Genetic fate-mapping reveals surface accumulation but not deep organ invasion of pleural and peritoneal cavity macrophages following injury.
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ABSTRACT:
SUBMITTER: Jin H
PROVIDER: S-EPMC8129080 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Recruitment of bone marrow derived monocytes via bloodstream and their subsequent conversion to CX3CR1+ macrophages in response to intestinal injury is dependent on CCR2, Nr4a1, and the microbiome. This process is critical for proper tissue repair; however, GATA6+ peritoneal cavity macrophages might represent an alternative, more readily available source of mature and functional myeloid cells at the damaged intestinal locations. Here we show, using spinning-disk confocal microscopy, that large F4/80hiGATA6+ peritoneal cavity macrophages promptly accumulate at damaged intestinal sites upon intestinal thermal injury and upon dextran sodium sulfate induced colitis in mice via a direct route from the peritoneal cavity. In contrast to bloodstream derived monocytes/macrophages, cavity macrophages do not depend on CCR2, Nr4a1 or the microbiome for recruitment, but rather on the ATP-release and exposed hyaluronan at the site of injury. They participate in the removal of necrotic cells, revascularization and collagen deposition and thus resolution of tissue damage. In summary, peritoneal cavity macrophages represent a rapid alternative route of intestinal tissue repair to traditional monocyte-derived macrophages.
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Project description:Macrophages resident in different organs express distinct genes, but understanding how this diversity fits into tissue-specific features is limited. Here, we show that selective expression of coagulation factor V (FV) by resident peritoneal macrophages in mice promotes bacterial clearance in the peritoneal cavity and serves to facilitate the well-known but poorly understood "macrophage disappearance reaction." Intravital imaging revealed that resident macrophages were nonadherent in peritoneal fluid during homeostasis. Bacterial entry into the peritoneum acutely induced macrophage adherence and associated bacterial phagocytosis. However, optimal control of bacterial expansion in the peritoneum also required expression of FV by the macrophages to form local clots that effectively brought macrophages and bacteria in proximity and out of the fluid phase. Thus, acute cellular adhesion and resident macrophage-induced coagulation operate independently and cooperatively to meet the challenges of a unique, open tissue environment. These events collectively account for the macrophage disappearance reaction in the peritoneal cavity.
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Project description:The goal of this study is to compare the transcriptome profile (RNA-seq) of peritoneal cavity macrophages of RXRa-deficient and WT mice to identify genes which are controlled by the expression of the TF RXRa
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Project description:The understanding of toxicological and pharmacological profiles of nanomaterials is an important step for the development and clinical application of nanomedicines. Carbon nanotubes (CNTs) have been extensively explored as a nanomedicine agent in pharmaceutical/biomedical applications, such as drug delivery, bioimaging, and tissue engineering. The biological durability of CNTs could affect the function of CNTs-based nanomedicines as well as their toxicity in cells and tissues. Therefore, it is crucial to assess the fate of nanomedicine in phagocytes. Herein, we investigated the candidate fate of acid-oxidized single-walled carbon nanotubes (SWNCTs) in non-activated primary mouse peritoneal macrophages (PMQ). The sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) results showed that the intracellular SWCNTs continued growing from 4 to 36 h in PMQ. After replacing the exposure medium, we found the exosome induced by SWCNTs on the surface of macrophages according to scanning electron microscope (SEM) observation. The near-infrared (NIR) absorption increase of the supernatant samples after post-exposure indicates that SWCNTs exocytosis occurred in PMQ. The decreasing intracellular SWCNTs amount suggested the incomplete biodegradation in PMQ, which was confirmed by Raman spectroscopy and transmission electron microscopy (TEM). The combined data reveal that SWCNTs could be retained for more than 60 h in macrophages. Then sustainable retention of SWCNTs in primary macrophages was coexist with exocytosis and biodegradation. The findings of this work will shed light on the bioimaging, diagnosis and other biomedical applications of CNTs-based nanomedicines.
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Project description:Peritoneal and pleural resident macrophages in the mouse share common features and in each compartment exist as two distinct subpopulations: F4/80(+) macrophages and MHC II(+) CD11c(+) macrophages. F4/80(+) macrophages derive from embryonic precursors, and their maintenance is controlled by Gata6. However, the origin and regulatory factors that maintain MHC II(+) macrophages remain unknown. Here, we show that the MHC II(+) macrophages arise postnatally from CCR2-dependent precursors that resemble monocytes. Monocytes continuously replenish this subset through adulthood. Gene expression analysis identified distinct surface markers like CD226 and revealed that the transcription factor IRF4 was selectively expressed in these macrophages relative to other organs. Monocytes first entered peritoneal or pleural cavities to become MHC II(+) cells that up-regulated CD226 and CD11c later as they continued to mature. In the absence of IRF4 or after administration of oral antibiotics, MHC II(+)CD226(-)CD11c(-) monocyte-derived cells accumulated in peritoneal and pleural cavities, but CD11c(+) CD226(+) macrophages were lost. Thus, MHC II(+) resident peritoneal and pleural macrophages are continuously replenished by blood monocytes recruited to the peritoneal and pleural cavities constitutively, starting after birth, where they require IRF4 and signals likely derived from the microbiome to fully differentiate.
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Project description:Microglia are the resident macrophages of the central nervous system and are associated with the pathogenesis of many neurodegenerative and brain inflammatory diseases; however, the origin of adult microglia remains controversial. We show that postnatal hematopoietic progenitors do not significantly contribute to microglia homeostasis in the adult brain. In contrast to many macrophage populations, we show that microglia develop in mice that lack colony stimulating factor-1 (CSF-1) but are absent in CSF-1 receptor-deficient mice. In vivo lineage tracing studies established that adult microglia derive from primitive myeloid progenitors that arise before embryonic day 8. These results identify microglia as an ontogenically distinct population in the mononuclear phagocyte system and have implications for the use of embryonically derived microglial progenitors for the treatment of various brain disorders.
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Project description:BackgroundThoracic endometriosis-related pneumothorax is a secondary spontaneous pneumothorax caused by thoracic endometriosis. Diaphragmatic endometriosis is well-studied, but visceral and/or parietal pleural lesions are not. Although surgery is an effective treatment, postoperative recurrence rates are unsatisfactory probably due to inadequate understanding of underlying pathophysiology. We aimed to clarify the clinicopathological features of thoracic endometriosis.MethodsIn total, 160 patients who underwent thoracoscopic surgery from a single institution with histopathologically proven thoracic endometriosis from January 2015 to December 2019 were included. Clinicopathological characteristics and surgical outcomes were assessed retrospectively.ResultsThe cohort median age was 41 (range 22-53) years. Pneumothorax was right-sided in 159 (99.4%) and left-sided in only 1 (0.6%) case. Visceral and parietal pleural lesions were diagnosed in 79 (49.4%) and 71 (44.4%) patients, respectively. In total, 104 visceral pleural lesions and 101 parietal pleural lesions were detected. The S4 region and the dorsal 6th intercostal space contained the largest number of visceral pleural (66 lesions) and parietal pleural lesions (25 lesions), respectively. Histopathological evaluation revealed endometriotic tissues, existing in the outer external elastic layer in all lesions, were localized or invaded deeply. The median follow-up period was 370 (range, 6-1824) days. The Kaplan-Meier method revealed that the 1- and 2-year postoperative recurrence rates were 13.8% and 19.3%, respectively.ConclusionsVisceral pleural endometriotic lesions may be disseminated from the visceral pleural surface and infiltrate into the pleura. Intraoperatively, careful observation of the specific sites, such as the visceral pleura of S4 and the parietal pleura of 6th intercostal space, is important to reduce postoperative recurrence.
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