ArticleAmerican journal of physiology. Renal physiology2014
Inflammasomes are important mediators of cyclophosphamide-induced bladder inflammation.
Article in American journal of physiology. Renal physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 78 citations in OpenAlex.
- Pathophysiology and multi-target prevention strategies for cyclophosphamide-induced bladder injury.iScience · 2026Review
- Urothelial Piezo1 channel contributes to BOO-induced inflammation, EMT, and bladder fibrosis via activation of NLRP3 inflammasome.Journal of translational medicine · 2026Article
- Targeting pattern recognition receptors for cancer therapy: Mechanisms and strategies.Acta pharmaceutica Sinica. B · 2025Review
- Dimethyl Fumarate Attenuates Cyclophosphamide-Induced Bladder Damage and Enhances Cytotoxic Activity Against SH-SY5Y Cells.Journal of biochemical and molecular toxicology · 2025Article
- Specialized pro-resolution mediators in the bladder: effects of resolvin E1 on diabetic bladder dysfunction in the type 1 diabetic male Akita mouse model.BMC urology · 2024Article
- Enzyme-induced hypoxia leads to inflammation in urothelial cells in vitro.International urology and nephrology · 2024Article
- Male Akita mice develop signs of bladder underactivity independent of NLRP3 as a result of a decrease in neurotransmitter release from efferent neurons.American journal of physiology. Renal physiology · 2023Article
- Immunogenic Cell Death Associated Molecular Patterns and the Dual Role of IL17RA in Interstitial Cystitis/Bladder Pain Syndrome.Biomolecules · 2023Article
- Microbiota Ecosystem in Recurrent Cystitis and the Immunological Microenvironment of Urothelium.Healthcare (Basel, Switzerland) · 2023Review
- Why Are Some People with Lower Urinary Tract Symptoms (LUTS) Depressed? New Evidence That Peripheral Inflammation in the Bladder Causes Central Inflammation and Mood Disorders.International journal of molecular sciences · 2023Review
- The Urinary Microbiome; Axis Crosstalk and Short-Chain Fatty Acid.Diagnostics (Basel, Switzerland) · 2022Review
- Diabetes causes NLRP3-dependent barrier dysfunction in mice with detrusor overactivity but not underactivity.American journal of physiology. Renal physiology · 2022Article
- Inhibition of hypoxia-inducible factor-prolyl hydroxylation protects from cyclophosphamide-induced bladder injury and urinary dysfunction.American journal of physiology. Renal physiology · 2022Article
- Diabetic bladder dysfunction progresses from an overactive to an underactive phenotype in a type-1 diabetic mouse model (Akita female mouse) and is dependent on NLRP3.Life sciences · 2022Article
- Flavonoid Nobiletin Attenuates Cyclophosphamide-Induced Cystitis in Mice through Mechanisms That Involve Inhibition of IL-1β Induced Connexin 43 Upregulation and Gap Junction Communication in Urothelial Cells.International journal of molecular sciences · 2022Article
- Specialized pro-resolution mediators in the bladder: Receptor expression and recovery of bladder function from cystitis.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- Loss of NLRP3 increases bacterial cystitis via IRAKM.Translational andrology and urology · 2022Article
- The Role of Inflammasomes in Mediating Urological Disease: A Short Literature Review.Journal of inflammation research · 2022Review
- The NLRP3 Inflammasome Inhibitor Dapansutrile Attenuates Cyclophosphamide-Induced Interstitial Cystitis.Frontiers in immunology · 2022Article
- Pyroptosis in sepsis: Comprehensive analysis of research hotspots and core genes in 2022.Frontiers in molecular biosciences · 2022Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Bladder inflammation (cystitis) underlies numerous bladder pathologies and is elicited by a plethora of agents such as urinary tract infections, bladder outlet obstruction, chemotherapies, and catheters. Pattern recognition receptors [Toll-like receptors (TLRs) and Nod-like receptors (NLRs)] that recognize pathogen- and/or damage-associated molecular patterns (PAMPs and/or DAMPs, respectively) are key components of the innate immune system that coordinates the production (TLRs) and maturation (NLRs) of proinflammatory IL-1β. Despite multiple studies of TLRs in the bladder, none have investigated NLRs beyond one small survey. We now demonstrate that NLRP3 and NLRC4, and their binding partners apoptosis-associated speck-like protein containing a COOH-terminal caspase recruitment domain (ASC) and NLR family apoptosis inhibitory protein (NAIP), are expressed in the bladder and localized predominantly to the urothelia. Activated NLRs form inflammasomes that activate caspase-1. Placement of a NLRP3- or NLRC4-activating PAMP or NLRP3-activating DAMPs into the lumen of the bladder stimulated caspase-1 activity. To investigate inflammasomes in vivo, we induced cystitis with cyclophosphamide (CP, 150 mg/kg ip) in the presence or absence of the inflammasome inhibitor glyburide. Glyburide completely blocked CP-induced activation of caspase-1 and the production of IL-1β at 4 h. At 24 h, glyburide reduced two markers of inflammation by 30-50% and reversed much of the inflammatory morphology. Furthermore, glyburide reversed changes in bladder physiology (cystometry) induced by CP. In conclusion, NLRs/inflammasomes are present in the bladder urothelia and respond to DAMPs and PAMPs, whereas NLRP3 inhibition blocks bladder dysfunction in the CP model. The coordinated response of NLRs and TLRs in the urothelia represents a first-line innate defense that may provide an important target for pharmacological intervention.
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