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Comment: Wikipedia is not a medical textbook. There is already a section in the granulopoiesis article on emergency granulopoiesis. Some material here could easily be merged there, without the overly complex detail here that is not appropriate to a general encyclopedia. WikiDan61ChatMe!ReadMe!! 13:19, 31 January 2024 (UTC)
Definition and Pathophysiology edit
Emergency granulopoiesis is a critical hematopoietic response mechanism, characterized by the expedited and augmented production of granulocytes, primarily neutrophils, in the bone marrow (BM) under acute infectious or inflammatory conditions. This physiological process serves as a rapid response mechanism to enhance innate immune capabilities in countering pathogen invasions.[1][2][3].
Molecular and Cellular Dynamics edit
In the context of emergency granulopoiesis, hematopoietic stem cells (HSCs) undergo significant transcriptional reprogramming. This reprogramming includes a pivotal transition from lymphoid-biased HSCs (expressing surface marker CD201) to myeloid-biased HSCs, thus altering the lineage commitment in favor of granulopoiesis[4]. Concurrently, the transcription factor CCAAT/enhancer binding protein β (C/EBPβ) is upregulated, playing a pivotal role in the early stages of granulocyte lineage commitment and proliferation, particularly during states of candidemia-induced granulopoiesis[5]
Genetic and Transcriptional Regulation edit
The role of genetic factors in emergency granulopoiesis is underscored by findings in TP53 haploinsufficient mice. In FANCC−/− (Fanconi C gene knockout) mice, the haploinsufficiency of TP53 rescues the impaired emergency granulopoiesis, highlighting the interplay between genetic predispositions and the granulopoietic response.[6]. Furthermore, the transcriptional control in emergency granulopoiesis involves direct and indirect pathogen sensing mechanisms. Hematopoietic stem and progenitor cells (HSPCs) express pathogen recognition receptors (PRRs), such as Toll-like receptors (TLRs), and respond to pathogen-associated molecular patterns (PAMPs) by initiating myeloid differentiation and proliferation[1]
Neutrophil Ontogeny in Emergency Granulopoiesis edit
Neutrophils, the primary effector cells of the innate immune system, originate from HSCs in a multistage differentiation process. Under homeostatic conditions, neutrophils are short-lived leukocytes, continuously replenished from the BM. During systemic inflammation, an increased demand for neutrophils triggers emergency granulopoiesis, characterized by cell cycle shortening in HSCs and progenitors, accelerated differentiation, and a shift towards myelopoiesis.[7]
Clinical Implications edit
Emergency granulopoiesis is critical for host survival during severe systemic infections, balancing the need for rapid neutrophil deployment against the risks of dysregulated immune responses, which can lead to conditions such as acute respiratory distress syndrome and sepsis-induced organ dysfunctions[3][7].
References edit
- ^ a b Paudel, Sagar; Ghimire, Laxman; Jin, Liliang; Jeansonne, Duane; Jeyaseelan, Samithamby (2022-09-05). "Regulation of emergency granulopoiesis during infection". Frontiers in Immunology. 13. doi:10.3389/fimmu.2022.961601. ISSN 1664-3224. PMC 9485265. PMID 36148240.
- ^ Kondo, Motonari; Wagers, Amy J.; Manz, Markus G.; Prohaska, Susan S.; Scherer, David C.; Beilhack, Georg F.; Shizuru, Judith A.; Weissman, Irving L. (April 2003). "Biology of Hematopoietic Stem Cells and Progenitors: Implications for Clinical Application". Annual Review of Immunology. 21 (1): 759–806. doi:10.1146/annurev.immunol.21.120601.141007. ISSN 0732-0582. PMID 12615892.
- ^ a b Manz, Markus G.; Boettcher, Steffen (May 2014). "Emergency granulopoiesis". Nature Reviews Immunology. 14 (5): 302–314. doi:10.1038/nri3660. ISSN 1474-1741. PMID 24751955. S2CID 26683941.
- ^ Vanickova, Karolina; Milosevic, Mirko; Ribeiro Bas, Irina; Burocziova, Monika; Yokota, Asumi; Danek, Petr; Grusanovic, Srdjan; Chiliński, Mateusz; Plewczynski, Dariusz; Rohlena, Jakub; Hirai, Hideyo; Rohlenova, Katerina; Alberich-Jorda, Meritxell (December 2023). "Hematopoietic stem cells undergo a lymphoid to myeloid switch in early stages of emergency granulopoiesis". The EMBO Journal. 42 (23): e113527. doi:10.15252/embj.2023113527. ISSN 0261-4189. PMC 10690458. PMID 37846891.
- ^ Satake, Sakiko; Hirai, Hideyo; Hayashi, Yoshihiro; Shime, Nobuaki; Tamura, Akihiro; Yao, Hisayuki; Yoshioka, Satoshi; Miura, Yasuo; Inaba, Tohru; Fujita, Naohisa; Ashihara, Eishi; Imanishi, Jiro; Sawa, Teiji; Maekawa, Taira (2012-11-01). "C/EBPβ Is Involved in the Amplification of Early Granulocyte Precursors during Candidemia-Induced "Emergency" Granulopoiesis". The Journal of Immunology. 189 (9): 4546–4555. doi:10.4049/jimmunol.1103007. ISSN 0022-1767. PMID 23024276.
- ^ Hu, Liping; Huang, Weiqi; Bei, Ling; Broglie, Larisa; Eklund, Elizabeth A. (2018-03-15). "TP53 Haploinsufficiency Rescues Emergency Granulopoiesis in FANCC −/− Mice". The Journal of Immunology. 200 (6): 2129–2139. doi:10.4049/jimmunol.1700931. ISSN 0022-1767. PMC 5834788. PMID 29427417.
- ^ a b Malengier-Devlies, Bert; Metzemaekers, Mieke; Wouters, Carine; Proost, Paul; Matthys, Patrick (2021-12-13). "Neutrophil Homeostasis and Emergency Granulopoiesis: The Example of Systemic Juvenile Idiopathic Arthritis". Frontiers in Immunology. 12. doi:10.3389/fimmu.2021.766620. ISSN 1664-3224. PMC 8710701. PMID 34966386.