middle ear effusion (MEE) between episodes. OME represents a spectrum of chronic disease states, ranging from serous to mucoid OM, and is associated with hearing loss, delayed speech development, permanent middle ear damage, and mucosal changes (1). Although COM remains a common problem in pediatric populations, its etiology and pathogenesis are not fully understood. Eustachian tube (ET) dysfunction is considered to be the underlying pathophysiologic event leading to most cases of OME in children. The most frequent causes of ET dysfunction include upper respiratory infections, adenoid tissue hypertrophy, and cleft palate (2, 3). In bacterial infection of COM, the majority of cases are caused by Gram-negative bacteria, whereas in acute OM, Gram-positive bacteria are also frequently isolated (4). Lipopolysaccharides are a component of Gram-negative bacteria that have been detected in human MEEs (5), and their levels are significantly higher in children with chronic OME than in children with acute OME (6). Lipopolysaccharides alone have also been shown to induce mucosal inflammation with the accumulation of effusion in the middle ears of animal models (7,8). Only 30% of MEEs from COM children yielded an unequivocally positive culture for aerobic bacteria (9). According to previous reports, components from Gram-negative bacteria are thought to induce COM in humans. However, recently, COM was reportedly associated with a persi...

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Mixed T Helper Cell Signatures In Chronic Rhinosinusitis with and without Polyps

Cited by 131 publications

References 26 publications

Chronic Rhinosinusitis: More Than Just “Asthma of the Upper Airway”

Chronic Rhinosinusitis: More Than Just “Asthma of the Upper Airway”

Searching for Distinct Mechanisms in Eosinophilic and Noneosinophilic Airway Inflammation

Accumulation of Regulatory T Cells and Chronic Inflammation in the Middle Ear in a Mouse Model of Chronic Otitis Media with Effusion Induced by Combined Eustachian Tube Blockage and Nontypeable Haemophilus influenzae Infection

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