Intestinal Lesions Containing Coronavirus-like Particles in Neonatal Necrotizing Enterocolitis: An Ultrastructural Analysis

PEDIATRICS ◽  
1984 ◽  
Vol 73 (2) ◽  
pp. 218-224
Author(s):  
S. Rousset ◽  
O. Moscovici ◽  
P. Lebon ◽  
J. P. Barbet ◽  
P. Helardot ◽  
...  

Since the outbreaks of neonatal necrotizing enterocolitis occurring in maternity hospitals of Paris and suburbs in 1979-1980, it has been possible to examine by light and electron microscopy gut specimens from ten newborns with this illness. Coronavirus-like particles, enclosed in intracytoplasmic vesicles of damaged epithelial cells of the intestinal mucosa, were observed in the small intestine, appendix, and colon. The ultrastructural study, supported by bacteriologic findings, suggests the role of coronavirus-like particles in the appearance of the lesions. Secondary proliferation of mainly anaerobic bacteria, probably responsible for pneumatosis, may aggravate the disease.

Author(s):  
J.E. Johnson

Although neuroaxonal dystrophy (NAD) has been examined by light and electron microscopy for years, the nature of the components in the dystrophic axons is not well understood. The present report examines nucleus gracilis and cuneatus (the dorsal column nuclei) in the brain stem of aging mice.Mice (C57BL/6J) were sacrificed by aldehyde perfusion at ages ranging from 3 months to 23 months. Several brain areas and parts of other organs were processed for electron microscopy.At 3 months of age, very little evidence of NAD can be discerned by light microscopy. At the EM level, a few axons are found to contain dystrophic material. By 23 months of age, the entire nucleus gracilis is filled with dystrophic axons. Much less NAD is seen in nucleus cuneatus by comparison. The most recurrent pattern of NAD is an enlarged profile, in the center of which is a mass of reticulated material (reticulated portion; or RP).


Life ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 579
Author(s):  
Fei Yang ◽  
Lingli Yang ◽  
Lanting Teng ◽  
Huimin Zhang ◽  
Ichiro Katayama

The role of Langerhans cells (LCs) in vitiligo pathogenesis remains unclear, with published studies reporting contradictory results regarding the quantity of LCs and no data on the features of LCs in vitiligo. Here, we aimed to analyze the presence, density, and morphological features of LCs in the epidermis of patients with vitiligo. Skin biopsies were stained for LCs using anti-CD1a/anti-langerin antibodies and analyzed by immunocytochemistry with light and electron microscopy. Compared with healthy controls, we detected significantly increased numbers of epidermal LCs in lesional skin from vitiligo in the progressive state. These LCs exhibited striking morphological alterations, including an elevated number of dendrites, with increased length and more branches than dendrites from controls. Ultrastructure examination via immuno-electron microscopy revealed markedly reduced Birbeck granules (BGs) and shorter BG rods in LCs from progressive vitiligo, with higher expression of langerin. Additionally, expression of S100B, the activity biomarker of vitiligo, was increased in these LCs. This work provides new insight on the cellular composition of LCs in vitiliginous skin, revealing altered morphology and increased LC numbers, with elevated S100B expression. Our data suggest LCs might play a critical role in vitiligo pathogenesis and thus may represent a novel therapeutic target for this disease.


PEDIATRICS ◽  
1980 ◽  
Vol 66 (6) ◽  
pp. 928-931 ◽  
Author(s):  
Randall Sturm ◽  
Joseph L. Staneck ◽  
Larry R. Stauffer ◽  
Wallace W. Neblett

The cause of neonatal necrotizing enterocolitis (NEC) is unknown. An association between NEC and clostridial infection has been reported from several centers, but the organisms have not been extensively characterized. Clostridium butyricum was isolated from the peritoneal fluid and cerebrospinal fluid of a neonate with NEC. The organism was resistant to the penicillins, but sensitive to vancomycin. Toxin production was demonstrated. Although the role of clostridial toxins in the pathogenesis of NEC is unknown, clostridial toxins are well established as the causes of two other intestinal diseases (antibiotic-associated pseudomembranous colitis and pig-bel). Further investigation of the role of clostridia in the pathogenesis of NEC and of the use of oral, nonabsorbable antibiotics in the treatment of NEC is needed.


1970 ◽  
Vol 44 (1) ◽  
pp. 151-171 ◽  
Author(s):  
Mary A. Bonneville ◽  
Melvyn Weinstock

The differentiation of the brush border which makes up the apical free surface of intestinal absorptive cells has been studied by electron microscopy. Specimens of Xenopus small intestine were fixed at various stages during metamorphosis, the time when a new intestinal epithelium forms. The interpretation of details described herein emphasizes the role of "surface-forming" vesicles. These vesicles are thought to provide membrane both for the initial expansion of the apical surface and for the later elongation of the microvilli. The latter are believed to be "molded" around filamentous cores that appear early in differentiation. The cores are attached to the apical membrane and extend vertically into the supranuclear cytoplasm. This interpretation rests chiefly on (a) the resemblance, both in morphology and in staining properties with colloidal thorium, between the membrane that limits the vesicles and that which limits the microvilli and (b) the distribution and time of appearance of the vesicles with respect to development of the microvilli. According to this view, the specific properties of surface membrane reside in preformed units that arise within the supranuclear cytoplasm. This morphogenetic process probably involves participation of the Golgi region as the site where the complex macromolecular architecture of the cell surface is assembled.


1988 ◽  
Vol 36 (7) ◽  
pp. 717-727 ◽  
Author(s):  
S J Hagen ◽  
J S Trier

We used post-embedding immunocytochemical techniques and affinity-purified anti-actin antibody to evaluate localization of actin in epithelial cells of small intestine by fluorescence and electron microscopy. Small intestine was fixed with 2% formaldehyde-0.1% glutaraldehyde and embedded in Lowicryl K4M. One-micron or thin sections were stained with antibody followed by rhodamine- or colloidal gold-labeled goat anti-rabbit IgG, respectively. Label was present overlying microvilli, the apical terminal web, and the cytoplasm directly adjacent to occluding and intermediate junctions. Label was associated with outer mitochondrial membranes of all cells and the supranuclear Golgi region of goblet cells. Lateral cytoplasmic interdigitations between mature cells and subplasmalemmal filaments next to intrusive cells were densely labeled. The cytoplasm adjacent to unplicated domains of lateral membrane was focally labeled. Label was prominent over organized filament bundles within the subplasmalemmal web at the base of mature cells, whereas there was focal labeling of the cytoplasm adjacent to the basal membrane of undifferentiated cells. Basolateral epithelial cell processes were labeled. Label was focally present overlying the cellular ground substance. Our results demonstrate that actin is distributed in a distinctive fashion within intestinal epithelial cells. This distribution suggests that in addition to its function as a structural protein, actin may participate in regulation of epithelial tight junction permeability, in motile processes including migration of cells from the crypt to the villus tip, in accommodation of intrusive intraepithelial cells and in adhesion of cells to one another and to their substratum.


2020 ◽  
Author(s):  
Xiuhao Zhao ◽  
Jin Zhou ◽  
Wenhua Liang ◽  
Qingfeng Sheng ◽  
Li Lu ◽  
...  

Abstract Background: Intestinal dysbiosis is believed to be one of the factors inducing neonatal necrotizing enterocolitis (NEC). Probiotics have been employed to treat NEC in a number of animal experiments and clinical trials, and some significant benefits of utilizing probiotics for the prevention or alleviation of NEC have been confirmed. However, the mechanism underlying the efficacy of probiotics in treating NEC has not been elucidated. Results: Impairment of the intestinal barrier, which was characterized by the decreased expression of tight junction components, was observed in the pathogenesis of NEC. The probiotic mixture alleviated this intestinal damage by enhancing the function of the barrier. Meanwhile, the probiotics remodeled the composition of the intestinal microbiota in NEC mice. Furthermore, increased expression of the pregnane X receptor ( PXR ) was observed after treatment with the probiotic mixture, and PXR overexpression in Caco-2 cells protected the barrier from lipopolysaccharide (LPS) damage. Further research showed that PXR could inhibit the phosphorylation of c-Jun N-terminal kinase (JNK) and could increase the expression of tight junction components. Conclusions: Our study confirmed that probiotics could ameliorate intestinal lesions by enhancing the function of the mucosal barrier. Specifically, probiotics may target PXR, which may subsequently enhance the expression of tight junction components by inhibiting the phosphorylation of JNK and enhancing the function of the barrier.


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