Omental and pleural milky spots: different reactivity patterns in mice infected with Schistosoma mansoni reveals coelomic compartmentalisation

Panasco, Mônica S; Pelajo-Machado, Marcelo; Lenzi, Henrique Leonel

doi:10.1590/s0074-02762010000400014

Cited by 11 publications

(8 citation statements)

References 25 publications

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“…Capillaries with high density and different levels constituted the basic skeleton of MS within the internal layer. Other H&E staining researches [ 11 , 27 , 42 , 46 , 47 ] found similar results that these purple cellular clusters stained by hematoxylin constitute MS together with pink blood vessels stained by eosin. However, immune cells could not be differentiated into specific types for further studies only by H&E staining.…”

Section: Histological Features Of Mssupporting

confidence: 63%

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Milky spots: omental functional units and hotbeds for peritoneal cancer metastasis

Liu

Geng

2016

Tumor Biol.

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As the most common metastatic disease of abdomen pelvic cavity cancer, peritoneal carcinomatosis (PC) renders significant negative impact on patient survival and quality of life. Invasive peritoneal exfoliated cancer cells (PECCs) preferentially select the omentum as a predominant target site for cancer cell colonization and proliferation compared with other tissues in the abdominal cavity. The precise pathogenic mechanism remains to be determined. As omental milky spots (MSs) are the major implantation site for malignant cells in peritoneal dissemination, researches on mechanisms of PC have been mainly focused on MS, primitive lymphoid tissues with unique structural features, and functional characteristics. To date, extensive biophysical and biochemical methods have been manipulated to investigate the MS exact function in the peritoneal cavity. This review summarized MS as hotbeds for PECC. The anatomical distribution was briefly described first. Then, MS histology was systematically reviewed, including morphological features, cellular constituents, and histological staining methods. At last, the roles of MS in PC pathological process were summarized with special emphasis on the distinct roles of macrophages.

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Section: Histological Features Of Mssupporting

confidence: 63%

“…Pleural and peritoneal cavities are repositories of MS [ 27 ]. In pleural cavity, MSs seem to be located mainly in the pleural fold behind the pericardium rather than lung parenchyma [ 27 ]. However, MS can be found in many tissues in abdomen pelvic cavities.…”

Section: Anatomical Distribution Of Msmentioning

confidence: 99%

Milky spots: omental functional units and hotbeds for peritoneal cancer metastasis

Liu

Geng

2016

Tumor Biol.

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“…Upon immune challenge, these structures support rapid activation of serous B cells and germinal center formation 13 15 . The existence of similar lymphoid structures has been reported in the adipose deposits of the pleural cavity, the mediastinum 13 16 17 18 and the pericardium 13 . Although the density of FALCs in pericardium and mediastinum is high 13 , the functional role of these clusters has not been investigated.…”

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confidence: 65%

Fat-associated lymphoid clusters control local IgM secretion during pleural infection and lung inflammation

et al. 2016

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Fat-associated lymphoid clusters (FALC) are inducible structures that support rapid innate-like B-cell immune responses in the serous cavities. Little is known about the physiological cues that activate FALCs in the pleural cavity and more generally the mechanisms controlling B-cell activation in FALCs. Here we show, using separate models of pleural nematode infection with Litomosoides sigmodontis and Altenaria alternata induced acute lung inflammation, that inflammation of the pleural cavity rapidly activates mediastinal and pericardial FALCs. IL-33 produced by FALC stroma is crucial for pleural B1-cell activation and local IgM secretion. However, B1 cells are not the direct target of IL-33, which instead requires IL-5 for activation. Moreover, lung inflammation leads to increased IL-5 production by type 2 cytokine-producing innate lymphoid cells (ILC2) in the FALC. These findings reveal a link between inflammation, IL-33 release by FALC stromal cells, ILC2 activation and pleural B-cell activation in FALCs, resulting in local and antigen-specific IgM production.

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“…During schistosomiasis, peritoneal cells react against S. mansoni antigens (Panasco et al 2010). The peritoneal cavity is a reservoir of circulating leukocytes, including monocytes, T and B lymphocytes and granulocytes frequently detected attached in the omentum and mesentery (Carlow et al 2009;Lenzi et al 1996).…”

Section: Discussionmentioning

confidence: 99%

Lack of galectin-3 up-regulates IgA expression by peritoneal B1 lymphocytes during B cell differentiation

et al. 2015

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Galectin-3 is a β-galactoside-binding protein with an inhibitory role in B cell differentiation into plasma cells in distinct lymphoid tissues. We use a model of chronic schistosomiasis, a well-characterized experimental disease hallmarked by polyclonal B cell activation, in order to investigate the role of galectin-3 in controlling IgA production through peritoneal B1 cells. Chronically infected, galectin-3-deficient mice (Lgals3 −/− ) display peritoneal fluid hypercellularity, increased numbers of atypical peritoneal IgM + /IgA + B1a and B1b lymphocytes and histological disturbances in plasma cell niches when compared with Lgals3 + / + mice. Similar to our infection model, peritoneal B1 cells from uninfected Lgals3 −/− mice show enhanced switching to IgA after in vitro treatment with interleukin-5 plus transforming growth factor-β (IL-5 + TGF-β1). A higher number of IgA + B1a lymphocytes was found in the peritoneal cavity of Lgals3 −/− -uninfected mice at 1 week after i.p. injection of IL-5 + TGF-β1; this correlates with the increased levels of secreted IgA detected in the peritoneal fluid of these mice after cytokine treatment. Interestingly, a higher number of degranulated mast cells is present in the peritoneal cavity of uninfected and Schistosoma mansoni-infected Lgals3 −/− mice, indicating that, at least in part, mast cells account for the enhanced differentiation of B1 into IgAproducing B cells found in the absence of galectin-3. Thus, a novel role is revealed for galectin-3 in controlling the expression of surface IgA by peritoneal B1 lymphocytes; this might have important implications for manipulating the mucosal immune response.

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Omental and pleural milky spots: different reactivity patterns in mice infected with Schistosoma mansoni reveals coelomic compartmentalisation

Cited by 11 publications

References 25 publications

Milky spots: omental functional units and hotbeds for peritoneal cancer metastasis

Milky spots: omental functional units and hotbeds for peritoneal cancer metastasis

Fat-associated lymphoid clusters control local IgM secretion during pleural infection and lung inflammation

Lack of galectin-3 up-regulates IgA expression by peritoneal B1 lymphocytes during B cell differentiation

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