Damage-associated molecular patterns stimulate interleukin-33 expression in nasal polyp epithelial c

[osisposis]

Damage-associated molecular patterns stimulate interleukin-33 expression in nasal polyp epithelial cells
http://onlinelibrary.wiley.com/doi/10.1002/alr.21237/full

 

[ukxmrv]

Thank you for posting that

"The present study demonstrates that SNECs derived from recalcitrant CRSwNP patients express the cytokine IL-33 in response to damage-associated molecular patterns in vitro. Moreover, whereas the expression of IL-33 is largely confined to the nuclei of basal epithelial cells in control subject ethmoid mucosa, tissue samples from recalcitrant CRSwNP frequently display IL-33 protein expression in the nuclei of more apically-located cells with extension into the cytoplasm. Because IL-33 has the capacity to activate Th2 cytokine-producing innate lymphoid cells residing in the sinus mucosa, dysregulation of this pathway may play a part in perpetuating eosinophilic inflammation in CRSwNP patients who are recalcitrant to medical and surgical therapy."

 

[South]

Can someone smarter than me translate that if possible, are there steps a person with candida and sinus problems might do with the study information? It is so far over my head. Is it more of a study proving some kind of background info, not really yet useable for people (and hopefully in the future more study might yield some steps real people can take)?

 

[osisposis]

Can someone smarter than me translate that if possible, are there steps a person with candida and sinus problems might do with the study information? It is so far over my head. Is it more of a study proving some kind of background info, not really yet useable for people (and hopefully in the future more study might yield some steps real people can take)?

I'm a pretty one tract thinker and I'd have to go bad and rap my mind around this , there is IL-33 treatment but it appears there might be other things that might need to be dealt with first, but at this time I cant really answer that question for you, I can post some other articles, maybe you can find answers there

Biomed Res Int. 2014;2014:587376. doi: 10.1155/2014/587376. Epub 2014 Jun 16.
Role of IL-33 and its receptor in T cell-mediated autoimmune diseases.
Zhao Q, Chen G.
Author information
Abstract

Interleukin-33 (IL-33) is a new cytokine of interleukin-1 family, whose specific receptor is ST2. IL-33 exerts its functions via its target cells and plays different roles in diseases. ST2 deletion and exclusion of IL-33/ST2 axis are accompanied by enhanced susceptibility to dominantly T cell-mediated organ-specific autoimmune diseases. It has been reported that IL-33/ST2 pathway plays a key role in host defense and immune regulation in inflammatory and infectious diseases. This review focuses on new findings in the roles of IL-33 and ST2 in several kinds of T cell-mediated autoimmune diseases.

http://www.ncbi.nlm.nih.gov/pubmed/25032216


http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4084552/


Curr Allergy Asthma Rep. 2013 Apr;13(2):196-202. doi: 10.1007/s11882-013-0338-z.
The role of interleukin-33 in rhinitis.
Rogala B1, Glück J.
Author information
Abstract

IL-33, a member of the IL-1 cytokine family and a ligand to receptor ST2, has great potential to induce a T helper 2-type inflammatory response. IL-33 is proven to be released by epithelial cells during their injury by different environmental stimuli such as airborne allergens, viruses, and air pollutants. IL-33 acting as an endogenous danger signal is termed an alarmin. As such, this cytokine is considered to play a crucial role in an allergic inflammatory disease such as rhinitis. Recent investigations regarding the IL-33/ST2 axis involvement in Th2 inflammatory response and pathogenesis of rhinitis have been reviewed. The role of IL-33 as a novel promising therapeutic target has also been discussed.

http://www.ncbi.nlm.nih.gov/pubmed/23381303


http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3585988/


Allergol Int. 2013 Mar;62(1):13-20. doi: 10.2332/allergolint.13-RAI-0538.
Role of interleukin-33 in innate-type immune cells in allergy.
Nakae S1, Morita H, Ohno T, Arae K, Matsumoto K, Saito H.
Author information
Abstract

Interleukin-33 (IL-33), a member of the IL-1 cytokine family, is preferentially and constitutively expressed in epithelial cells, and it is especially localized in the cells' nucleus. The nuclear IL-33 is released by necrotic cells after tissue injury and/or trauma, and subsequently provokes local inflammation as an alarmin, like high-mobility group box protein-1 (HMGB-1) and IL-1α. IL-33 mainly activates Th2 cells and such innate-type immune cells as mast cells, basophils, eosinophils and natural helper cells that express IL-33R (a heterodimer of IL-1 receptor-like 1 [IL-1RL1; also called ST2, T1, Der4, fit-1] and IL-1 receptor accessory protein [IL-1RAcP]). That activation causes the cells to produce Th2 cytokines, which contribute to host defense against nematodes. On the other hand, excessive and/or inappropriate production of IL-33 is also considered to be involved in the development of such disorders as allergy. In this review, we summarize current knowledge regarding the pathogenic roles of IL-33 in the development of allergic inflammation by focusing on its effects on innate-type immune cells.

http://www.ncbi.nlm.nih.gov/pubmed/23439054
Am J Rhinol Allergy. 2010 Mar-Apr;24(2):105-9. doi: 10.2500/ajra.2010.24.3446.
Treatment-recalcitrant chronic rhinosinusitis with polyps is associated with altered epithelial cell expression of interleukin-33.
Reh DD1, Wang Y, Ramanathan M Jr, Lane AP.
Author information
Abstract
BACKGROUND:

Abnormalities in host mucosal immunity exist in chronic rhinosinusitis with nasal polyps (CRSwNPs), but it is unclear whether this is a cause or an effect of the eosinophilic inflammation and frequent microbial colonization that characterizes the disease. Sinonasal epithelial cells (SNECs) are critical participants in healthy antimicrobial innate immune defense. They also can promote Th2 inflammation with various mediators, including interleukin (IL)-33, which induces T helper cells to produce Th2 cytokines.
METHODS:

CRSwNP SNECs were obtained during sinus surgery and stored. Patients were subsequently classified as either treatment responsive or treatment recalcitrant, based on long-term outcomes of medical and surgical therapy. Epithelial cells from these patients were grown in air-liquid interface (ALI) culture and treated with IL-13, as well as the bacteria-associated molecule, CpG. Expression of IL-33 mRNA was determined by real-time polymerase chain reaction.
RESULTS:

Recalcitrant CRSwNP epithelial cells had increased baseline expression of IL-33 compared with responsive CRSwNPs, which was further increased by 24-hour exposure to CpG. Treatment-responsive epithelial cells were not induced by CpG to express IL-33. Prolonged treatment with IL-13 during differentiation at the ALI diminished the baseline expression of IL-33 and prevented the subsequent induction of IL-33 by CpG.
CONCLUSION:

Mucosal innate immunity likely plays an important role in CRSwNP pathogenesis. A definitive link between infectious triggers and the development of Th2 inflammation has been elusive. We have found constitutive IL-33 expression by SNECs in recalcitrant CRSwNPs, which can be further induced by a bacteria-associated molecular pattern. Dysregulated epithelial cell immune interactions between host and environment may contribute to Th2 inflammation in CRSwNPs.

http://www.ncbi.nlm.nih.gov/pubmed/20338108



ScientificWorldJournal. 2014;2014:340690. Epub 2014 Jul 21.
The Role of IL-33 in Host Response to Candida albicans.
Rodríguez-Cerdeira C1, Lopez-Bárcenas A2, Sánchez-Blanco B3, Arenas R4.
Author information
Abstract

Background. Interleukin (IL) 33 is a recently identified pleiotropic cytokine that influences the activity of multiple cell types and orchestrates complex innate and adaptive immune responses. Methods. We performed an extensive review of the literature published between 2005 and 2013 on IL-33 and related cytokines, their functions, and their regulation of the immune system following Candida albicans colonization. Our literature review included cross-references from retrieved articles and specific data from our own studies. Results. IL-33 (IL-1F11) is a recently identified member of the IL-1 family of cytokines. Accumulating evidence suggests a pivotal role of the IL-33/ST2 axis in host immune defense against fungal pathogens, including C. albicans. IL-33 induces a Th2-type inflammatory response and activates both innate and adaptive immunity. Studies in animal models have shown that Th2 inflammatory responses have a beneficial role in immunity against gastrointestinal and systemic infections by Candida spp. Conclusions. This review summarizes the most important clinical studies and case reports describing the beneficial role of IL-33 in immunity and host defense mechanisms against pathogenic fungi. The finding that the IL-33/ST2 axis is involved in therapeutic target has implications for the prevention and treatment of inflammatory diseases, including acute or chronic candidiasis.

http://www.ncbi.nlm.nih.gov/pubmed/25136658

IL-33 (IL-1F11) is a recently identified member of the IL-1 family of cytokines. Accumulating evidence suggests a pivotal role of the IL-33/ST2 axis in host immune defense against fungal pathogens, including C. albicans. IL-33 induces a Th2-type inflammatory response and activates both innate and adaptive immunity.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4130336/