Biology:PANoptosis

From HandWiki

PANoptosis is a prominent innate immune, inflammatory, and lytic cell death pathway initiated by innate immune sensors and driven by caspases and receptor-interacting protein kinases (RIPKs) through multiprotein PANoptosome complexes.[1][2] The assembly of the PANoptosome cell death complex occurs in response to germline-encoded pattern-recognition receptors (PRRs) sensing pathogens, including bacterial, viral, and fungal infections, as well as pathogen-associated molecular patterns, damage-associated molecular patterns, and cytokines that are released during infections, inflammatory conditions, and cancer.[1][3][4][5][6][7][8][9][10][11][12][13][14][15][16] Several PANoptosome complexes, such as the ZBP1-, AIM2-, RIPK1-, NLRP3 and NLRC5- and NLRP12-PANoptosomes, have been characterized so far.[1][17][18][19][20][21][22][23][24]

Emerging genetic, molecular, and biochemical studies have identified extensive crosstalk among the molecular components across various cell death pathways in response to a variety of pathogens and innate immune triggers.[3][4] Historically, inflammatory caspase-mediated pyroptosis and RIPK-driven necroptosis were described as two major inflammatory cell death pathways. While the PANoptosis pathway has some molecular components in common with pyroptosis and necroptosis, as well as with the non-lytic apoptosis pathway, these mechanisms are separate processes that are associated with distinct triggers, protein complexes, and execution pathways.[2] Inflammasome-dependent pyroptosis involves inflammatory caspases, including caspase-1 and caspase-11 in mice, and caspases-1, -4, and -5 in humans, and is executed by gasdermin D.[25][26][27][28][29][30][31] In contrast, necroptosis occurs via RIPK1/3-mediated MLKL activation, which is downstream of caspase-8 inhibition.[32][33][34][35] On the other hand, PANoptosis is [TDK1] driven by caspases and RIPKs and is executed by gasdermins, MLKL, NINJ1, and potentially other yet to be identified molecules cleaved by caspases.[36][37][38][39][40][41][19][21] Moreover, caspase-8 is essential for cell death in PANoptosis[42][43] but needs to be inactivated or inhibited to induce necroptosis.[44][45]

Summary of the different morphologies, mechanisms and outcomes of apoptosis, pyroptosis, necroptosis, and PANoptosis

Characteristics Apoptosis Pyroptosis Necroptosis PANoptosis
Morphology Cell lysis No Yes Yes Yes
Pore formation No Yes Yes Yes
Mechanism Caspase activation Yes Yes No Yes
Gasdermin activation No Yes No Yes
RIPK1 Yes No Yes Yes
RIPK3 No No Yes Yes
Outcome IL-1b and IL-18 release No Yes No Possible
DAMP release No Yes Yes Yes
Inflammation No Yes Yes Yes
Programmed cell death Yes Yes Yes Yes

Disease Relevance

Activation of PANoptosis can support host defense by clearing damaged and infected cells. Additionally, PANoptosis has been implicated in inflammatory diseases, neurological diseases, and cancer.[46][47][48][49][50][51][52][53][54][55]

Viral Infections

PANoptosis has now been identified in a variety of infections, including influenza A virus, herpes simplex virus 1 (HSV1), and coronavirus. For example, PANoptosis is important for host defense during influenza infection through the ZBP1-PANoptosome and during HSV1 infections through the AIM2-PANoptosome. Studies with beta-coronaviruses have shown that IFN can induce ZBP1-mediated PANoptosis during SARS-CoV-2 infection, thereby limiting the efficacy of IFN treatment during infection and resulting in morbidity and mortality. This suggests that inhibiting ZBP1 may improve the therapeutic efficacy of IFN therapy during SARS-CoV-2 infection and possibly other inflammatory conditions where IFN-mediated cell death and pathology occur.[56][57]

Bacterial Infections

In Yersinia pseudotuberculosis infections, PANoptosis is induced through the RIPK1-PANoptosome, and the deletion of caspase-8 and RIPK3 prevents cell death. During Francisella novicida infection, PANoptosis occurs through the AIM2-PANoptosome.[5][7][17][19] PANoptosis has also been observed in Salmonella enterica and Listeria monocytogenes infections, where the combined loss of caspases and RIPK3 significantly protects cells from death.[58]

Fungal Infections

PANoptosis also occurs in fungal infections, including those caused by Candida albicans and Aspergillus fumigatus.[59]

Cancer

Treatment of cancer cells with the PANoptosis-inducing agents TNF and IFN-γ[60][6] can reduce tumor size in preclinical models.[61] The combination of the nuclear export inhibitor selinexor and IFN can also cause PANoptosis and regress tumors in preclinical models.[3][62]

Hematologic disorders

More recent evidence suggests that NLRC5- NLRP12-mediated PANoptosis is activated by heme, which can be released by red blood cell lysis during infection or inflammatory disease, in combination with specific components of infection or cellular damage. Deletion of NLRP12 protects against pathology in animal models of hemolytic disease, suggesting this could also act as a therapeutic target. Similarly, the NLRC5-PANoptosome, which also contains NLRP12, was identified as a response to NAD+ depletion downstream of heme-containing triggers. Deletion of NLRC5 protects against not only hemolytic disease models, but also colitis and HLH models.[22][23]

Fever

Additionally, PANoptosis can be induced by heat stress (HS), such as fever, during infection, and NINJ1 is a key executioner in this context. Deletion of NINJ1 in a murine model of HS and infection reduces mortality; furthermore, deleting essential PANoptosis effectors upstream completely rescues the mice from mortality, thereby identifying NINJ1 and PANoptosis effectors as potential therapeutic targets.[63]

Therapeutic Potential

The regulation of PANoptosis involves numerous PANoptosomes, which include multiple sensor molecules such as NLRP3, ZBP1, AIM2, NLRC5, and NLRP12, along with complex-forming molecules such as caspases and RIPKs. These components activate various downstream cell death executioners and play a role in disease. Therefore, modulating the components of this pathway has potential for therapy. However, excessive activation of PANoptosis can lead to inflammation, inflammatory disease, and cytokine storm syndromes.[6][11][64][21][1] Treatments that block TNF and IFN-γ to prevent PANoptosis have provided therapeutic benefit in preclinical models of cytokine storm syndromes, including cytokine shock, SARS-CoV-2 infection, sepsis, and hemophagocytic lymphohistiocytosis, suggesting the therapeutic potential of modulating this pathway.[6][65]

References

  1. ↑ 1.0 1.1 1.2 1.3 "St. Jude finds NLRP12 as a new drug target for infection, inflammation and hemolytic diseases" (in en). https://www.stjude.org/media-resources/news-releases/2023-medicine-science-news/st-jude-finds-nlrp12-as-a-new-drug-target.html. 
  2. ↑ 2.0 2.1 Pandeya, Ankit; Kanneganti, Thirumala-Devi (January 2024). "Therapeutic potential of PANoptosis: innate sensors, inflammasomes, and RIPKs in PANoptosomes". Trends in Molecular Medicine 30 (1): 74–88. doi:10.1016/j.molmed.2023.10.001. ISSN 1471-499X. PMID 37977994. 
  3. ↑ 3.0 3.1 3.2 "Promising preclinical cancer therapy harnesses a newly discovered cell death pathway" (in en). https://www.stjude.org/media-resources/news-releases/2021-medicine-science-news/promising-preclinical-cancer-therapy-harnesses-a-newly-discovered-cell-death-pathway.html. 
  4. ↑ 4.0 4.1 "ZBP1 links interferon treatment and dangerous inflammatory cell death during COVID-19" (in en). https://www.stjude.org/media-resources/news-releases/2022-medicine-science-news/zbp1-links-interferon-treatment-and-cell-death-during-covid-19.html. 
  5. ↑ 5.0 5.1 "The PANoptosome: a new frontier in innate immune responses" (in en). https://www.stjude.org/media-resources/news-releases/2021-medicine-science-news/the-panoptosome-a-new-frontier-in-innate-immune-responses.html. 
  6. ↑ 6.0 6.1 6.2 6.3 "In the lab, St. Jude scientists identify possible COVID-19 treatment" (in en). https://www.stjude.org/media-resources/news-releases/2020-medicine-science-news/in-the-lab-st-jude-scientists-identify-possible-covid-19-treatment.html. 
  7. ↑ 7.0 7.1 "Discovering the secrets of the enigmatic caspase-6" (in en). https://www.stjude.org/media-resources/news-releases/2020-medicine-science-news/discovering-the-secrets-of-the-enigmatic-caspase-6.html. 
  8. ↑ "Breaking the dogma: Key cell death regulator has more than one way to get the job done" (in en). https://www.stjude.org/media-resources/news-releases/2019-medicine-science-news/key-cell-death-regulator-gets-job-done.html. 
  9. ↑ Kuriakose, Teneema; Man, Si Ming; Malireddi, R.K. Subbarao; Karki, Rajendra; Kesavardhana, Sannula; Place, David E.; Neale, Geoffrey; Vogel, Peter et al. (2016-08-05). "ZBP1/DAI is an innate sensor of influenza virus triggering the NLRP3 inflammasome and programmed cell death pathways". Science Immunology 1 (2). doi:10.1126/sciimmunol.aag2045. ISSN 2470-9468. PMID 27917412. 
  10. ↑ Karki, Rajendra; Sharma, Bhesh Raj; Lee, Ein; Banoth, Balaji; Malireddi, R.K. Subbarao; Samir, Parimal; Tuladhar, Shraddha; Mummareddy, Harisankeerth et al. (2020-06-18). "Interferon regulatory factor 1 regulates PANoptosis to prevent colorectal cancer". JCI Insight 5 (12). doi:10.1172/jci.insight.136720. ISSN 2379-3708. PMID 32554929. 
  11. ↑ 11.0 11.1 "Diet affects mix of intestinal bacteria and the risk of inflammatory bone disease" (in en). https://www.stjude.org/media-resources/news-releases/2014-medicine-science-news/diet-affects-mix-of-intestinal-bacteria-and-the-risk-of-inflammatory-bone-disease.html. 
  12. ↑ Malireddi, R. K. Subbarao; Karki, Rajendra; Sundaram, Balamurugan; Kancharana, Balabhaskararao; Lee, SangJoon; Samir, Parimal; Kanneganti, Thirumala-Devi (2021-07-21). "Inflammatory Cell Death, PANoptosis, Mediated by Cytokines in Diverse Cancer Lineages Inhibits Tumor Growth". ImmunoHorizons 5 (7): 568–580. doi:10.4049/immunohorizons.2100059. ISSN 2573-7732. PMID 34290111. 
  13. ↑ Karki, Rajendra; Sharma, Bhesh Raj; Tuladhar, Shraddha; Williams, Evan Peter; Zalduondo, Lillian; Samir, Parimal; Zheng, Min; Sundaram, Balamurugan et al. (2021-01-07). "Synergism of TNF-α and IFN-γ Triggers Inflammatory Cell Death, Tissue Damage, and Mortality in SARS-CoV-2 Infection and Cytokine Shock Syndromes". Cell 184 (1): 149–168.e17. doi:10.1016/j.cell.2020.11.025. ISSN 1097-4172. PMID 33278357. 
  14. ↑ Karki, Rajendra; Lee, SangJoon; Mall, Raghvendra; Pandian, Nagakannan; Wang, Yaqiu; Sharma, Bhesh Raj; Malireddi, Rk Subbarao; Yang, Dong et al. (2022-05-19). "ZBP1-dependent inflammatory cell death, PANoptosis, and cytokine storm disrupt IFN therapeutic efficacy during coronavirus infection". Science Immunology 7 (74). doi:10.1126/sciimmunol.abo6294. ISSN 2470-9468. PMID 35587515. 
  15. ↑ Wang, Yaqiu; Pandian, Nagakannan; Han, Joo-Hui; Sundaram, Balamurugan; Lee, SangJoon; Karki, Rajendra; Guy, Clifford S.; Kanneganti, Thirumala-Devi (2022-09-28). "Single cell analysis of PANoptosome cell death complexes through an expansion microscopy method". Cellular and Molecular Life Sciences 79 (10): 531. doi:10.1007/s00018-022-04564-z. ISSN 1420-9071. PMID 36169732. 
  16. ↑ Sundaram, Balamurugan; Pandian, Nagakannan; Mall, Raghvendra; Wang, Yaqiu; Sarkar, Roman; Kim, Hee Jin; Malireddi, R.K. Subbarao; Karki, Rajendra et al. (June 2023). "NLRP12-PANoptosome activates PANoptosis and pathology in response to heme and PAMPs" (in en). Cell 186 (13): 2783–2801.e20. doi:10.1016/j.cell.2023.05.005. PMID 37267949. 
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  19. ↑ 19.0 19.1 19.2 Lee, SangJoon; Karki, Rajendra; Wang, Yaqiu; Nguyen, Lam Nhat; Kalathur, Ravi C.; Kanneganti, Thirumala-Devi (September 2021). "AIM2 forms a complex with pyrin and ZBP1 to drive PANoptosis and host defence". Nature 597 (7876): 415–419. doi:10.1038/s41586-021-03875-8. ISSN 1476-4687. PMID 34471287. Bibcode: 2021Natur.597..415L. 
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  22. ↑ 22.0 22.1 Sundaram, Balamurugan; Pandian, Nagakannan; Kim, Hee Jin; Abdelaal, Hadia M.; Mall, Raghvendra; Indari, Omkar; Sarkar, Roman; Tweedell, Rebecca E. et al. (June 2024). "NLRC5 senses NAD+ depletion, forming a PANoptosome and driving PANoptosis and inflammation". Cell 187 (15): 4061–4077.e17. doi:10.1016/j.cell.2024.05.034. ISSN 0092-8674. PMID 38878777. 
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  55. ↑ Zhu, Peng; Ke, Zhuo-Ran; Chen, Jing-Xian; Li, Shi-Jin; Ma, Tian-Liang; Fan, Xiao-Lei (2023). "Advances in mechanism and regulation of PANoptosis: Prospects in disease treatment". Frontiers in Immunology 14. doi:10.3389/fimmu.2023.1120034. ISSN 1664-3224. PMID 36845112. 
  56. ↑ Oh, SuHyeon; Lee, SangJoon (2023). "Recent advances in ZBP1-derived PANoptosis against viral infections". Frontiers in Immunology 14. doi:10.3389/fimmu.2023.1148727. ISSN 1664-3224. PMID 37261341. 
  57. ↑ Schifanella, Luca; Anderson, Jodi; Wieking, Garritt; Southern, Peter J.; Antinori, Spinello; Galli, Massimo; Corbellino, Mario; Lai, Alessia et al. (2023-05-29). "The Defenders of the Alveolus Succumb in COVID-19 Pneumonia to SARS-CoV-2 and Necroptosis, Pyroptosis, and PANoptosis". The Journal of Infectious Diseases 227 (11): 1245–1254. doi:10.1093/infdis/jiad056. ISSN 1537-6613. PMID 36869698. 
  58. ↑ Christgen, Shelbi; Zheng, Zhen; Kesavardhana, Sannula; Karki, Rajendra; Malireddi, R K Subbarao; Banoth, Balaji; Place, David E; Sharma, Bhesh Raj et al. (2020). "Identification of the PANoptosome: A Molecular Platform Triggering Pyroptosis, Apoptosis, and Necroptosis (PANoptosis)". Frontiers in Cellular and Infection Microbiology 29:10:237.: 237. doi:10.3389/fcimb.2020.00237. PMID 32547960. 
  59. ↑ Banoth, Balaji; Tuladhar, Shraddha; Karki, Rajendra; Sharma, Bhesh Raj; Briard, Benoit; Kesavardhana, Sannula; Burton, Amanda; Kanneganti, Thirumala-Devi (2020). "ZBP1 promotes fungi-induced inflammasome activation and pyroptosis, apoptosis, and necroptosis (PANoptosis)". J Biol Chem 52 (295): 18276–18283. doi:10.1074/jbc.RA120.015924. PMID 33109609. 
  60. ↑ Karki, Rajendra; Sharma, Bhesh Raj; Tuladhar, Shraddha; Williams, Evan Peter; Zalduondo, Lillian; Samir, Parimal; Zheng, Min; Sundaram, Balamurugan et al. (2021-01-07). "Synergism of TNF-α and IFN-γ Triggers Inflammatory Cell Death, Tissue Damage, and Mortality in SARS-CoV-2 Infection and Cytokine Shock Syndromes". Cell 184 (1): 149–168.e17. doi:10.1016/j.cell.2020.11.025. ISSN 1097-4172. PMID 33278357. 
  61. ↑ Subbarao Malireddi, R.K.; Karki, Rajendra; Sundaram, Balamurugan; Kancharana, Balabhaskararao; Lee, SangJoon; Samir, Parimal; Kanneganti, Thirumala-Devi (2021-07-21). "Inflammatory cell death, PANoptosis, mediated by cytokines in diverse cancer lineages inhibits tumor growth". ImmunoHorizons 5 (7): 568–580. doi:10.4049/immunohorizons.2100059. ISSN 2573-7732. PMID 34290111. 
  62. ↑ Karki, Rajendra; Sundaram, Balamurugan; Sharma, Bhesh Raj; Lee, SangJoon; Malireddi, R.K. Subbarao; Nguyen, Lam Nhat; Christgen, Shelbi; Zheng, Min et al. (2021-10-19). "ADAR1 restricts ZBP1-mediated immune response and PANoptosis to promote tumorigenesis". Cell Reports 37 (3). doi:10.1016/j.celrep.2021.109858. ISSN 2211-1247. PMID 34686350. 
  63. ↑ Han, Joo-Hui; Karki, Rajendra; Malireddi, R. K. Subbarao; Mall, Raghvendra; Sarkar, Roman; Sharma, Bhesh Raj; Klein, Jonathon; Berns, Harmut et al. (2024-02-26). "NINJ1 mediates inflammatory cell death, PANoptosis, and lethality during infection conditions and heat stress". Nature Communications 15 (1): 1739. doi:10.1038/s41467-024-45466-x. ISSN 2041-1723. PMID 38409108. Bibcode: 2024NatCo..15.1739H. 
  64. ↑ Karki, Rajendra; Kanneganti, Thirumala-Devi (August 2021). "The 'Cytokine Storm': molecular mechanisms and therapeutic prospects". Trends in Immunology 42 (8): 681–705. doi:10.1016/j.it.2021.06.001. ISSN 1471-4906. PMID 34217595. 
  65. ↑ Karki, Rajendra; Sharma, Bhesh Raj; Tuladhar, Shraddha; Williams, Evan Peter; Zalduondo, Lillian; Samir, Parimal; Zheng, Min; Sundaram, Balamurugan et al. (2021-01-07). "Synergism of TNF-α and IFN-γ Triggers Inflammatory Cell Death, Tissue Damage, and Mortality in SARS-CoV-2 Infection and Cytokine Shock Syndromes". Cell 184 (1): 149–168.e17. doi:10.1016/j.cell.2020.11.025. ISSN 0092-8674. PMID 33278357. 



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