Inflammatory cell death: how macrophages sense neighbouring cell infection and damage

Abstract

Programmed cell death is a critical host defence strategy during viral infection. Neighbouring cells deal with this death in distinct ways depending on how the infected cell dies. While apoptosis is considered immunologically silent, the lytic pathways of necroptosis and pyroptosis trigger inflammatory responses by releasing inflammatory host molecules. All these pathways have been implicated in influenza A virus infection. Here, we review how cells sense neighbouring infection and death and how sensing shapes ensuing inflammatory responses.

Unraveling the relationship among inflammatory responses, oxidative damage, and host susceptibility to Opisthorchis viverrini infection: A comparative analysis in animal models

“…The pathogenesis of O. viverrini-induced inflammation is believed to be attributed to the somatic and excretory/secretory antigens released by this parasite, which stimulate and recruit inflammatory cells to the bile duct, where they reside. In addition, chemoattractant molecules and damage-associated molecular patterns along with microbial bacteria enhance or exert a synergistic effect on the attraction of inflammatory cells [24][25][26]. In hamster studies on the response to helminth infection, inflammatory cells, such as neutrophils, mononuclear cells, eosinophils, and mast cells, have been reported as common white blood cells [12,18,21,27].…”

Interaction among inflammasome, PANoptosise, and innate immune cells in infection of influenza virus: Updated review

“…MLKL is transferred into the plasma membrane which leads to the efflux of potassium, resulting in activating NLRP3 intrinsically (Figure 2). 21,82,103 To prevent excessive inflammatory reactions, MQs phagocyte apoptotic bodies are infected with IV which is almost found in alveolar routes and lung tissue. However, pyroptosis and necroptosis are observed, along with the inflammation due to releasing necrotic cells and applying specific mechanisms, especially inflammasomes.…”

“…However, studies have shown that IV has multiple evade mechanisms that allow it to escape innate immunity. To propagate and amplify an infection, IV needs to evade the innate immune response 82,83 …”

“…To propagate and amplify an infection, IV needs to evade the innate immune response. 82,83 Generally, it has been believed that IV can accelerate the speed of its replication to evade from cellular death pathway. 83 On the other hand, NS1, an Influenza protein, can limit the assembly of NLRP3 inflammasome through the suppression of recruitment of the downstream adaptor proteins.…”

“…MLKL is transferred into the plasma membrane which leads to the efflux of potassium, resulting in activating NLRP3 intrinsically (Figure 2 ). 21 , 82 , 103 …”