Human Monocytopoiesis in Acute and Chronic Inflammation

Meuret, G.; Detel, U.; Kilz, H.P.; Senn, Hans; Lessen, H. van

doi:10.1159/000208094

Cited by 18 publications

(5 citation statements)

References 10 publications

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“…It did not reach the level of proliferating human erythroblasts [13] or granulopoietic cells [2], Higher values of promonocyte DNA synthesis activity, however, were found in the septicaemia patient. This is in accord with observations in patients under going surgical operations which demonstrated a rapid rise in promonocyte proliferation activity during the early phase of the inflammatory response [12]. From these findings it can be derived that normal monocytopoiesis is endowed with a proliferation reserve in the proliferation pool of the system.…”

Section: Discussionsupporting

confidence: 88%

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Monocytopoiesis in Normal Man: Pool Size, Proliferation Activity and DNA Synthesis Time of Promonocytes

Meuret¹,

Batara²,

Fürste³

1975

Acta Haematol

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Monocytopoiesis was analyzed in the bone marrow of healthy individuals. Promonocytes were identified by simultaneous determination of sodium-fluoride-sensitive and resistent naphthol-AS-D-acetate esterases. DNA synthesis activity of enzyme-positive promocytes was determined by ³H-thymidine (³H-TDR) incorporation in vitro. DNA synthesis time of these cells was measured by a double labelling technique (³H-TDR in vivo, ¹⁴C-TDR in vitro) as well as by serial injections of ³H-TDR. The relative number of promonocytes in the myelogram averaged 2.9 % corresponding to a medullar promonocyte pool of about 600 × 10^B cells per kilogram body weight. The promonocytes were classified into 4 groups on the basis of nucleus morphology: type I promonocytes with small lymphocyte-like nuclei (mean frequency of occurence, F = 5 %; mean ³H-TDR labelling index, LI = 7.1 %; type II promonocytes with large round or oval nuclei (F = 31%; LI = 9.7%); type III promonocytes with large, slightly folded nuclei (F = 51%; LI = 10.1%); type IV promonocytes with large, distinctly folded nuclei (F = 13%; LI = 24.9%). LI of pooled promonocytes was 12.0%. Mean DNA synthesis times of the different types of promonocytes was similar and approximated 10 h (range 6.6–13.3 h). This was true under normal conditions as well as in septicaemia.

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Section: Discussionsupporting

confidence: 88%

“…This proliferation reserve is utilized under conditions of enhanced cell demand such as infection and inflammation. Several results indicate [8,12] that the small lymphocyte-like type I promonocytes possess the highest proliferation reserve.…”

Section: Discussionmentioning

confidence: 99%

Monocytopoiesis in Normal Man: Pool Size, Proliferation Activity and DNA Synthesis Time of Promonocytes

Meuret¹,

Batara²,

Fürste³

1975

Acta Haematol

Self Cite

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“…The mature monocyte travels into the circulation and then undergoes extravasation from the blood to peripheral tissues. The rate at which monocytes are produced into the circulation is elevated in response to inflammation [5,6].…”

Section: Introductionmentioning

confidence: 99%

PK1/EG-VEGF induces monocyte differentiation and activation

Dorsch

Qiu

Soler

et al. 2005

Journal of Leukocyte Biology

109

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Macrophages exist as sentinels in innate immune response and react by expressing proinflammatory cytokines and up-regulating antigen-presenting and costimulatory molecules. We report a novel function for prokineticin-1 (PK1)/endocrine gland-derived vascular endothelial growth factor. Screening of murine tissue sections and cells for specific binding site leads to the identification of macrophages as an in vivo cellular target for PK1. We demonstrate PK1 induces differentiation of murine and human bone marrow cells into the monocyte/macrophage lineage. Human peripheral blood monocytes respond to PK1 by morphological changes and down-regulation of B7-1, CD14, CC chemokine receptor 5, and CXC chemokine receptor 4. Monocytes treated with PK1 have elevated interleukin (IL)-12 and tumor necrosis factor alpha and down-regulated IL-10 production in response to lipopolysaccharide. PK1 induces a distinct monocyte-derived cell population, which is primed for release of proinflammatory cytokines that favor a T helper cell type 1 response.

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“…In summary, acute inflammation and chronic inflammation are two different types of inflammation that occur in the body, and they differ in duration, underlying causes, and features. 54 Acute inflammation is a short-term, rapid, and self-limited response of the human body to an injury, infection, or other harmful stimuli. It helps to recruit immune cells to the site of injury or infection, remove damaged tissue, and promote tissue repair.…”

Section: Acute and Chronic Inflammation: Acute-to-chronic Transitionmentioning

confidence: 99%

Role of Mitochondria in the Chronification of Inflammation: Focus on Dysfunctional Mitophagy and Mitochondrial DNA Mutations

Orekhov,

Summerhill,

Khotina

et al. 2023

Gene Expr

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Inflammation is a natural reaction of the innate immune system that evolved primarily to protect the human body from invading pathogens and to heal injuries. There are two different types of inflammation, acute and chronic inflammation, differing in duration, underlying causes, and characteristics. The acute-to-chronic transition can be determined by several pathomechanisms, including dysregulation of immune response and failure to eliminate the underlying cause. Moreover, epigenetic changes that refer to modifications in gene expression that are heritable but do not involve changes to the underlying DNA sequence can also contribute to prolonged inflammation. Emerging evidence suggests that dysfunctional mitochondria can promote the development of chronic inflammation. In this respect, the mechanisms triggering defective mitophagy, a selective form of autophagy that exterminates dysfunctional mitochondria to maintain cellular homeostasis, attracted special attention. The hypothesis on the pivotal role of mutations in mitochondrial DNA causing defective mitophagy stimulated the area of the research that applies editing of the mitochondrial genome. The mitoCAS9 vector and two single guide RNAs to the G15059A mutation were used to eliminate the mutation from the macrophage-like cells. The normal activity of the initially defective mitophagy was restored in intact macrophage-like cells, confirming the causal role of the G15059A mutation in the disruption of the mitophagy process. The unraveling of the underlying mechanisms of chronic inflammation will help to develop targeted therapeutic approaches aimed at restoring mitochondrial health and alleviating chronic inflammation that can be used for the treatment of a wide range of chronic inflammatory diseases.

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Human Monocytopoiesis in Acute and Chronic Inflammation

Cited by 18 publications

References 10 publications

Monocytopoiesis in Normal Man: Pool Size, Proliferation Activity and DNA Synthesis Time of Promonocytes

Monocytopoiesis in Normal Man: Pool Size, Proliferation Activity and DNA Synthesis Time of Promonocytes

PK1/EG-VEGF induces monocyte differentiation and activation

Role of Mitochondria in the Chronification of Inflammation: Focus on Dysfunctional Mitophagy and Mitochondrial DNA Mutations

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