In women, endometrial breakdown, which is experienced as menstruation, is characterised by high concentrations of inflammatory mediators and immune cells which account for ~40% of the stromal compartment during tissue shedding. These inflammatory cells are known to play a pivotal role in tissue breakdown but their contribution to the rapid scarless repair of endometrium remains poorly understood. In the current study we used a mouse model of menstruation to investigate dynamic changes in mononuclear phagocytes during endometrial repair and remodelling. Menstruation was simulated in MacGreen mice to allow visualisation of CSF1R+ mononuclear phagocytes. Immunohistochemistry revealed dynamic spatio-temporal changes in numbers and location of CSF1R-EGFP+ cells and Ly6G+ neutrophils. Flow cytometry confirmed a striking increase in numbers of GFP+ cells during repair (24 h): influxed cells were 66% F4/80+Gr-1+ and 30% F4/80−Gr-1+. Immunostaining identified distinct populations of putative ‘classical’ monocytes (GFP+F4/80−), monocyte-derived macrophages (GFP+F4/80+) and a stable population of putative tissue-resident macrophages (GFP-F4/80+) localised to areas of breakdown, repair and remodelling respectively. Collectively, these data provide the first compelling evidence to support a role for different populations of monocytes/macrophages in endometrial repair and provide the platform for future studies on the role of these cells in scarless healing.

/pdf/evidence-for-a-dynamic-role-for-mononuclear-phagocytes-54vhnj6e5j.pdf

Evidence for a dynamic role for mononuclear phagocytes during endometrial repair and remodelling

Phagocytosis is the necessary corollary of apoptosis. It leads to the clearance of apoptotic cells by phagocytes, which can be 'professional' or 'amateur'. I review the known molecular aspects of phagocytosis of apoptotic corpses in mammals, Caenorhabditis elegans and Drosophila melanogaster from the point of view of the phagocyte and the apoptotic corpse. I highlight recent advances made in the field and discuss the physiological outcomes and consequences of this process. Indeed, phagocytosis of apoptotic cells is important in shaping or remodeling tissues to maintain their integrity and specialized functions during development and wound healing. It also contributes to the development of inflammation and/or its resolution after an injury or infection. This perhaps explains why the molecular mechanisms of phagocytosis of apoptotic cells are redundant and complex in mammals and suggests why they appear to have been mostly conserved through evolution. Caenorhabditis elegans has already proven to be useful in genetically dissecting the molecular mechanisms underlying phagocytosis of apoptotic corpses by 'amateur' neighboring cells. Drosophila melanogaster will become the model of choice in genetically dissecting the molecular mechanisms underlying phagocytosis of apoptotic cells by 'professional' phagocytes such as macrophages.

Phagocytosis of apoptotic cells in mammals, caenorhabditis elegans and drosophila melanogaster: molecular mechanisms and physiological consequences

Background Estrogens are known to orchestrate reproductive events and to regulate the immune system during infections and following tissue damage. Recent findings suggest that, in the absence of any danger signal, estrogens trigger the physiological expansion and functional specialization of macrophages, which are immune cells that populate the female reproductive tract (FRT) and are increasingly being recognized to participate in tissue homeostasis beyond their immune activity against infections. Although estrogens are the only female gonadal hormones that directly target macrophages, a comprehensive view of this endocrine-immune communication and its involvement in the FRT is still missing. Objective and rationale Recent accomplishments encourage a revision of the literature on the ability of macrophages to respond to estrogens and induce tissue-specific functions required for reproductive events, with the aim to envision macrophages as key players in FRT homeostasis and mediators of the regenerative and trophic actions of estrogens. Search methods We conducted a systematic search using PubMed and Ovid for human, animal (rodents) and cellular studies published until 2018 on estrogen action in macrophages and the activity of these cells in the FRT. Outcomes Our search identified the remarkable ability of macrophages to activate biochemical processes in response to estrogens in cell culture experiments. The distribution at specific locations, interaction with selected cells and acquisition of distinct phenotypes of macrophages in the FRT, as well as the cyclic renewal of these properties at each ovarian cycle, demonstrate the involvement of these cells in the homeostasis of reproductive events. Moreover, current evidence suggests an association between estrogen-macrophage signaling and the generation of a tolerant and regenerative environment in the FRT, although a causative link is still missing. Wider implications Dysregulation of the functions and estrogen responsiveness of FRT macrophages may be involved in infertility and estrogen- and macrophage-dependent gynecological diseases, such as ovarian cancer and endometriosis. Thus, more research is needed on the physiology and pharmacological control of this endocrine-immune interplay.

/pdf/the-estrogen-macrophage-interplay-in-the-homeostasis-of-the-4yzvkis8q7.pdf

The estrogen-macrophage interplay in the homeostasis of the female reproductive tract.

Colony-stimulating factor-1 (CSF-1), also known as macrophage-colony stimulating factor (M-CSF), is the primary growth factor regulating survival, proliferation and differentiation of macrophages It is also a potent chemokine for macrophages and monocytes Signaling via the CSF-1 receptor (CSF-1R) is necessary for the production of almost all tissue resident macrophage populations and these macrophages participate, via trophic mechanisms, in the normal development and homeostasis of tissues and organs in which they reside, including the mammary gland The drawback of this close interaction between macrophages and parenchymal cells is that dysregulation of macrophage trophic functions assists in the development and progression of many cancers, including breast cancer Furthermore, tumour cells secrete CSF-1 to attract more macrophages to the tumour microenvironment where CSF-1R signaling frequently drives the behaviour of these tumour-associated macrophages (TAMs) to promote tumour progression and metastasis Evidence is mounting that treated tumours secrete more CSF-1 and the increased recruitment of TAMs limits treatment efficacy Thus, therapeutic targeting of the CSF-1R to inhibit TAM function is likely to enhance tumour response and improve patient outcomes in the treatment of cancer, including breast cancer

CSF-1R Signaling in Health and Disease: A Focus on the Mammary Gland

One-fifth of cancer deaths are associated with obesity. Because the molecular mechanisms by which obesity affects the progression of ovarian cancer (OC) are poorly understood, we investigated if obesity could promote the progression of OC cells using the postmenopausal ob/ob mouse model and peritoneal dissemination of mouse ID8 OC cells. Compared to lean mice, obese mice had earlier OC occurrence, greater metastasis throughout the peritoneal cavity, a trend toward shorter survival, and higher circulating glucose and proinflammatory chemokine CXCL1 levels. Ascites in obese mice had higher levels of macrophages (Mφ) and chemokines including CCL2, CXCL12, CXCL13, G-CSF and M-CSF. Omental tumor tissues in obese mice had more adipocytes than lean mice. Our data suggest that obesity may accelerate the peritoneal dissemination of OC through higher production of pro-inflammatory chemokines and Mφ recruitment.

Obesity-Induced Peritoneal Dissemination of Ovarian Cancer and Dominant Recruitment of Macrophages in Ascites

There are large numbers of macrophages in the uterus of normal mice. During estrus and metestrus endometrial epithelial cells express macrophage colony-stimulating factor (M-CSF). Numbers of uterine macrophages showed cyclic changes and accumulated beneath the endometrial epithelial cells at estrus and metestrus. However, numbers of uterine macrophages in osteopetrotic (op/op) mice were reduced tenfold compared with normal littermate mice and op/op mouse macrophages were ultrastructurally immature throughout the estrous cycle. Several macrophage chemokines were produced in the uterus. However, administration of antibody against the macrophage colony stimulating factor receptor (c-fms) severely diminished the number of uterine macrophages in normal littermate mice, implying that M-CSF plays a major role in macrophage recruitment in the uterus. Endometrial epithelial cells underwent apoptosis at estrus and metestrus and were disposed into the uterine lumen in op/op mice and littermate mice. In littermate mice a large number of macrophages accumulated beneath the endometrial epithelial cells and actively removed apoptotic cells. In contrast, there were few macrophages in op/op mice and clearance of apoptotic cells by macrophages was defective in the uterus of these mice. Thus M-CSF plays important roles in the recruitment and differentiation of macrophages and in scavenging effete epithelial cells in the uterus.

Defective macrophage recruitment and clearance of apoptotic cells in the uterus of osteopetrotic mutant mice lacking macrophage colony-stimulating factor (M-CSF).

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Defective macrophage recruitment and clearance of apoptotic cells in the uterus of osteopetrotic mutant mice lacking macrophage colony-stimulating factor (M-CSF).