Proinflammatory M1 Macrophages Inhibit RANKL-Induced Osteoclastogenesis

In response to a defined panel of stimuli, immature macrophages can be classified into two major phenotypes: proinflammatory (M1) and anti-inflammatory (M2). Although both phenotypes have been implicated in several chronic inflammatory diseases, their direct role in bone resorption remains unclear. The present study investigated the possible effects of M1 and M2 macrophages on RANKL-induced osteoclastogenesis. In osteoclastogenesis assays using RAW264.7 cells or bone marrow cells as osteoclast precursors, addition of M1 macrophages significantly suppressed RANKL-induced osteoclastogenesis compared to nonstimulated conditions (M0), addition of M2 macrophages, or no macrophage addition (P< 0.05), suggesting that M1 macrophages can downregulate osteoclastogenesis. This effect was maintained when direct contact between M1 and osteoclast precursors was interrupted by cell culture insertion, indicating engagement of soluble factors released from M1. M1 macrophages developed from interferon gamma (IFN-γ) knockout (IFN-γ–KO) mice lost the ability to downregulate osteoclastogenesis. Antibody-based neutralization of interleukin-12 (IL-12), but not IL-10, produced by M1 macrophages also abrogated M1-mediated downregulation of osteoclastogenesis. Real-time PCR analyses showed that IFN-γ suppressed gene expression of NFATc1, a master regulator of osteoclastogenesis, whereas IL-12 increased the apoptosis of osteoclasts, suggesting molecular mechanisms underlying the possible roles of IFN-γ or IL-12 in M1-mediated inhibition of osteoclastogenesis. These findings were confirmed in anin vivoligature-induced mouse periodontitis model in which adoptive transfer of M1 macrophages showed a significantly lower level of bone loss and less tartrate-resistant acid phosphatase (TRAP)-positive cell induction than M0 or M2 macrophage transfer. In conclusion, by its secretion of IFN-γ and IL-12, M1, but not M0 or M2, was demonstrated to inhibit osteoclastogenesis.

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Abstract 660: Macrophage Specific Deficiency of the Transient Receptor Potential Canonical 3 Channel Reduces Apoptosis and Necrosis in Advanced Atherosclerotic Plaques

Arteriosclerosis Thrombosis and Vascular Biology ◽

10.1161/atvb.36.suppl_1.660 ◽

2016 ◽

Vol 36 (suppl_1) ◽

Author(s):

Sumeet A Solanki ◽

Guillermo Vazquez

Keyword(s):

Bone Marrow ◽

Transient Receptor Potential ◽

Receptor Potential ◽

Atherosclerotic Plaques ◽

M2 Macrophage ◽

M2 Macrophages ◽

M1 Macrophages ◽

Transient Receptor Potential Canonical ◽

Transient Receptor ◽

Apoptosis And Necrosis

Background: Macrophage apoptosis plays a critical role in progression of atherosclerosis. Previous studies suggest that M1 and M2 macrophage phenotypes dominate atherosclerosis. Recently, we showed that advanced lesions in the aortic root of Apoe -/- mice transplanted with bone marrow deficient in the calcium-permeable channel Transient Receptor Potential Canonical 3 (TRPC3) are characterized by reduced areas of necrosis and less apoptotic macrophages. However, the donor mice used in these studies had global deficiency of TRPC3, raising the question whether the observed phenotype was also contributed by TRPC3-deficient non-myeloid cells which could undermine the true impact of macrophage deletion of TRPC3. To address this important question, we generated mice with macrophage-specific loss of TRPC3 function (MacTrpc3 -/- ). Methods & results: 13 six week-old female Ldlr -/- mice were irradiated and transplanted with Ldlr -/- (control) or MacTrpc3 -/- Ldlr -/- (experimental) bone marrow and kept on high fat diet for 14 weeks. At the end of the diet period, aortic roots were sectioned and processed for atherosclerotic lesion analysis. Total lesion size (H&E), neutral lipid (Oil Red O) and macrophage content (CD68 staining) were not different between groups. However, we found a 1.7 fold decrease (P=0.01) in percent necrotic area in advanced lesions of MacTrpc3 -/- Ldlr -/- mice (23.12 ± 2.07%, n=10) compared to controls (39.63 ± 5.93%, n=10). Using in situ TUNEL we found that MacTrpc3 -/- Ldlr -/- lesions have less apoptotic cells compared to controls, and these overlapped with CD68 + areas. Using iNOS and mannose receptor as markers for M1 and M2 macrophages, respectively, we found that both subsets overlapped with CD68 + and TUNEL + positive areas, with no differences between groups (n=5). Previously, we showed that M1, but not M2 macrophages derived from MacTrpc3 -/- mice, had reduced apoptosis. This suggests that reduced plaque necrosis of MacTrpc3 -/- Ldlr -/- mice may be due to reduced apoptosis of M1 macrophages. In sum, these in vivo studies indicate that macrophage-specific deficiency of TRPC3 has a genuine beneficial effect on advanced atherosclerotic plaques, reducing apoptosis and necrosis, probably due to a selective effect of TRPC3 on M1 macrophages.

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Crosstalk between adipocytes and M2 macrophages compensates for osteopenic phenotype in the Lrp5-deficient mice

Experimental Biology and Medicine ◽

10.1177/1535370220972320 ◽

2020 ◽

pp. 153537022097232

Author(s):

Lisha Li ◽

Xuemin Qiu ◽

Na Zhang ◽

Yan Sun ◽

Yan Wang ◽

...

Keyword(s):

Bone Marrow ◽

Wnt Signaling ◽

Macrophage Polarization ◽

Myeloid Cells ◽

Osteogenic Potential ◽

Enzyme Linked Immunosorbent Assay ◽

Tartrate Resistant Acid Phosphatase ◽

M2 Macrophage ◽

M2 Macrophages ◽

Alizarin Red

A loss-of-function mutation in the Lrp5 gene in mice leads to a low bone mass disorder due to the inhibition of the canonical Wnt signaling pathway; however, the role of bone marrow microenvironment in mice with this mutation remains unclear. In this study, we evaluated proliferation and osteogenic potential of mouse osteoblasts using the MTT assay and Alizarin red staining. The levels of alkaline phosphatase, tartrate-resistant acid phosphatase, and adiponectin in culture supernatants were measured using the enzyme-linked immunosorbent assay. Osteoclast bone resorbing activity was evaluated by toluidine staining and the number and area of bone resorption pits were determined. We observed increased osteogenesis in osteoblasts co-cultured with the BM-derived myeloid cells compared to the osteoblasts cultured alone. Mice with global Lrp5 deletion had a relatively higher bone density compared to the mice carrying osteoblast/osteocyte-specific Lrp5 deletion. An increased frequency of M2 macrophages and reduced expression of inflammatory cytokines were detected in the myeloid cells derived from the bone marrow of mice with global Lrp5 deletion. Higher adipogenic potential and elevated levels of adiponectin in the global Lrp5 deletion mice contributed to the preferential M2 macrophage polarization. Here, we identified a novel systemic regulatory mechanism of bone formation and degradation in mice with global Lrp5 deletion. This mechanism depends on a crosstalk between the adipocytes and M2 macrophages in the bone marrow and is responsible for partly rescuing osteopenia developed as a result of decreased Wnt signaling.

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Tumor-derived exosomal miR-934 induces macrophage M2 polarization to promote liver metastasis of colorectal cancer

Journal of Hematology & Oncology ◽

10.1186/s13045-020-00991-2 ◽

2020 ◽

Vol 13 (1) ◽

Author(s):

Senlin Zhao ◽

Yushuai Mi ◽

Bingjie Guan ◽

Binbin Zheng ◽

Ping Wei ◽

...

Keyword(s):

Colorectal Cancer ◽

Liver Metastasis ◽

Molecular Mechanisms ◽

Macrophage Polarization ◽

In Vitro Assays ◽

Luciferase Reporter ◽

M2 Macrophage ◽

M2 Macrophages ◽

Premetastatic Niche ◽

Niche Formation

Abstract Background Mounting evidence has demonstrated the vital importance of tumor-associated macrophages (TAMs) and exosomes in the formation of the premetastatic niche. However, the molecular mechanisms by which tumor-derived exosomal miRNAs interact with TAMs underlying premetastatic niche formation and colorectal cancer liver metastasis (CRLM) remain largely unknown. Methods Transmission electron microscopy and differential ultracentrifugation were used to verify the existence of exosomes. In vivo and in vitro assays were used to identify roles of exosomal miR-934. RNA pull-down assay, dual-luciferase reporter assay, etc. were applied to clarify the mechanism of exosomal miR-934 regulated the crosstalk between CRC cells and M2 macrophages. Results In the present study, we first demonstrated the aberrant overexpression of miR-934 in colorectal cancer (CRC), especially in CRLM, and its correlation with the poor prognosis of CRC patients. Then, we verified that CRC cell-derived exosomal miR-934 induced M2 macrophage polarization by downregulating PTEN expression and activating the PI3K/AKT signaling pathway. Moreover, we revealed that hnRNPA2B1 mediated miR-934 packaging into exosomes of CRC cells and then transferred exosomal miR-934 into macrophages. Interestingly, polarized M2 macrophages could induce premetastatic niche formation and promote CRLM by secreting CXCL13, which activated a CXCL13/CXCR5/NFκB/p65/miR-934 positive feedback loop in CRC cells. Conclusions These findings indicate that tumor-derived exosomal miR-934 can promote CRLM by regulating the crosstalk between CRC cells and TAMs. These findings reveal a tumor and TAM interaction in the metastatic microenvironment mediated by tumor-derived exosomes that affects CRLM. The present study also provides a theoretical basis for secondary liver cancer.

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Phenotype and function of macrophage polarization in monocrotaline-induced pulmonary arterial hypertension rat model

Physiological Research ◽

10.33549/physiolres.934456 ◽

2021 ◽

Author(s):

Yong Fan ◽

Yanjie Hao ◽

Dai Gao ◽

Lan Gao ◽

Guangtao Li ◽

...

Keyword(s):

Endothelial Cell ◽

Pulmonary Arterial Hypertension ◽

Arterial Hypertension ◽

Lung Tissue ◽

Rat Model ◽

Macrophage Polarization ◽

M2 Macrophage ◽

M2 Macrophages ◽

M1 Macrophages ◽

Pulmonary Arterial

Pulmonary arterial hypertension (PAH) is a fatal disease characterized by vascular remodeling and chronic inflammation. Macrophages are the key orchestrators of inflammatory and repair responses, and have been demonstrated to be vital in the pathogenesis of PAH. However, specific phenotype of macrophage polarization (M1 & M2 macrophage) in the development of PAH and the underlying mechanisms how they work are still largely unclear. A rat model of monocrotaline (MCT) induced PAH was used. Hemodynamic analysis and histopathological experiments were conducted at day 3, 7, 14, 21 and 28, respectively. In PAH rat lung tissue, confocal microscopic images showed that CD68+NOS2+ M1-like macrophages were remarkably infiltrated on early stage, but dramatically decreased in mid-late stage. Meanwhile, CD68+CD206+ M2-like macrophages in lung tissue accumulated gradually since day 7 to day 28, and the relative ratio of M2/M1 macrophage increased over time. Results detected by western blot and immunohistochemistry were consistent. Further vitro functional studies revealed the possible mechanism involved in this pathophysiological process. By using Transwell co-culture system, it was found that M1 macrophages induced endothelial cell apoptosis, while M2 macrophages significantly promoted proliferation of both endothelial cell and smooth muscle cell. These data preliminarily demonstrated a temporal dynamic change of macrophage M1/M2 polarization status in the development of experimental PAH. M1 macrophages participated in the initial stage of inflammation by accelerating apoptosis of endothelial cell, while M2 macrophages predominated in the reparative stage of inflammation and the followed stage of aberrant tissue remodeling.

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Lung Tumor Cell-Derived Exosomes Promote M2 Macrophage Polarization

Cells ◽

10.3390/cells9051303 ◽

2020 ◽

Vol 9 (5) ◽

pp. 1303 ◽

Cited By ~ 2

Author(s):

Alexandra Pritchard ◽

Sultan Tousif ◽

Yong Wang ◽

Kenneth Hough ◽

Saad Khan ◽

...

Keyword(s):

Bone Marrow ◽

Tumor Cells ◽

Bone Marrow Cells ◽

Lung Tumor ◽

Macrophage Polarization ◽

M2 Macrophage ◽

M2 Macrophages ◽

M2 Macrophage Polarization ◽

The Impact ◽

M2 Phenotype

Cellular cross-talk within the tumor microenvironment (TME) by exosomes is known to promote tumor progression. Tumor promoting macrophages with an M2 phenotype are suppressors of anti-tumor immunity. However, the impact of tumor-derived exosomes in modulating macrophage polarization in the lung TME is largely unknown. Herein, we investigated if lung tumor-derived exosomes alter transcriptional and bioenergetic signatures of M0 macrophages and polarize them to an M2 phenotype. The concentration of exosomes produced by p53 null H358 lung tumor cells was significantly reduced compared to A549 (p53 wild-type) lung tumor cells, consistent with p53-mediated regulation of exosome production. In co-culture studies, M0 macrophages internalized tumor-derived exosomes, and differentiated into M2 phenotype. Importantly, we demonstrate that tumor-derived exosomes enhance the oxygen consumption rate of macrophages, altering their bioenergetic state consistent with that of M2 macrophages. In vitro co-cultures of M0 macrophages with H358 exosomes demonstrated that exosome-induced M2 polarization may be p53 independent. Murine bone marrow cells and bone marrow-derived myeloid-derived suppressor cells (MDSCs) co-cultured with lewis lung carcinoma (LLC)-derived exosomes differentiated to M2 macrophages. Collectively, these studies provide evidence for a novel role for lung tumor-exosomes in M2 macrophage polarization, which then offers new therapeutic targets for immunotherapy of lung cancer.

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Spatial analysis of tumor immune microenvironment (TIME) in patients treated with Bintrafusp alfa.

Journal of Clinical Oncology ◽

10.1200/jco.2020.38.15_suppl.3070 ◽

2020 ◽

Vol 38 (15_suppl) ◽

pp. 3070-3070

Author(s):

Houssein Abdul Sater ◽

Jeffrey Robinson ◽

Julius Strauss ◽

Margaret Elena Gatti-Mays ◽

Jason Redman ◽

...

Keyword(s):

T Cell ◽

Immune Cell ◽

Nk Cell ◽

Cd8 T Cell ◽

Tumor Control ◽

M2 Macrophage ◽

M2 Macrophages ◽

M1 Macrophages ◽

Linear Discriminant ◽

Number Of Patients

3070 Background: Bintrafusp alfa is a first-in-class bifunctional fusion protein composed of the extracellular domain of TGF-βRII receptor (TGF-β “trap”) fused to a human IgG1 mAb blocking PD-L1. In preclinical models, bintrafusp alfa treatment promoted CD8+ T cell and NK cell activation, and both immune cell (IC) populations were required for optimal bintrafusp alfa mediated tumor control. However, the effect of bintrafusp alfa on TIME in humans has not been reported. Methods: In this unplanned interim analysis of a biomarker expansion cohort (NCT 02517398), patients (pts) with advanced non-small cell lung cancer (NSCLC) underwent paired biopsies (bx) before and on treatment with bintrafusp alfa (~ 50 days apart). The objective was to evaluate frequency and localization of tumor infiltrated ICs by IHC. Out of 12 pts, 7 had matched (Pre vs Post) tumor-containing specimens sufficient for multiplex immunofluorescence (MxIF) analysis of TIME. Four pts were excluded as Post bx histology for 3/12 [2 PR (partial response), 1 SD (stable disease)] was negative for tumor (necrosis or fibrosis) and 1/12 did not have a Post bx performed. Results: TIME study shows CD8 T cell infiltrates were increased in Post compared to Pre bx (median 161 vs 62/mm²; interquartile range [IQR] 65–396/mm² vs 31–135/mm²; p = 0·04). While M2 macrophages were also increased (median 800 vs 367/mm²; IQR 776–1131/mm² vs 171–831/mm²; p = 0·04), the ratio of M1/M2 was reversed in pts with SD (↑) compared to pts with PD (↓). Other ICs such as CD4, T-regs, NK cells and M1 macrophages were not changed. On average compared to baseline, M2 macrophages were > 2 fold closer to every other IC in pts with PD, but > 2 fold further from any IC in pts with SD. Tregs were relatively closer to other IC in PD pts. Linear Discriminant Analysis was also performed and results indicate that differential IC densities (mainly M1 macrophages and CD4 T cells) do perform as classifiers between long ( > 5 months) and short ( < 5 months) term responses. Conclusions: This study suggests that bintrafusp alfa not only can enhance intratumoral effector IC infiltrates (CD8) but also has a modulating effect on the spatial distribution of both M1/M2 macrophages within the NSCLC TIME. The differential proximity of M2 macrophages to other IC infiltrates and changes in M1/M2 ratios in association with response suggests that an M1/M2 macrophage balance is directly involved in response and/or resistance to bintrafusp alfa. Given the limited number of patients in this cohort, we intend to study effects of bintrafusp alfa in a larger cohort of patients. Clinical trial information: 02517398 .

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Characterization of Early Gamma Interferon (IFN-γ) Expression during Murine Listeriosis: Identification of NK1.1+ CD11c+ Cells as the Primary IFN-γ-Expressing Cells

Infection and Immunity ◽

10.1128/iai.01026-06 ◽

2006 ◽

Vol 75 (3) ◽

pp. 1167-1176 ◽

Cited By ~ 13

Author(s):

Shu-Rung Chang ◽

Kung-Jiun Wang ◽

Yan-Feng Lu ◽

Lii-Jia Yang ◽

Wei-Jie Chen ◽

...

Keyword(s):

Bone Marrow ◽

Lymph Node ◽

Bone Marrow Cells ◽

Intracellular Cytokine Staining ◽

Gamma Interferon ◽

Interleukin 12 ◽

Innate Defense ◽

Ifn Γ ◽

Almost All

ABSTRACT Though it is well established that gamma interferon (IFN-γ) is crucial to the early innate defense of murine listeriosis, its sources remain controversial. In this study, intracellular cytokine staining of IFN-γ-expressing splenocytes early after Listeria monocytogenes infection revealed that NK1.1+, CD11c+, CD8+ T, and CD4+ T cells expressed IFN-γ 24 h after infection. Contrary to the previous report, most IFN-γ+ dendritic cells (DC) were CD8α− DC. Unexpectedly, almost all CD11c+ IFN-γ-expressing cells also expressed NK1.1. These NK1.1+ CD11c+ cells represented primary IFN-γ-expressing cells after infection. In situ studies showed these NK1.1+ CD11c+ cells were recruited to the borders of infectious foci and expressed IFN-γ. A significant NK1.1+ CD11c+ population was found in uninfected spleen, lymph node, blood, and bone marrow cells. And its number increased significantly in spleen, lymph node, and bone marrow after L. monocytogenes infection. Using interleukin-12 (IL-12) p40−/− mice, IFN-γ expression was found to be largely IL-12 p40 dependent, and the number of IFN-γ-expressing cells was only about one-third of that of wild-type mice. Moreover, the IFN-γ expression was absolutely dependent on live L. monocytogenes infection, as no IFN-γ was detected after inoculation of heat-killed L. monocytogenes. Our findings not only provide an insight into IFN-γ expression after in vivo infection but may also change the current perceptions of DC and natural killer cells.

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12/15-Lipoxygenase-Dependent Myeloid Production of Interleukin-12 Is Essential for Resistance to Chronic Toxoplasmosis

Infection and Immunity ◽

10.1128/iai.00560-09 ◽

2009 ◽

Vol 77 (12) ◽

pp. 5690-5700 ◽

Cited By ~ 15

Author(s):

Melissa K. Middleton ◽

Alicia M. Zukas ◽

Tanya Rubinstein ◽

Michelle Kinder ◽

Emma H. Wilson ◽

...

Keyword(s):

Molecular Mechanisms ◽

Ex Vivo ◽

Acute Infection ◽

Chronic Phase ◽

Parasite Burden ◽

Brain Inflammation ◽

Interleukin 12 ◽

Unsaturated Lipids ◽

Ifn Γ ◽

Deficient Mice

ABSTRACT Interleukin-12 (IL-12) is critical for resistance to Toxoplasma gondii during both the acute and chronic stages of infection. However, the cellular and molecular pathways that regulate IL-12 production during chronic toxoplasmosis are incompletely defined. We recently discovered that 12/15-lipoxygenase (12/15-LOX), which oxidizes unsaturated lipids in macrophages, is a novel and selective regulator of IL-12 production. We now demonstrate the essential role of this enzyme in the chronic phase of toxoplasmosis. Although 12/15-LOX-deficient mice were resistant to acute T. gondii infection, 80% of 12/15-LOX-deficient mice died during chronic toxoplasmosis, compared to no deaths in wild-type controls. The morbidity of chronically infected 12/15-LOX mice was associated with an increase in brain inflammation and parasite burden. These data suggest that the evolution of the immune response to T. gondii is accompanied by an increasing requirement for 12/15-LOX-mediated signaling. Consistent with this conclusion, 12/15-LOX activity was enhanced during chronic, but not acute, toxoplasmosis. Furthermore, the enhanced susceptibility of 12/15-LOX-deficient mice to chronic toxoplasmosis was associated with reduced production of IL-12 and gamma interferon (IFN-γ) that was not evident during acute infection. Importantly, ex vivo IFN-γ production by 12/15-LOX-deficient splenocytes could be rescued by the addition of recombinant IL-12. These data establish that 12/15-LOX is a critical mediator of the chronic type 1 inflammatory response and that immune mediators can be subject to distinct cellular and/or molecular mechanisms of regulation at different stages of inflammation.

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A Population of M2 Macrophages Associated With Bone Formation

Frontiers in Immunology ◽

10.3389/fimmu.2021.686769 ◽

2021 ◽

Vol 12 ◽

Author(s):

Elizabeth Olmsted-Davis ◽

Julio Mejia ◽

Elizabeth Salisbury ◽

Zbigniew Gugala ◽

Alan R. Davis

Keyword(s):

Bone Formation ◽

Tissue Regeneration ◽

Cell Sorting ◽

Brown Adipocyte ◽

M2 Macrophage ◽

M2 Macrophages ◽

Defect Model ◽

Specific Population ◽

M1 Macrophages ◽

Macrophage Populations

We previously identified transient brown adipocyte-like cells associated with heterotopic ossification (HO). These ancillary cells support new vessel synthesis essential to bone formation. Recent studies have shown that the M2 macrophage contributes to tissue regeneration in a similar way. To further define the phenotype of these brown adipocyte-like cells they were isolated and characterized by single-cell RNAseq (scRNAseq). Analysis of the transcriptome and the presence of surface markers specific for macrophages suggest that these cells are M2 macrophages. To validate these findings, clodronate liposomes were delivered to the tissues during HO, and the results showed both a significant reduction in these macrophages as well as bone formation. These cells were isolated and shown in culture to polarize towards either M1 or M2 similar to other macrophages. To confirm that these are M2 macrophages, mice received lipopolysacheride (LPS), which induces proinflammation and M1 macrophages. The results showed a significant decrease in this specific population and bone formation, suggesting an essential role for M2 macrophages in the production of bone. To determine if these macrophages are specific to HO, we isolated these cells using fluorescence-activated cell sorting (FACS) from a bone defect model and subjected them to scRNAseq. Surprisingly, the macrophage populations overlapped between the two groups (HO-derived versus callus) suggesting that they may be essential ancillary cells for bone formation in general and not selective to HO. Of further note, their unique metabolism and lipogenic properties suggest the potential for unique cross talk between these cells and the newly forming bone.

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M1 M2 macrophage expression in menstrual blood flakes of women with endometriosis

Majalah Obstetri & Ginekologi ◽

10.20473/mog.v24i2.4562 ◽

2017 ◽

Vol 24 (2) ◽

pp. 62

Author(s):

Yulisa Haslinda ◽

Hendy Hendarto ◽

Faroek Hoesin

Keyword(s):

Immunohistochemical Staining ◽

Menstrual Blood ◽

Control Group ◽

M2 Macrophage ◽

M2 Macrophages ◽

Cross Sectional ◽

M1 Macrophages ◽

Parametric Test ◽

Menstrual Cycles ◽

And Control

Objectives: to measure and prove the increase of panmacrophage, macrophages M1 and M2 expression and decrease of ratio of M1/M2 in menstrual blood flakes of women with endometriosis. Materials and Methods: This study was a cross sectional observational analytic study conducted on 30 subjects with endometriosis and non-endometriosis. Immunohistochemical staining was done on a sample of menstrual blood flakes of subjects study who were taken at the second or third day of menstrual cycles with CD68 and CD163 antibody to measure the expression of panmacrophage and M2 macrophages. Expression of M1 macrophages is the approach of a reduction expression of panmacrophage with M2 macrophages.Results: Expression of M1, M2 and the ratio M1/M2 in the both of groups had a normal distribution then continued by independent t-test with one-tailed α (0.05). Probability was considered statistically significant at p <0.05 with a confidence interval of 95%. Based on the statistical result, Mφ macrophage expression in endometriosis and control group amounted to 3.62 ± 0.50 and 2.80 ± 0.64 (p =0.0005) with non parametric test. The expression of M1 macrophages in endometriosis group and non endometriosis were respectively 1.40 ± 0.35 and 1.33 ± 0.40 (p =0.3005) and the expression of M2 in both of group, respectively of 2.23 ± 0.41 and 1.47 ± 0.36 (p =0.0005). The ratio of M1/M2, the endometriosis group and non endometriosis, respectively of 0.65 ± 0.20 and 0.92 ± 0.24 (p =0.0015).Conclusion: this study were significant increased in the panmacrophage Mφ, M2 macrophages expression on a woman's menstrual blood flakes endometriosis and significant decreased in ratio M1/M2 in the woman's menstrual blood flakes endometriosis.

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