scholarly journals Study on the Mechanism of Injury of Chicken Tracheal Epithelium Caused by Mycoplasma Gallisepticum Infection

2021 ◽  
Author(s):  
Chunlin WU ◽  
Lemiao Zhong ◽  
Ligen Zhang ◽  
Wenji Li ◽  
Binhui Liu ◽  
...  
Keyword(s):  
Immunohistochemical Analysis ◽  
Mycoplasma Gallisepticum ◽  
Chronic Respiratory Disease ◽  
Immune Defense ◽  
Sequencing Analysis ◽  
Tracheal Mucosa ◽  
Respiratory Epithelial Cells ◽  
Epithelial Injury ◽  
Junction Protein ◽  
Respiratory Epithelial

Abstract Mycoplasma gallisepticum (MG) is a pathogenic microorganism that is seriously harmful to the poultry industry. It mainly adsorbs on the cilia and mucosa of respiratory epithelial cells, resulting in tracheal mucosal epithelial injury or ciliary shedding, causing chronic respiratory disease (CRD). In order to study the damage of tracheal mucosal epithelium induced by MG infection in chickens and explore its possible mechanism, SPF chicks were challenged with the wild-type Mycoplasma gallisepticum strain MG-HY strain. Then, transcriptome sequencing analysis was performed to study the mechanism of MG tracheal mucosal epithelial injury. During infection, MG localizes and proliferates in the chicken trachea, and induces mucosal epithelial damage.A total of 3112 significantly (P < 0.01) differentially expressed genes (DEGs) were selected by RNA-seq, including 1646 up-regulated genes and 1466 down-regulated genes. Functional analysis showed increased expression levels of genes involved in immune defense response and mechanical barrier of tracheal mucosa in infected chicks. The expression level of pro-inflammatory cytokines (TNF-α) increased, activating the upstream protein Ras of the ERK-MLCK signaling pathway, Ras causing ERK1/2 phosphorylation levels to rise and MLCK activation, thus causing phosphationalization of MLC, and further regulating the expression and mucous distribution of tight junction protein (TJ), leading to tracheal mucosal epithelial injury in chicks. The results of qRT-PCR assay and immunohistochemical analysis were consistent with the results of transcriptome analysis. Overall, our results provide a basis for further investigation of the mechanisms underlying the epithelial damage of the tracheal membrane in chicks caused by MG-infection, contributing to the understanding of how MG affects avian respiratory diseases.

X-Ray Microanalysis of Respiratory Epithelial Cells in the Study of Cystic Fibrosis

1990 ◽  
Vol 48 (2) ◽  
pp. 352-353
Author(s):  
Godfried M. Roomans ◽  
Samuel Sagström ◽  
Joke L.M. Ceulemans ◽  
Jan Bijman
Keyword(s):  
Cystic Fibrosis ◽  
Epithelial Cells ◽  
Water Transport ◽  
Clinical Symptoms ◽  
Chloride Secretion ◽  
Tracheal Mucosa ◽  
Respiratory Epithelial Cells ◽  
X Ray ◽  
Airway Infections ◽  
Respiratory Epithelial

One of the most important clinical symptoms associated with cystic fibrosis (CF) is obstructive airway disease and recurrent airway infections. The smaller airways in CF patients are blocked by viscous mucus, and infections are common and difficult to manage. Generally, lung disease is directly or indirectly the cause of death in CF. The viscous mucus in CF is likely to be a result of defective water transport in the respiratory epithelium. Water transport is coupled to chloride secretion, and it is strongly suspected that a defective chloride channel in the apical membrane of the respiratory epithelial cells is the basic error in CF. We therefore studied changes in the intracellular concentration of chloride (and other ions) by x-ray microanalysis of cultured respiratory epithelial cells under a variety of conditions.Tissues were obtained from material excised during polypectomy. The tracheal mucosa was digested with collagenase and the dispersed cells were plated onto Milliporefilters coated with human placental collagen.

scholarly journals Differential Response of the Chicken Trachea to Chronic Infection with Virulent Mycoplasma gallisepticum Strain Ap3AS and Vaxsafe MG (Strain ts-304): a Transcriptional Profile

2020 ◽  
Vol 88 (5) ◽  
Author(s):  
Sathya N. Kulappu Arachchige ◽  
Neil D. Young ◽  
Pollob K. Shil ◽  
Alistair R. Legione ◽  
Anna Kanci Condello ◽  
...  
Keyword(s):  
Cytokine Production ◽  
Mycoplasma Gallisepticum ◽  
Chronic Respiratory Disease ◽  
Tracheal Mucosa ◽  
Content Type ◽  
Motor Movement ◽  
Cilia Formation ◽  
Junctional Complexes ◽  
Protein Classes ◽  
Gene Ontologies

ABSTRACT Mycoplasma gallisepticum is the primary etiological agent of chronic respiratory disease in chickens. Live attenuated vaccines are most commonly used in the field to control the disease, but current vaccines have some limitations. Vaxsafe MG (strain ts-304) is a new vaccine candidate that is efficacious at a lower dose than the current commercial vaccine strain ts-11, from which it is derived. In this study, the transcriptional profiles of the trachea of unvaccinated chickens and chickens vaccinated with strain ts-304 were compared 2 weeks after challenge with M. gallisepticum strain Ap3AS during the chronic stage of infection. After challenge, genes, gene ontologies, pathways, and protein classes involved in inflammation, cytokine production and signaling, and cell proliferation were upregulated, while those involved in formation and motor movement of cilia, formation of intercellular junctional complexes, and formation of the cytoskeleton were downregulated in the unvaccinated birds compared to the vaccinated birds, reflecting immune dysregulation and the pathological changes induced in the trachea by infection with M. gallisepticum. Vaccination appears to protect the structural and functional integrity of the tracheal mucosa 2 weeks after infection with M. gallisepticum.

scholarly journals SARS-CoV-2 drives JAK1/2-dependent local complement hyperactivation

2021 ◽  
Vol 6 (58) ◽  
pp. eabg0833
Author(s):  
Bingyu Yan ◽  
Tilo Freiwald ◽  
Daniel Chauss ◽  
Luopin Wang ◽  
Erin West ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Clinical Manifestations ◽  
Lung Epithelial Cells ◽  
Complement Factor ◽  
Respiratory Epithelial Cells ◽  
Signature Genes ◽  
Wide Range ◽  
Lung Epithelial ◽  
Gene Transcripts ◽  
Respiratory Epithelial

Patients with coronavirus disease 2019 (COVID-19) present a wide range of acute clinical manifestations affecting the lungs, liver, kidneys and gut. Angiotensin converting enzyme (ACE) 2, the best-characterized entry receptor for the disease-causing virus SARS-CoV-2, is highly expressed in the aforementioned tissues. However, the pathways that underlie the disease are still poorly understood. Here, we unexpectedly found that the complement system was one of the intracellular pathways most highly induced by SARS-CoV-2 infection in lung epithelial cells. Infection of respiratory epithelial cells with SARS-CoV-2 generated activated complement component C3a and could be blocked by a cell-permeable inhibitor of complement factor B (CFBi), indicating the presence of an inducible cell-intrinsic C3 convertase in respiratory epithelial cells. Within cells of the bronchoalveolar lavage of patients, distinct signatures of complement activation in myeloid, lymphoid and epithelial cells tracked with disease severity. Genes induced by SARS-CoV-2 and the drugs that could normalize these genes both implicated the interferon-JAK1/2-STAT1 signaling system and NF-κB as the main drivers of their expression. Ruxolitinib, a JAK1/2 inhibitor, normalized interferon signature genes and all complement gene transcripts induced by SARS-CoV-2 in lung epithelial cell lines, but did not affect NF-κB-regulated genes. Ruxolitinib, alone or in combination with the antiviral remdesivir, inhibited C3a protein produced by infected cells. Together, we postulate that combination therapy with JAK inhibitors and drugs that normalize NF-κB-signaling could potentially have clinical application for severe COVID-19.

scholarly journals Lycopene Inhibits Toll-Like Receptor 4-Mediated Expression of Inflammatory Cytokines in House Dust Mite-Stimulated Respiratory Epithelial Cells

Molecules ◽  
2021 ◽  
Vol 26 (11) ◽  
pp. 3127
Author(s):  
Jiyeon Choi ◽  
Joo Weon Lim ◽  
Hyeyoung Kim
Keyword(s):  
Epithelial Cells ◽  
A549 Cells ◽  
Cytokine Expression ◽  
Ros Production ◽  
Toll Like Receptor ◽  
Respiratory Epithelial Cells ◽  
Toll Like Receptor 4 ◽  
Mitochondrial Ros ◽  
Tlr4 Activation ◽  
Respiratory Epithelial

House dust mites (HDM) are critical factors in airway inflammation. They activate respiratory epithelial cells to produce reactive oxygen species (ROS) and activate Toll-like receptor 4 (TLR4). ROS induce the expression of inflammatory cytokines in respiratory epithelial cells. Lycopene is a potent antioxidant nutrient with anti-inflammatory activity. The present study aimed to investigate whether HDM induce intracellular and mitochondrial ROS production, TLR4 activation, and pro-inflammatory cytokine expression (IL-6 and IL-8) in respiratory epithelial A549 cells. Additionally, we examined whether lycopene inhibits HDM-induced alterations in A549 cells. The treatment of A549 cells with HDM activated TLR4, induced the expression of IL-6 and IL-8, and increased intracellular and mitochondrial ROS levels. TAK242, a TLR4 inhibitor, suppressed both HDM-induced ROS production and cytokine expression. Furthermore, lycopene inhibited the HDM-induced TLR4 activation and cytokine expression, along with reducing the intracellular and mitochondrial ROS levels in HDM-treated cells. These results collectively indicated that the HDM induced TLR4 activation and increased intracellular and mitochondrial ROS levels, thus resulting in the induction of cytokine expression in respiratory epithelial cells. The antioxidant lycopene could inhibit HDM-induced cytokine expression, possibly by suppressing TLR4 activation and reducing the intracellular and mitochondrial ROS levels in respiratory epithelial cells.

scholarly journals Dolosigranulum pigrum Modulates Immunity against SARS-CoV-2 in Respiratory Epithelial Cells

Pathogens ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 634
Author(s):  
Md. Aminul Islam ◽  
Leonardo Albarracin ◽  
Vyacheslav Melnikov ◽  
Bruno G. N. Andrade ◽  
Rafael R. C. Cuadrat ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Specific Effect ◽  
Commensal Bacteria ◽  
Cellular Damage ◽  
Poly I:C ◽  
Respiratory Epithelial Cells ◽  
Promising Alternative ◽  
Immunological Mechanisms ◽  
Syncytial Virus ◽  
Respiratory Epithelial

In a previous work, we demonstrated that nasally administered Dolosigranulum pigrum 040417 beneficially modulated the respiratory innate immune response triggered by the activation of Toll-like receptor 3 (TLR3) and improved protection against Respiratory Syncytial Virus (RSV) in mice. In this work, we aimed to evaluate the immunomodulatory effects of D. pigrum 040417 in human respiratory epithelial cells and the potential ability of this immunobiotic bacterium to increase the protection against Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). The respiratory commensal bacterium D. pigrum 040417 differentially modulated the production of IFN-β, IL-6, CXCL8, CCL5 and CXCL10 in the culture supernatants of Calu-3 cells stimulated with poly(I:C) or challenged with SARS-CoV-2. The differential cytokine profile induced by the 040417 strain was associated with a significant reduction in viral replication and cellular damage after coronavirus infection. Of note, D. pigrum 030918 was not able to modify the resistance of Calu-3 cells to SARS-CoV-2 infection, indicating a strain-specific immunomodulatory effect for respiratory commensal bacteria. The findings of this work improve our understanding of the immunological mechanisms involved in the modulation of respiratory immunity induced by respiratory commensal bacteria, by demonstrating their specific effect on respiratory epithelial cells. In addition, the results suggest that particular strains such as D. pigrum 040417 could be used as a promising alternative for combating SARS-CoV-2 and reducing the severity of COVID-19.

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