What role does pyroptosis play in microbial infection?

Abstract

Pyroptosis, a type of programmed cell death mediated by gasdermin, is characterized by the swelling and rupture of cells, release of cellular contents and a strong inflammatory response, which is critical for controlling microbial infection. Pattern recognition receptors recognize the intracellular and extracellular pathogenic microbial components and stimulate the organism's inflammatory response by activating the pyroptosis signaling pathway and releasing interleukin‐1β (IL‐1β), IL‐18, and other inflammatory factors to promote pathogen clearance and prevent infection. In the process of continuous evolution, pathogens have developed multiple strategies to modulate the occurrence of pyroptosis and thus enhance their ability to induce disease; that is, the competition between host cells and pathogens controls the occurrence of pyroptosis. Competition can directly affect tissue inflammation outbreaks and even alter cell survival. Studies have shown that various bacterial infections, including Shigella flexneri, Salmonella, Listeria monocytogenes, and Legionella pneumophila, can lead to pyroptosis. Pyroptosis is associated with the occurrence and development of various diseases caused by microbial infection, and the identification of molecules related to the pyroptosis signaling pathway may provide new drug targets for the treatment of related diseases. This study reviews the molecular mechanisms of pyroptosis and the role of pyroptosis in microbial infection‐related diseases.

Cytolethal distending toxin‐induced release of interleukin‐1β by human macrophages is dependent upon activation of glycogen synthase kinase 3β, spleen tyrosine kinase (Syk) and the noncanonical inflammasome

“…Our observations demonstrate that Cdt‐induced release of IL‐1β is dependent upon caspase‐4 activation; this finding is significant as this caspase is involved in not only, the noncanonical inflammasome, but also pyroptosis, a form of inflammatory caspase‐mediated lytic cell death (Martel, Lai, Ko, Young, & Ojcius, ; Taabazuing, Okondo, & Bachovchin, ; Xia, Wang, Zheng, Jiang, & Hu, ). In the next series of experiments, we focused on the relationship between Cdt, caspase‐4 activation, pyroptosis and ultimately the release of cytokines.…”

“…Pyroptosis was first recognised as a form of cell death that was distinct from apoptosis as it was independent of caspase‐3 (Tang, Kang, Berghe, Vandenabeele, & Kroemer, ; Xia et al, ). The two forms of cell death exhibit other distinguishing characteristics.…”

“…Cell death mediated by this complex is referred to as canonical pyroptosis and typically occurs in monocytes, macrophages and dendritic cells (Russo, Behl, Banerjee, & Rathinam, ; Shi et al, ). In contrast, noncanonical pyroptosis is mediated by activated caspases‐4, ‐5, ‐11 and occurs in a variety of cell types (Shi et al, ; Xia et al, ). Activation of this pathway was initially identified as occurring as a result of direct interaction between intracellular bacterial lipopolysaccharide (LPS) and caspase‐4/5; cell surface interactions involving TLR4‐LPS do not activate these caspases (Shi et al, ).…”

Stoking the Fire: How Dying Cells Propagate Inflammatory Signalling through Extracellular Vesicle Trafficking

“…Pyroptosis is an inflammatory cell death pathway activated in response to microbial infection as well as during sterile inflammatory pathologies [ 88 , 89 ]. A cell’s commitment to pyroptotic death culminates from initial cell surface receptor engagement with extracellular PAMPs, DAMPs or toxins, leading to PRR-mediated activation of one of several intracellular inflammasome complexes, the most well-studied being the NLRP3 inflammasome, which is comprised of nucleotide-binding domain leucine-rich repeat (NLR) and pyrin domain containing receptor 3 (NLRP3), apoptosis-associated speck-like protein containing a CARD (ASC) and pro-caspase 1.…”

Mechanisms for Salmonella Infection and Potential Management Options in Chicken

“…The pyroptosis occurs when a pathogen such as Salmonella in the macrophage cell express TTSS-1 effectors (SipB) into the cytoplasm to activate caspase-1. The typical inflammasomes that identify Salmonella in the cytoplasm are NOD-like receptor (NLR) family of proteins, namely NLRP3 and NLRC4 (Xia et al, 2019). This is because all classic inflammasomes contain NLRs (Behnsen et al, 2015).…”