Macrophages display proinflammatory phenotypes in the eutopic endometrium of women with endometriosis with relevance to an infectious etiology of the disease.
Fertil Steril
; 112(6): 1118-1128, 2019 12.
Article
in En
| MEDLINE
| ID: mdl-31843088
ABSTRACT
OBJECTIVE:
To phenotype transcriptomically M1 macrophages (MÏ1) and M2 macrophages (MÏ2) in the endometrium of women with endometriosis.DESIGN:
Prospective experimental study.SETTING:
University research laboratory. PATIENT(S) Six women with endometriosis and five controls without disease, in the secretory phase of the menstrual cycle. INTERVENTION(S) MÏ1, MÏ2, uterine natural killer, and T regulatory cells were isolated from human endometrium using a uniquely designed cell-specific fluorescence activating cell sorting panel. Transcriptome profiles were assessed by RNA high sequencing, bioinformatics, and biological pathway analyses. MAIN OUTCOMES MEASURE(S) Differential gene expression between MÏ1 and MÏ2 in women with and without endometriosis and in MÏ1 versus MÏ2 in each group was determined and involved different biologic and signaling pathways. RESULT(S) Flow cytometry analysis showed no significant differences in total numbers of leukocytes between control and endometriosis groups, although MÏ1 were higher in the endometriosis group versus controls. Statistical transcriptomic analysis was performed only in MÏ1 and MÏ2 populations due to larger sample sizes. Bioinformatic analyses revealed that in women with endometriosis, endometrial MÏ1 are more proinflammatory than controls and that MÏ2 paradoxically have a proinflammatory phenotype. CONCLUSION(S) As MÏ are phenotypically plastic and their polarization state depends on their microenvironment, the altered endometrial environment in women with endometriosis may promote endometrial MÏ2 polarization and an MÏ1 proinflammatory phenotype. Moreover, aberrant phenotypes of MÏ may contribute to abnormal gene expression of the eutopic endometrium and a proinflammatory environment in women with endometriosis relevant to the pathophysiology of the disease and compromised reproductive outcomes.Key words
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Endometriosis
/
Endometrium
/
Transcriptome
/
Cell Plasticity
/
Macrophage Activation
/
Macrophages
Type of study:
Etiology_studies
/
Observational_studies
Limits:
Adult
/
Female
/
Humans
/
Middle aged
Language:
En
Journal:
Fertil Steril
Year:
2019
Document type:
Article