AI Article Synopsis
- The airway epithelium and innate immune cells serve as the first defense against lung pathogens by recognizing harmful molecules through specific receptors.
- Inflammasomes, particularly the non-canonical caspase-11 inflammasome, play a crucial role in activating inflammation and initiating cell death when bacteria like Gram-negative pathogens are detected.
- The review discusses how caspase-11 responds to cytosolic LPS in the lungs, as well as the tactics pathogens may use to avoid detection by this immune response.
Article Abstract
The airway epithelium and underlying innate immune cells comprise the first line of host defense in the lung. They recognize pathogen-associated molecular patterns (PAMPs) using membrane-bound receptors, as well as cytosolic receptors such as inflammasomes. Inflammasomes activate inflammatory caspases, which in turn process and release the inflammatory cytokines IL-1β and IL-18. Additionally, inflammasomes trigger a form of lytic cell death termed pyroptosis. One of the most important inflammasomes at the host-pathogen interface is the non-canonical caspase-11 inflammasome that responds to LPS in the cytosol. Caspase-11 is important in defense against Gram-negative pathogens, and can drive inflammatory diseases such as LPS-induced sepsis. However, pathogens can employ evasive strategies to minimize or evade host caspase-11 detection. In this review, we present a comprehensive overview of the function of the non-canonical caspase-11 inflammasome in sensing of cytosolic LPS, and its mechanism of action with particular emphasis in the role of caspase-11 in the lung. We also explore some of the strategies pathogens use to evade caspase-11.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7472987 | PMC |
| http://dx.doi.org/10.3389/fimmu.2020.01895 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Functional interplay between non-canonical inflammasomes and autophagy in inflammatory responses and diseases.
Korean J Physiol Pharmacol
November 2024
Department of Life Sciences, Kyonggi University, Suwon 16227, Korea.
The inflammasome is a cytosolic multiprotein platform that plays a key role in the inflammatory response, an essential innate immune response that protects the body from pathogens and cellular danger signals. Autophagy is a fundamental cellular mechanism that maintains homeostasis through the elimination and recycling of dysfunctional molecules and subcellular elements. Many previous studies have demonstrated a functional interplay between canonical inflammasomes that were earlier discovered and autophagy in inflammatory responses and diseases.
View Article and Find Full Text PDFInterferon signalling and non-canonical inflammasome activation promote host protection against multidrug-resistant Acinetobacter baumannii.
Commun Biol
November 2024
Division of Immunology and Infectious Disease, The John Curtin School of Medical Research, the Australian National University, Canberra, Australian Capital Territory, Australia.
Multidrug-resistant (MDR) Acinetobacter baumannii are of major concern worldwide due to their resistance to last resort carbapenem and polymyxin antibiotics. To develop an effective treatment strategy, it is critical to better understand how an A. baumannii MDR bacterium interacts with its mammalian host.
View Article and Find Full Text PDFactivates pyroptotic pathways in a mouse model of meningitis: role of a two-partner secretion system.
Front Cell Infect Microbiol
October 2024
Department of Molecular Medicine and Medical Biotecnologies, University of Naples "Federico II", Naples, Italy.
Article Synopsis
- * A study using a reference strain and a knockout mutant showed that the HrpA/HrpB system is essential for disease progression, as the mutant exhibited impaired spreading and replication in the brain of infected mice.
- * Analysis of infected brain samples revealed that the mutant had reduced activation of key pyroptosis pathways and inflammatory markers, indicating that HrpA/HrpB is crucial for inducing pyroptosis during meningococcal infection.
Molecular mechanisms of emerging inflammasome complexes and their activation and signaling in inflammation and pyroptosis.
Immunol Rev
October 2024
Division of Immunology and Infectious Diseases, The John Curtin School of Medical Research, The Australian National University, Canberra, Australia.
Inflammasomes are multi-protein complexes that assemble within the cytoplasm of mammalian cells in response to pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs), driving the secretion of the pro-inflammatory cytokines IL-1β and IL-18, and pyroptosis. The best-characterized inflammasome complexes are the NLRP3, NAIP-NLRC4, NLRP1, AIM2, and Pyrin canonical caspase-1-containing inflammasomes, and the caspase-11 non-canonical inflammasome. Newer inflammasome sensor proteins have been identified, including NLRP6, NLRP7, NLRP9, NLRP10, NLRP11, NLRP12, CARD8, and MxA.
View Article and Find Full Text PDFRole of caspase-11 non-canonical inflammasomes in retinal ischemia/reperfusion injury.
Mol Med
September 2024
Department of Ophthalmology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, Shaanxi, China.
Article Synopsis
- Retinal ischemia/reperfusion injury is linked to various eye diseases and involves the inflammatory factor interleukin-1β (IL-1β), but how IL-1β is regulated during this injury remains unclear.
- This study used C57BL/6J mice to investigate the role of caspase-11 non-canonical inflammasomes in retinal IR injury, comparing knockout mice with wild-type mice to evaluate changes in retinal function and IL-1β expression.
- Results showed that caspase-11 knockout mice experienced less retinal ganglion cell death, edema, and improved b-wave amplitude in electroretinography, alongside decreased levels of IL-1β and related proteins in their
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!