Coronavirus?

To the Editor.— We read with great interest the paper by Rousset et al1 in which the presence of coronavirus-like particles in intestinal lesions of neonates with necrotizing enterocolitis was described. The presence of viral particles in thin-sectioned material is often difficult to demonstrate because of the striking similarity of some viral particles to normal cell organelles and structures. We agree with the authors that coronavirus-like particles may be an etiologic agent in some cases of neonatal necrotizing enterocolitis of nonbacterial origin2,3; we do not agree, however, that their published electron micrographs unequivocally demonstrate viral particles.

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

PEDIATRICS ◽

10.1542/peds.73.2.218 ◽

1984 ◽

Vol 73 (2) ◽

pp. 218-224

Author(s):

S. Rousset ◽

O. Moscovici ◽

P. Lebon ◽

J. P. Barbet ◽

P. Helardot ◽

...

Keyword(s):

Electron Microscopy ◽

Small Intestine ◽

Necrotizing Enterocolitis ◽

Intestinal Mucosa ◽

Light And Electron Microscopy ◽

Anaerobic Bacteria ◽

Intestinal Lesions ◽

Maternity Hospitals ◽

Neonatal Necrotizing Enterocolitis

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.

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Probiotics Mixture Reinforces Barrier Function to Ameliorate Necrotizing Enterocolitis by Regulating PXR-JNK Pathway

10.21203/rs.3.rs-61658/v2 ◽

2020 ◽

Author(s):

Xiuhao Zhao ◽

Jin Zhou ◽

Wenhua Liang ◽

Qingfeng Sheng ◽

Li Lu ◽

...

Keyword(s):

Tight Junction ◽

Necrotizing Enterocolitis ◽

Animal Experiments ◽

Intestinal Barrier ◽

Pregnane X Receptor ◽

Mucosal Barrier ◽

Intestinal Damage ◽

Jnk Pathway ◽

Intestinal Lesions ◽

Neonatal Necrotizing Enterocolitis

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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Probiotics mixture reinforces barrier function to ameliorate necrotizing enterocolitis by regulating PXR-JNK pathway

Cell & Bioscience ◽

10.1186/s13578-021-00530-7 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Xiuhao Zhao ◽

Jin Zhou ◽

Wenhua Liang ◽

Qingfeng Sheng ◽

Li Lu ◽

...

Keyword(s):

Tight Junction ◽

Necrotizing Enterocolitis ◽

Animal Experiments ◽

Intestinal Barrier ◽

Pregnane X Receptor ◽

Mucosal Barrier ◽

Intestinal Damage ◽

Jnk Pathway ◽

Intestinal Lesions ◽

Neonatal Necrotizing Enterocolitis

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 enhance the function of the barrier.

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Probiotics Mixture Reinforces Barrier Function to Ameliorate Necrotizing Enterocolitis by Regulating PXR-JNK Pathway

10.21203/rs.3.rs-61658/v1 ◽

2020 ◽

Author(s):

Xiuhao Zhao ◽

Jin Zhou ◽

Wenhua Liang ◽

Qingfeng Sheng ◽

Li Lu ◽

...

Keyword(s):

Tight Junction ◽

Necrotizing Enterocolitis ◽

Animal Experiments ◽

Intestinal Barrier ◽

Pregnane X Receptor ◽

Mucosal Barrier ◽

Intestinal Damage ◽

Jnk Pathway ◽

Intestinal Lesions ◽

Neonatal Necrotizing Enterocolitis

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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Probiotics Mixture Reinforces Barrier Function to Ameliorate Necrotizing Enterocolitis by Regulating PXR-JNK Pathway

10.21203/rs.3.rs-61658/v3 ◽

2021 ◽

Author(s):

Xiuhao Zhao ◽

Jin Zhou ◽

Wenhua Liang ◽

Qingfeng Sheng ◽

Li Lu ◽

...

Keyword(s):

Tight Junction ◽

Necrotizing Enterocolitis ◽

Animal Experiments ◽

Intestinal Barrier ◽

Pregnane X Receptor ◽

Mucosal Barrier ◽

Intestinal Damage ◽

Jnk Pathway ◽

Intestinal Lesions ◽

Neonatal Necrotizing Enterocolitis

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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A rapid method for the direct identification of paramyxovirus in canine CSF by ultracentrifugation and negative staining as a rule out for distemper

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100160522 ◽

1990 ◽

Vol 48 (3) ◽

pp. 594-595

Author(s):

W.L. Steffens ◽

M.B. Ard ◽

C.E. Greene ◽

A. Jaggy

Keyword(s):

Subacute Sclerosing Panencephalitis ◽

Clinical Signs ◽

Viral Disease ◽

Etiologic Agent ◽

Mucosal Inflammation ◽

Worldwide Distribution ◽

Negative Stain ◽

Viral Particles ◽

Systemic Manifestations ◽

Rule Out

Canine distemper is a multisystemic contagious viral disease having a worldwide distribution, a high mortality rate, and significant central neurologic system (CNS) complications. In its systemic manifestations, it is often presumptively diagnosed on the basis of clinical signs and history. Few definitive antemortem diagnostic tests exist, and most are limited to the detection of viral antigen by immunofluorescence techniques on tissues or cytologic specimens or high immunoglobulin levels in CSF (cerebrospinal fluid). Diagnosis of CNS distemper is often unreliable due to the relatively low cell count in CSF (<50 cells/μl) and the binding of blocking immunoglobulins in CSF to cell surfaces. A more reliable and definitive test might be possible utilizing direct morphologic detection of the etiologic agent. Distemper is the canine equivalent of human measles, in that both involve a closely related member of the Paramyxoviridae, both produce mucosal inflammation, and may produce CNS complications. In humans, diagnosis of measles-induced subacute sclerosing panencephalitis is through negative stain identification of whole or incomplete viral particles in patient CSF.

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