Exacerbation of allergic rhinitis by the commensal bacterium Streptococcus salivarius

Tackling Severe Neutrophilic Inflammation in Airway Disorders with Functionalized Nanosheets

“…Subsequently, the mice were sacrificed, and nasal mucosa was collected for cytokine mRNA expression examination via quantitative real-time polymerase chain reaction (qRT-PCR). 46 As shown in Figures 6B and S24, the expression levels of several inflammatory cytokines, including IL-1β, IL-6, TNF-α, and IFN-γ, did not markedly change in the sham mice treated with BP-PGA 50 or PGA 50 NPs, while the levels of these cytokines significantly increased after LPS treatment, again confirming the upper-airway inflammation in these model mice. Interestingly, BP-PGA 50 nanosheets decreased the expression levels of the above cytokines, indicating their outstanding therapeutic effect for nasal inflammation, while this modulatory effect was much weaker in the PGA 50 NP and BP nanosheet-treated mice (Figures 6B and S23 and S24).…”

“…However, in the inflammatory model mice, BP-PGA 50 nanosheets effectively reduced the cfDNA level in the NALF (from 376.4 ± 58.6 to 187.3 ± 76.1 ng/mL), demonstrating higher in vivo cfDNA-scavenging efficacy than PGA 50 NPs (Figure A). Subsequently, the mice were sacrificed, and nasal mucosa was collected for cytokine mRNA expression examination via quantitative real-time polymerase chain reaction (qRT-PCR) . As shown in Figures B and S24, the expression levels of several inflammatory cytokines, including IL-1β, IL-6, TNF-α, and IFN-γ, did not markedly change in the sham mice treated with BP-PGA 50 or PGA 50 NPs, while the levels of these cytokines significantly increased after LPS treatment, again confirming the upper-airway inflammation in these model mice.…”

Functional 2D Nanoplatforms Alleviate Eosinophilic Chronic Rhinosinusitis by Modulating Eosinophil Extracellular Trap Formation

“…Subsequently, the experimental mice were sacrificed and their nasal mucosal tissues were collected for quantification of inflammatory cytokines expression with qRT‐PCR. [ 54 ] TLPG A treatment effectively reduced the expression of inflammatory cytokines, especially IL‐4 (by ≈70%) and IL‐5 (by ≈80%), in the nasal mucosa of mice with inflammation (Figure 7C ; Figure S21 , Supporting Information). Although LPG A treatment slightly reduced the expression of these cytokines (e.g., IL‐4 reduced by ≈30%), its efficacy was much lower than that of TLPG A .…”

Intranasal Morphology Transformation Nanomedicines for Long-Term Intervention of Allergic Rhinitis

“…Allergic rhinitis (AR) is a heterogeneous respiratory system inflammatory disorder syndrome, caused by immunoglobulin E (IgE)-mediated reactions to inhaled allergens, and jointly participated in by a variety of immune cells and cytokines. 1,2 AR exhibits the main symptoms of running nose, sneezing, and nasal congestion and is closely related to the morbidity of asthma, sinusitis, and conjunctivitis. 3 AR is hardly completely cured, usually persists throughout life, and seriously affects people's quality of life worldwide.…”

“…Allergic rhinitis (AR) is a heterogeneous respiratory system inflammatory disorder syndrome, caused by immunoglobulin E (IgE)-mediated reactions to inhaled allergens, and jointly participated in by a variety of immune cells and cytokines. , AR exhibits the main symptoms of running nose, sneezing, and nasal congestion and is closely related to the morbidity of asthma, sinusitis, and conjunctivitis . AR is hardly completely cured, usually persists throughout life, and seriously affects people’s quality of life worldwide. , In the early stage of AR, mast cells release histamine, leukotrienes, and other inflammatory mediators, which play a key role in the induction and maintenance of typical allergic symptoms. , Afterward, inflammatory mediators stimulate the nasal mucosal epithelium to secrete chemokine eotaxin, which combines with CC chemokine receptor 3 (CCR3) highly expressed on the surface of mast cells and eosinophils (EOS), inducing the recruitment and infiltration of inflammatory cells in the nasal mucosa and further aggravating the inflammatory reaction in the late phase (Figure S1).…”