[Expert consensus on the diagnosis and treatment of respiratory diseases exacerbated by nonsteroidal anti-inflammatory drugs （2024, Chengdu）].

Non-steroidal anti-inflammatory drugs-exacerbated respiratory disease （N-ERD） is a chronic respiratory disease characterized by eosinophilic inflammation, featuring chronic rhinosinusitis （CRS）, asthma, and intolerance to cyclooxygenase 1 （COX-1） inhibitors. The use of these medications can lead to an acute worsening of rhinitis and asthma symptoms. This condition has not yet received sufficient attention in China, with a high rate of misdiagnosis and a lack of related research.

Chinese Expert Consensus on the Use of Biologics in Patients with Chronic Rhinosinusitis (2022, Zhuhai).

Background: Chronic rhinosinusitis (CRS) is a common inflammatory disease in otolaryngology, mainly manifested as nasal congestion, nasal discharge, facial pain/pressure, and smell disorder. CRS with nasal polyps (CRSwNP), an important phenotype of CRS, has a high recurrence rate even after receiving corticosteroids and/or functional endoscopic sinus surgery. In recent years, clinicians have focused on the application of biological agents in CRSwNP.

Circadian rhythm disruption exacerbates Th2-like immune response in murine allergic airway inflammation.

Background: Chronic jet lag (CJL)-induced circadian rhythm disruption (CRD) is positively correlated with an increased risk of allergic diseases. However, little is known about the mechanism involved in allergic rhinitis (AR).

Methods: Aberrant light/dark cycles-induced CRD mice were randomly divided into negative control (NC) group, AR group, CRD+NC group, and CRD+AR group (n = 8/group).

Livin in synergy with Ras induces and sustains corticosteroid resistance in the airway mucosa.

: Corticosteroid resistance (CR) seriously affects the therapeutic effects of steroids on many chronic inflammatory disorders, including airway allergy. The mechanism of CR development is unclear. Recent research indicates that livin, an apoptosis inhibitor, is associated with the regulation in cell activities.

Interaction between Ras and Bcl2L12 in B cells suppresses IL-10 expression.

The pathogenesis of recurrent tonsillitis is to be further investigated. B cell-derived interleukin (IL)-10 plays a critical role in immune regulation. Ras activation plays an important role in cancer and many immune disorders.

Period2 gene regulates diurnal changes of nasal symptoms in an allergic rhinitis mouse model.

Background: Allergic rhinitis (AR) symptoms exhibit prominent 24-hour variations associated with the biological clock. Although endogenous glucocorticoids synchronize circadian oscillator in the nasal mucosa, the precise mechanism of AR remains unclear. Therefore, using a mouse model, we investigated the association between circadian-clock genes and AR symptoms at various time-points.

Role of FcRI in Antigen-Dependent Eosinophil Activation in Patients With Allergic Rhinitis.

Background: The eosinophil (Eo) activation is a crucial factor evoking allergic rhinitis (AR) attacks; factors; the mechanism of triggering Eo activation remains to be further investigated. The interaction of antigen (Ag) and antibody plays a critical role in evoking allergy attacks. This study aims to elucidate the role of FcγRI, the high affinity receptor of IgG, in the Ag-mediated Eo activation.

Probiotic extracts ameliorate nasal allergy by inducing interleukin-35-producing dendritic cells in mice.

Background: The therapeutic efficacy of allergic rhinitis (AR) needs to be improved. Probiotics have immunoregulatory functions. In this study we evaluated the effects of protein extracts of probiotics in the amelioration of AR.

B cell lymphoma-2-like protein-12 association with T-helper 2 inflammation in chronic rhinosinusitis with allergy.

Background: T-helper 2 (Th2) polarization plays a critical role in the pathogenesis of chronic rhinosinusitis (CRS) with accompanying nasal allergy. Recent studies indicate that B cell lymphoma-2-like protein-12 (Bcl2L12) is associated with immune dysregulation. The purpose of this study was to elucidate the role of Bcl2L12 in the pathogenesis of Th2 polarization of CRS patients.

The 3-methyl-4-nitrophenol (PNMC) compromises airway epithelial barrier function.

Background And Aims: It is recognized that the air pollution is associated with the pathogenesis of airway diseases. This study aims to elucidate the role of the 3-methyl-4-nitrophenol (PNMC), one of the components of diesel-exhaust particles, in compromising the airway epithelial barrier integrity.

Methods: A549 cells, an airway epithelial cell line, were cultured to monolayers to be used as an in vitro epithelial barrier model.

[Preliminary study on Aspergillus fumigatus-induced IKKα controlled maspin protein expression in respiratory epithelial cells of rats].

Objective: To study if the expression of maspin protein in respiratory epithelial cells was downregulated through IκB kinase-α (IKKα)-controlled mechanism in an Aspergillus fumigatus-induced model in rat.

Methods: Inactivated Aspergillus fumigatus hyphae (AFH) suspension was used to induce respiratory epithelial cells (REC) cultured in vitro in rat, with PBS buffer as control. By RT-PCR, the mRNA expression of maspin was quantified, and by immunocytochemistry, the expression of maspin and IKKα in REC was observed.

Staphylococcal enterotoxin B-derived haptens promote sensitization.

T helper 2 (Th2) polarization is a major pathological feature in allergic diseases; its etiology is not fully understood. This study aims to elucidate the adjuvant effect of the microbial product-derived small peptides in the initiation of antigen-specific Th2 polarization. In this study, a clinical survey of patients with chronic rhinosinusitis (CRS) and food allergy (FA) was carried out.

Ubiquitin E3 ligase A20 facilitates processing microbial product in nasal epithelial cells.

Microbial products play a role in the pathogenesis of allergic diseases; ubiquitin E3 ligase A20 (A20) is an important molecule in regulating inflammation in the body. The present study aims to elucidate the role of A20 in processing the absorbed microbial products in nasal epithelial cells. Human nasal mucosal specimens were collected from patients with or without chronic rhinitis and analyzed by immunohistochemistry.

[Immunoglobulin domain and mucin domain-1 in helper T lymphocytes in allergic rhinitis].

Objective: To investigate the significance of T cell immunoglobulin domain and mucin domain-1 (TIM-1) expression in helper T lymphocyte in allergic rhinitis (AR) patients.

Methods: Peripheral blood samples were collected from 20 AR patients, 9 males and 11 females, aged 31.4 (20-54), and 20 healthy persons, 12 males and 8 females, aged 38, 6 (18-60).

[Effects of sulphur dioxide inhalation on allergic rhinitis in mice].

Objective: To observe the effect of sulphur dioxide (SO2) inhalation on the pathogenesis of allergic rhinitis (AR) in mice, and investigate the toxic effect of SO2 on respiratory tract mucosa.

Methods: Fifty male Kunming strain mice were randomly allocated to five groups, i. e.

[Preliminary investigation into the allergic rhinitis complicated with acute bacterial sinusitis in mice].

Objective: To develop a mouse model of bacterial rhinosinusitis superposed on allergic rhinitis (AR), and to explore whether ongoing allergic rhinitis enhance the acute sinus infection and inflammation associated with Streptococcus pneumoniae (SP).

Methods: Fourty mice of C57BL6/J were randomly divided on average into 4 groups: A [ovalbumin (OVA) + SP], B [OVA + normal saline (NS)], C [phosphate buffered solution (PBS) + SP] and D (PBS + NS). (1) Group A and B were sensitized by intraperitoneal injection with 200 microl (10%) OVA on days 1 through 9, and exposed to OVA (6%) intranasally on days 10 through 17, to induce allergic inflammation.

[Alteration of cytokines and mucin in lower respiratory tract in allergic rhinitis model in rats].

Objective: To investigate the relationship between allergic rhinitis (AR) and asthma as well as the mechanisms related with it.

Methods: Sixty healthy rats were randomly divided into AR group and control group. AR model was established by intraperitoneal injection of ovalbumin (OVA) and nasal challenge with OVA.