scholarly journals Polarization of macrophage cellular center during endometrioid cyst evolution

2021 ◽  
Vol 36 (2) ◽  
pp. 84-91
Author(s):  
R. V. Ukrainets ◽  
Y. S. Korneva
Keyword(s):  
Ovarian Cyst ◽  
Cyst Wall ◽  
Macrophage Polarization ◽  
Visual Fields ◽  
Cell Populations ◽  
Fibrous Layer ◽  
Macrophage Cell ◽  
Subsequent Formation ◽  
Hematoxylin And Eosin ◽  
Homeostasis Regulation

Introduction. Macrophages are the center of homeostasis regulation in endometrioid heterotopia tissue. Being one of the most important elements in understanding the pathogenesis of endometriosis, macrophages control the changes in the cooperation of cellular elements.Aim. The aim of the study was to assess the location, nature, and strength of correlation relationships between the macrophages/ siderophages and other cell populations in the endometrioid cysts wall at various stages of their formation.Material and Methods. The study comprised 57 patients with a histologically verified diagnosis of endometrioid ovarian cyst. All the studied endometrioid cysts were divided into “young”, “mature”, and “old” based on the morphological features. The macrophages/siderophages, lymphocytes, neutrophils, and eosinophils were counted in 10 visual fields in the cyst wall after staining with hematoxylin and eosin at ×400 magnification at the different layers of cyst wall.Results. The dynamics of changes in the location, direction, and strength of correlations showed that the functional destruction of macrophage cell center occurred during maturation and aging of the ovarian endometrioid cyst. This process was caused by an insufficient vascularization of endometrioid heterotopia, increasing pressure inside the cyst, and the gradual compaction of underlying fibrous layer, which lead to the atrophy of endometrioid lining and inability of macrophage cell center to maintain homeostasis. These changes caused a complete depletion of macrophage cell center due to macrophage polarization and subsequent formation of siderophages.Conclusion. In the absence of endometrium-associated macrophage pool renewal, endometrioid heterotopia eventually subside due to the destruction of macrophage cell center that controls its homeostasis.

scholarly journals The Role of Macrophages in the Host’s Defense against Sporothrix schenckii

Pathogens ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 905
Author(s):  
Estela Ruiz-Baca ◽  
Armando Pérez-Torres ◽  
Yolanda Romo-Lozano ◽  
Daniel Cervantes-García ◽  
Carlos A. Alba-Fierro ◽  
...  
Keyword(s):  
Immune Responses ◽  
Macrophage Polarization ◽  
Sporothrix Schenckii ◽  
Macrophage Cell ◽  
Cell Recruitment ◽  
Host Pathogen Interaction ◽  
Interaction Processes ◽  
Host Pathogen ◽  
Molecular Patterns

The role of immune cells associated with sporotrichosis caused by Sporothrix schenckii is not yet fully clarified. Macrophages through pattern recognition receptors (PRRs) can recognize pathogen-associated molecular patterns (PAMPs) of Sporothrix, engulf it, activate respiratory burst, and secrete pro-inflammatory or anti-inflammatory biological mediators to control infection. It is important to consider that the characteristics associated with S. schenckii and/or the host may influence macrophage polarization (M1/M2), cell recruitment, and the type of immune response (1, 2, and 17). Currently, with the use of new monocyte-macrophage cell lines, it is possible to evaluate different host–pathogen interaction processes, which allows for the proposal of new mechanisms in human sporotrichosis. Therefore, in order to contribute to the understanding of these host–pathogen interactions, the aim of this review is to summarize and discuss the immune responses induced by macrophage-S. schenckii interactions, as well as the PRRs and PAMPs involved during the recognition of S. schenckii that favor the immune evasion by the fungus.

The Fine Structure of the Cyst Wall of the Metacercaria of Fasciola hepatica

1964 ◽  
Vol s3-105 (72) ◽  
pp. 385-389
Author(s):  
K. E. DIXON ◽  
E. H. MERCER
Keyword(s):  
Fine Structure ◽  
Electron Microscope ◽  
Cyst Wall ◽  
Fasciola Hepatica ◽  
Fibrous Layer ◽  
Protein Layer ◽  
Compact Layer

Observations with the electron microscope have shown that 4 major layers can be distinguished in the cyst wall: (a) an outer tanned-protein layer, consisting of a meshwork of irregular bodies made up of cigar-shaped particles; (b) a predominantly mucopolysaccharide, finely-fibrous layer, closely adherent to the tanned layer; (c) an inner, mainly mucopolysaccharide layer, which can be resolved into two layers differing in fine texture; (d) a dense, compact layer, composed of numerous protein sheets stabilized by disulphide linkages. This layer is formed from tightly wound scrolls, developed in intracellular vacuoles, which are unrolled at the surface of the animal after secretion.

scholarly journals Prognostic Significance of Immune Cell Populations Identified by Machine Learning in Colorectal Cancer Using Routine Hematoxylin and Eosin–Stained Sections

2020 ◽  
Vol 26 (16) ◽  
pp. 4326-4338 ◽  
Author(s):  
Juha P. Väyrynen ◽  
Mai Chan Lau ◽  
Koichiro Haruki ◽  
Sara A. Väyrynen ◽  
Andressa Dias Costa ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Machine Learning ◽  
Immune Cell ◽  
Prognostic Significance ◽  
Cell Populations ◽  
Hematoxylin And Eosin

scholarly journals Dynamics of Macrophage Cell Populations During Murine Pulmonary Tuberculosis

2003 ◽  
Vol 171 (6) ◽  
pp. 3128-3135 ◽  
Author(s):  
Mercedes Gonzalez-Juarrero ◽  
Tae Sun Shim ◽  
Andre Kipnis ◽  
Ana Paula Junqueira-Kipnis ◽  
Ian M. Orme
Keyword(s):  
Pulmonary Tuberculosis ◽  
Cell Populations ◽  
Macrophage Cell

The Complex Role of Target Cells in the Effects of Soluble Substances Released by Monocyte-Macrophage Cell Populations

1978 ◽  
Vol 8 (2) ◽  
pp. 81-89 ◽  
Author(s):  
M. P. ARALA-CHAVES ◽  
M. KEY ◽  
J. W. FETT ◽  
M. T. PORTO ◽  
H. H. FUDENBERG
Keyword(s):  
Cell Populations ◽  
Target Cells ◽  
Macrophage Cell

Version up-date: The CDKN2B-AS1/ MIR497/TXNIP axis regulated macrophages

2021 ◽  
Author(s):  
JianZhong Xu
Keyword(s):  
Rheumatoid Arthritis ◽  
Macrophage Polarization ◽  
Critical Role ◽  
M2 Macrophages ◽  
Macrophage Cell Line ◽  
Macrophage Cell ◽  
Surface Polarization ◽  
M2 Polarization ◽  
M1 Polarization ◽  
Healthy Donors

Abstract The polarization of macrophages plays a critical role in the pathophysiology of rheumatoid arthritis. The macrophages can have pro-inflammatory M1 polarization and various types of alternative anti-inflammatory M2 polarization. Our preliminary results showed that the CDKN2B-AS1/MIR497/TXNIP axis might regulate macrophages of rheumatoid arthritis patients. Therefore, we hypothesized that this axis regulated the polarization of rheumatoid macrophages. Flow cytometry was used to determine the surface polarization markers in M1 or M2 macrophages from healthy donors and rheumatoid arthritis patients. The QPCR and Western Blotting were used to compare the expression of the CDKN2B-AS1/MIR497/TXNIP axis in these macrophages. We Knocked down and overexpressed the axis in the macrophage cell line MD to test its roles in macrophage polarization. Compared to cells from healthy donors, cells from rheumatoid arthritis patients expressed higher levels of CD40 and CD80 and lower levels of CD16, CD163, CD206, and CD200R after polarization, they also expressed higher CDKN2B-AS1, lower MIR497, and higher TXNIP. In macrophages from healthy donors, there was no correlation among CDKN2B-AS1, MIR497, and TXNIP. But in macrophages from patients, there were significant correlations. The CDKN2B-AS1 knockdown, MIR497 mimics suppressed the M1 polarization but promoted the M2 polarization in MD cells, while the MIR497 knockdown and the TXNIP overexpression did the opposite. This study demonstrated that elevated CDKN2B-AS1 in macrophages promotes the M1 polarization and inhibited the M2 polarization of macrophages by the CDKN2B-AS1/ MIR497/TXNIP axis.

Deletion of Myeloid Interferon Regulatory Factor 4 (Irf4) in Mouse Model Protects against Kidney Fibrosis after Ischemic Injury by Decreased Macrophage Recruitment and Activation

2021 ◽  
pp. ASN.2020071010
Author(s):  
Kensuke Sasaki ◽  
Andrew S. Terker ◽  
Yu Pan ◽  
Zhilian Li ◽  
Shirong Cao ◽  
...  
Keyword(s):  
Renal Fibrosis ◽  
Macrophage Polarization ◽  
Kidney Injury ◽  
Significant Inhibition ◽  
Macrophage Infiltration ◽  
Wild Type ◽  
Regulatory Factor ◽  
Macrophage Cell ◽  
Kidney Fibrosis ◽  
M2 Phenotype

BackgroundAKI is characterized by abrupt and reversible kidney dysfunction, and incomplete recovery leads to chronic kidney injury. Previous studies by us and others have indicated that macrophage infiltration and polarization play key roles in recovery from AKI. The role in AKI recovery played by IFN regulatory factor 4 (IRF4), a mediator of polarization of macrophages to the M2 phenotype, is unclear.MethodsWe used mice with myeloid or macrophage cell–specific deletion of Irf4 (MΦ Irf4−/−) to evaluate Irf4’s role in renal macrophage polarization and development of fibrosis after severe AKI.ResultsSurprisingly, although macrophage Irf4 deletion had a minimal effect on early renal functional recovery from AKI, it resulted in decreased renal fibrosis 4 weeks after severe AKI, in association with less-activated macrophages. Macrophage Irf4 deletion also protected against renal fibrosis in unilateral ureteral obstruction. Bone marrow–derived monocytes (BMDMs) from MΦ Irf4−/− mice had diminished chemotactic responses to macrophage chemoattractants, with decreased activation of AKT and PI3 kinase and increased PTEN expression. PI3K and AKT inhibitors markedly decreased chemotaxis in wild-type BMDMs, and in a cultured macrophage cell line. There was significant inhibition of homing of labeled Irf4−/− BMDMs to postischemic kidneys. Renal macrophage infiltration in response to AKI was markedly decreased in MΦ Irf4−/− mice or in wild-type mice with inhibition of AKT activity.ConclusionsDeletion of Irf4 from myeloid cells protected against development of tubulointerstitial fibrosis after severe ischemic renal injury in mice, due primarily to inhibition of AKT-mediated monocyte recruitment to the injured kidney and reduced activation and subsequent polarization into a profibrotic M2 phenotype.

The structure and histochemistry of the cyst wall of the metacercaria of Fasciola hepatica L.

Parasitology ◽  
1965 ◽  
Vol 55 (2) ◽  
pp. 215-226 ◽  
Author(s):  
K. E. Dixon
Keyword(s):  
Cyst Wall ◽  
Fasciola Hepatica ◽  
Acid Mucopolysaccharide ◽  
Toxic Substances ◽  
Relative Importance ◽  
Lipid Matrix ◽  
External Layer ◽  
Fibrous Layer ◽  
Ventral Region ◽  
Layer I

The cyst wall which encloses the metacercaria of Fasciola hepatica consists of four major layers, one of which is further divisible into three sublayers. These layers are numbered I to IV, the first being the external layer. Layers I and II form the outer cyst which may be separated from the inner cyst formed from layers III and IV.Layer I, the thick incomplete external layer, covers the metacercaria dorsally and laterally. It is composed of tanned protein.Layer II is a thin fibrous layer closely adherent to the inner surface of layer I and is composed of mucoprotein and acid mucopolysaccharide.Layer III is made up of three separate sublayers, the relative widths of which vary in different regions of the cyst. In general IIIa consists of mucoprotein, IIIb of acid mucopolysaccharide and IIIc of neutral mucopolysaccharide.In the dorsal and lateral regions, layer IV appears to be formed of lamellae held in a protein–lipid matrix. The lamellae are composed of protein stabilized by disulphide linkages.In the ventral region of layer IV there is a thickened mucopolysaccharide area, the ventral plug, through which the metacercaria excysts.The relative importance of these resistant layers in providing protection against desiccation, toxic substances and attack by other organisms is discussed.This work was carried out during the tenure of a Commonwealth Post Graduate Scholarship. The author is grateful to Professor J. D. Smyth and Dr J. A. Clegg for advice and encouragement during the course of this work and in preparation of the manuscript.

Detection of monocyte/macrophage cell populations in effusions: A comparative study using flow cytometric immunophenotyping and immunocytochemistry

2001 ◽  
Vol 25 (4) ◽  
pp. 214-219 ◽  
Author(s):  
Bj�rn Risberg ◽  
Ben Davidson ◽  
S�ren Nielsen ◽  
Hiep P. Dong ◽  
Jette Christensen ◽  
...  
Keyword(s):  
Comparative Study ◽  
Cell Populations ◽  
Macrophage Cell ◽  
Flow Cytometric Immunophenotyping ◽  
Flow Cytometric

scholarly journals The CDKN2B-AS1/ MIR497/TXNIP axis regulated macrophages

2021 ◽  
Author(s):  
Jianzhong Xu ◽  
Yu Li ◽  
Chenxi Gu ◽  
Guanlei Liu ◽  
Yang Yu
Keyword(s):  
Rheumatoid Arthritis ◽  
Macrophage Polarization ◽  
Critical Role ◽  
Macrophage Cell Line ◽  
Macrophage Cell ◽  
Surface Polarization ◽  
M2 Polarization ◽  
M1 Polarization ◽  
Healthy Donors ◽  
And Function

Abstract Abstract The polarization of macrophages plays a critical role in the pathophysiology of rheumatoid arthritis. The polarization states include pro-inflammatory M1 polarization and various alternative anti-inflammatory M2 polarization. Our preliminary results showed that CDKN2B-AS1/MIR497/TXNIP axis might play a role in macrophages extracted from rheumatoid arthritis patients. Therefore, we hypothesized that this axis regulated the polarization of rheumatoid macrophages. Flow cytometry was used to determine the surface polarization markers in M1 or M2 macrophages from healthy donors and rheumatoid arthritis patients. QPCR and western blotting were used to compare the expression of the CDKN2B-AS1/MIR497/TXNIP axis in these macrophages. We interfered with the expression and function of the axis from upstream to downstream in the macrophage cell line MD to test its roles in macrophage polarization. Compared to cells from healthy donors, cells from rheumatoid arthritis patients expressed a higher level of CD40 and CD80 and a lower level of CD16, CD163, CD206, and CD200R after polarization, they also expressed higher CDKN2B-AS1, lower MIR497, and higher TXNIP. In macrophages from healthy donors, there was no correlation among CDKN2B-AS1, MIR497, and TXNIP. But in macrophages patients, they showed significant correlations. The CDKN2B-AS1 knockdown, MIR497 mimics suppressed M1 polarization but promoted M2 polarization in MD cells, while MIR497 knockdown and TXNIP overexpression did the opposite. This study demonstrated that elevated CDKN2B-AS1 in macrophages promotes M1 polarization and inhibits M2 polarization of macrophage by negatively regulating MIR497, thereby upregulated the expression of TXNIP.

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