scholarly journals Colonic Mucosal Immune Activation in Mice with Ovalbumin-Induced Allergic Airway Disease: Association between Allergic Airway Disease and Irritable Bowel Syndrome

2021 ◽  
Vol 23 (1) ◽  
pp. 181
Author(s):  
Sanghyun Kim ◽  
Bora Keum ◽  
Junhyoung Byun ◽  
Byoungjae Kim ◽  
Kijeong Lee ◽  
...  

Recent studies on the pathophysiology of irritable bowel syndrome (IBS) have focused on the role of mast cells (MCs) in intestinal mucosal immunity. A link between allergic airway diseases (AADs) and IBS has been suggested because both diseases have similar pathophysiology. We aimed to investigate whether the induction of AAD in mice could lead to inflammation of the colonic mucosa, similar to IBS. We also evaluated whether this inflammatory response could be suppressed by administering a therapeutic agent. Mice were divided into three groups: control, AAD-induced, and salbutamol-treated. An AAD mouse model was established by intraperitoneal injection and nasal challenge with ovalbumin. Mice with AAD were intranasally administered salbutamol. Analyses of cytokine levels, MC count, and tryptase levels in the intestinal mucosa were performed to compare the changes in inflammatory responses among the three groups. Inflammation was observed in the intestinal mucosa of mice in the AAD group. This inflammation in AAD mice was suppressed after salbutamol treatment. Our study demonstrates that AAD induces an inflammatory response similar to that in IBS, suggesting a possible association between IBS and AADs. In patients with IBS with such allergic components, salbutamol may have the potential to alleviate the inflammatory response.

2021 ◽  
Vol 55 (2) ◽  
pp. 108-114
Author(s):  
Yu.M. Stepanov ◽  
I.Ya. Budzak ◽  
Yu.A. Gaidar

The article presents modern data on morphological changes in the intestinal mucosa in patients with irritable bowel syndrome. There were analyzed the studies of different years on the morphological manifestations of irritable bowel syndrome. It has been shown that this pathology has an unusual low-grade inflammation. Mast cells play an important role in these inflammatory disorders, they have an effect on motility disorders, visceral hypersensitivity and other pathogenetic factors of irritable bowel syndrome. Disorders of intercellular tight junctions in this category of patients were also analyzed. The role of proteins involved in intercellular contacts (occludin, claudin, ZO) has been characterized. An analysis of the studies investigating these disorders has been carried out. The article provides examples of the analysis of biopsies in patients with irritable bowel syndrome using various methods of their assessment.


Author(s):  
Philippe Gevaert ◽  
Kit Wong ◽  
Lauren A. Millette ◽  
Tara F. Carr

AbstractImmunoglobulin E (IgE) is a well-known key factor in allergic airway disease; however, its central role in non-allergic airway inflammation is often underestimated. In some airway diseases, IgE is produced as a result of allergic sensitization. However, in others, IgE production occurs despite the lack of a specific allergen. Although multiple pathways contribute to the production of IgE in airway disease, it is its activity in mediating the inflammatory response that is associated with disease. Therefore, an understanding of IgE as the unifying component of upper and lower airway diseases has important implications for both diagnosis and treatment. Understanding the role of IgE in each upper and lower airway disease highlights its potential utility as a diagnostic marker and therapeutic target. Further classification of these diseases by whether they are IgE mediated or non–IgE mediated, rather than by the existence of an underlying allergic component, accounts for both systemic and localized IgE activity. Improvements in diagnostic methodologies and standardization of clinical practices with this classification in mind can help identify patients with IgE-mediated diseases. In doing so, this group of patients can receive optimal care through targeted anti-IgE therapeutics, which have already demonstrated efficacy across numerous IgE-mediated upper and lower airway diseases.


2020 ◽  
Vol 0 (3) ◽  
pp. 29-36
Author(s):  
I. A. Derkach ◽  
A. E. Dorofeyev ◽  
M. M. Rudenko ◽  
G. A. Dorofeyeva ◽  
Yu. Z. Dynia

2016 ◽  
Vol 16 (18) ◽  
pp. 1462-1469 ◽  
Author(s):  
Agata Jarmu| ◽  
Marta Zieli|ska ◽  
Karolina Le| ◽  
Martyna Banaszek ◽  
Martin Storr ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Shinjini Chakraborty ◽  
Veronika Eva Winkelmann ◽  
Sonja Braumüller ◽  
Annette Palmer ◽  
Anke Schultze ◽  
...  

AbstractSingular blockade of C5a in experimental models of sepsis is known to confer protection by rescuing lethality and decreasing pro-inflammatory responses. However, the role of inhibiting C5a has not been evaluated in the context of sterile systemic inflammatory responses, like polytrauma and hemorrhagic shock (PT + HS). In our presented study, a novel and highly specific C5a L-aptamer, NoxD21, was used to block C5a activity in an experimental murine model of PT + HS. The aim of the study was to assess early modulation of inflammatory responses and lung damage 4 h after PT + HS induction. NoxD21-treated PT + HS mice displayed greater polymorphonuclear cell recruitment in the lung, increased pro-inflammatory cytokine levels in the bronchoalveolar lavage fluids (BALF) and reduced myeloperoxidase levels within the lung tissue. An in vitro model of the alveolar-capillary barrier was established to confirm these in vivo observations. Treatment with a polytrauma cocktail induced barrier damage only after 16 h, and NoxD21 treatment in vitro did not rescue this effect. Furthermore, to test the exact role of both the cognate receptors of C5a (C5aR1 and C5aR2), experimental PT + HS was induced in C5aR1 knockout (C5aR1 KO) and C5aR2 KO mice. Following 4 h of PT + HS, C5aR2 KO mice had significantly reduced IL-6 and IL-17 levels in the BALF without significant lung damage, and both, C5aR1 KO and C5aR2 KO PT + HS animals displayed reduced MPO levels within the lungs. In conclusion, the C5aR2 could be a putative driver of early local inflammatory responses in the lung after PT + HS.


2018 ◽  
Vol 76 (2) ◽  
pp. 111-120 ◽  
Author(s):  
Nicola Principi ◽  
Rita Cozzali ◽  
Edoardo Farinelli ◽  
Andrea Brusaferro ◽  
Susanna Esposito

RSC Advances ◽  
2016 ◽  
Vol 6 (69) ◽  
pp. 64208-64214 ◽  
Author(s):  
Shenglan Yang ◽  
Danfang Deng ◽  
Yingying Luo ◽  
Yanran Wu ◽  
Rui Zhu ◽  
...  

In this study, the alleviating role of hydrogen sulfide (H2S) was investigated in a Post-Infectious Irritable Bowel Syndrome (PI-IBS) murine model and Caco-2 cells.


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