Respiratory Physiology & Neurobiology, Год журнала: 2024, Номер unknown, С. 104387 - 104387
Опубликована: Дек. 1, 2024
Язык: Английский
Immunologic Research, Год журнала: 2025, Номер 73(1)
Опубликована: Янв. 14, 2025
Язык: Английский
Процитировано
0
Russian Journal of Archive of Pathology, Год журнала: 2025, Номер 87(1), С. 68 - 68
Опубликована: Фев. 12, 2025
Polyposis rhinosinusitis (CRSwNP) is a heterogeneous proliferative disease characterized by inflammatory hyperplasia of the nasal mucosa with dysregulation apoptosis and cell differentiation. The review summarizes data on molecular cellular mechanisms CRSwNP presents concept intercellular signaling during polyposis growth. Various factors that form specific endotype are involved in development polyp. Features morphogenesis make it possible to distinguish edematous, eosinophilic fibrous NP. In all cases, markers neurogenic inflammation, impaired expression proinflammatory cytokines, NO synthase, BMP-2 other morphogenetic molecules arerecorded. growing polyp reaction damage epithelium mucous membrane bone wall cavity. Interleukin-1β an integrative link pathogenesis these events.
Язык: Английский
Процитировано
0
Immunological Reviews, Год журнала: 2025, Номер 331(1)
Опубликована: Март 31, 2025
Type 2-mediated immune responses protect the body against environmental threats at barrier surfaces, such as large parasites and toxins, facilitate repair of inflammatory tissue damage. However, maladaptive to typically nonpathogenic substances, commonly known allergens, can lead development allergic diseases. 2 immunity involves a series prototype TH2 cytokines (IL-4, IL-5, IL-13) alarmins (IL-33, TSLP) that promote generation adaptive CD4+ helper cells humoral products allergen-specific IgE. Mast basophils are integral players in this network, serving primary effectors IgE-mediated responses. These bind IgE via high-affinity receptors (FcεRI) expressed on their surface and, upon activation by release variety mediators regulate responses, attract modulate other cells, contribute repair. Here, we review biology effector mechanisms these focusing primarily role mediating both physiological pathological contexts.
Язык: Английский
Процитировано
0
Molecular Neurobiology, Год журнала: 2024, Номер unknown
Опубликована: Авг. 9, 2024
Язык: Английский
Процитировано
3
Environment International, Год журнала: 2024, Номер 190, С. 108890 - 108890
Опубликована: Июль 17, 2024
The growing consensus links exposure to fine particulate matter (PM2.5) with an increased risk of respiratory diseases. However, little is known about the additional effects on brainstem function in allergic rhinitis (AR). Furthermore, it unknown what extent PM2.5-induced affect inflammatory response AR. This study aimed determine effects, mechanisms and consequences neural activity altered by allergenic stimulation PM2.5 exposure. Using AR model ovalbumin (OVA) elicitation whole-body exposure, metabolic profile post-allergen was characterized through vivo proton magnetic resonance imaging (1H-MRS). Then, transient receptor potential vanilloid-1 (TRPV1) neuronal expression sensitivity trigeminal nerve were investigated. link between TRPV1 differential metabolites also determined. Finally, we evaluated mediating brain-spleen axis Exposure allergens led changes profiles brainstem, particularly affecting levels glutamine (Gln) glutamate (Glu). TRPV1+ neurons nerve, closely linked metabolism Glu Gln. Moreover, p38, while phosphorylation p38 ERK, resulting upregulation expression. Gln found partially mediate impact inflammation, which supported presence pro-inflammatory axis. Brainstem are under allergen via sensitization exacerbates brain-splenic
Язык: Английский
Процитировано
2
Brazilian Journal of Otorhinolaryngology, Год журнала: 2024, Номер 91(1), С. 101500 - 101500
Опубликована: Сен. 7, 2024
Язык: Английский
Процитировано
1
Respiratory Physiology & Neurobiology, Год журнала: 2024, Номер unknown, С. 104387 - 104387
Опубликована: Дек. 1, 2024
Язык: Английский
Процитировано
0