Glaesserella parasuis serotype 4 HPS4-YC disrupts the integrity of the swine tracheal epithelial barrier and facilitates bacterial translocation

AbstractGlaesserella parasuis (G. parasuis) is a commensal bacterium in the upper respiratory tract of pigs that can also cause the swine Glässer disease, which induces an intensive inflammatory response and results in significant economic losses to the swine industry worldwide. G. parasuis can cause disease through infection of the respiratory tract, resulting in systemic infection, but the mechanism is largely unknown. Recently we showed that Glaesserella parasuis serotype 4 (GPS4) increased swine tracheal epithelial barrier permeability, resulting in easier bacterial translocation. Tight junction proteins (TJ) play a crucial role in maintaining the integrity and impermeability of the epithelial barrier. GPS4 decreased the expression of the TJ ZO-1 and occludin in swine tracheal epithelial cells (STEC). Furthermore, the proinflammatory cytokines IL-6, IL-8 and TNF-α were significantly upregulated in GPS4-infected STEC, and both the MAPK and NF-κB signaling pathways were activated and contributed to the expression of TNF-α. We demonstrate that the production of proinflammatory cytokines, especially TNF-α, during GPS4 infection was involved in barrier dysfunction. Additionally, animal challenge experiments confirmed that GPS4 infection downregulated TJ in the lungs of piglets and induced a severe inflammatory response. In general, G. parasuis infection downregulated the expression of TJ and induced massive secretion of proinflammatory cytokines, resulting in epithelial barrier disruption and favoring bacterial infection. This study allowed us to better understand the mechanism by which G. parasuis crosses the respiratory tract of pigs.

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Correlation between cyclical epithelial barrier dysfunction and bacterial translocation in the relapses of intestinal inflammation

Inflammatory Bowel Diseases ◽

10.1097/01.mib.0000231571.88806.62 ◽

2006 ◽

Vol 12 (9) ◽

pp. 843-852 ◽

Cited By ~ 43

Author(s):

Monica Porras ◽

Maria Teresa Martín ◽

Ping-Chang Yang ◽

Jennifer Jury ◽

Mary H. Perdue ◽

...

Keyword(s):

Bacterial Translocation ◽

Intestinal Inflammation ◽

Epithelial Barrier ◽

Barrier Dysfunction ◽

Epithelial Barrier Dysfunction

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Absence of Mycoplasma spp. in nightingales (Luscinia megarhynchos) and blue (Cyanistes caeruleus) and great tits (Parus major) in Germany and its potential implication for evolutionary studies in birds

European Journal of Wildlife Research ◽

10.1007/s10344-021-01554-7 ◽

2021 ◽

Vol 68 (1) ◽

Author(s):

Luisa Fischer ◽

Franca Möller Palau-Ribes ◽

Silke Kipper ◽

Michael Weiss ◽

Conny Landgraf ◽

...

Keyword(s):

Respiratory Tract ◽

Bird Species ◽

Respiratory Pathogen ◽

Economic Losses ◽

Rrna Gene ◽

Upper Respiratory Tract ◽

Healthy Individuals ◽

Cyanistes Caeruleus ◽

Potential Implication ◽

Free Ranging

AbstractMycoplasma spp. are important pathogens in poultry and cause high economic losses for poultry industry worldwide. In other bird species (e.g. white storks, birds of prey, and several waterfowl species), Mycoplasma spp. are regularly found in healthy individuals, hence, considered apathogenic or part of the microbiota of the upper respiratory tract. However, as Mycoplasma spp. are absent in healthy individuals of some wild bird species, they might play a role as respiratory pathogen in these bird species, e.g. Mycoplasma gallisepticum in house finches. The knowledge on the occurrence of Mycoplasma spp. in wild birds is limited. To evaluate the relevance of Mycoplasma spp. in free-ranging nightingales and tits, 172 wild caught birds were screened for the presence of mycoplasmas. The birds were sampled via choanal swabs and examined via molecular methods (n = 172) and, when possible, via culture (n = 142). The Mycoplasma sp. was determined by sequencing the 16S rRNA gene and 16S-23S Intergenic Transcribed Spacer Region. All birds were tested negative for mycoplasmas via PCR and/or mycoplasmal culture. Hence, free-ranging nightingales and tits do not show any mycoplasma in their microbial flora of the respiratory tract. Therefore, these songbird species may suffer from clinical mycoplasmosis when being infected. We hypothesize that birds relying on their vocal ability for reproduction have excluded mycoplasmas from their respiratory flora compared to other bird species.

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Tea polyphenols protect gingival keratinocytes against TNF-α-induced tight junction barrier dysfunction and attenuate the inflammatory response of monocytes/macrophages

Cytokine ◽

10.1016/j.cyto.2018.12.009 ◽

2019 ◽

Vol 115 ◽

pp. 64-75 ◽

Cited By ~ 7

Author(s):

Amel Ben Lagha ◽

Daniel Grenier

Keyword(s):

Inflammatory Response ◽

Tight Junction ◽

Tea Polyphenols ◽

Barrier Dysfunction ◽

Tnf Α

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The Role of the Immune Response in the Pathogenesis of Bronchiectasis

BioMed Research International ◽

10.1155/2018/6802637 ◽

2018 ◽

Vol 2018 ◽

pp. 1-12 ◽

Cited By ~ 3

Author(s):

Paul T. King

Keyword(s):

Immune Response ◽

Inflammatory Response ◽

Respiratory Tract ◽

Lower Respiratory Tract ◽

Therapeutic Potential ◽

Small Airways ◽

Upper Respiratory Tract ◽

Causative Factors ◽

Triggering Factor

Bronchiectasis is a prevalent respiratory condition characterised by permanent and abnormal dilation of the lung airways (bronchi). There are a large variety of causative factors that have been identified for bronchiectasis; all of these compromise the function of the immune response to fight infection. A triggering factor may lead to the establishment of chronic infection in the lower respiratory tract. The bacteria responsible for the lower respiratory tract infection are usually found as commensals in the upper respiratory tract microbiome. The consequent inflammatory response to infection is largely responsible for the pathology of this condition. Both innate and adaptive immune responses are activated. The literature has highlighted the central role of neutrophils in the pathogenesis of bronchiectasis. Proteases produced in the lung by the inflammatory response damage the airways and lead to the pathological dilation that is the pathognomonic feature of bronchiectasis. The small airways demonstrate infiltration with lymphoid follicles that may contribute to localised small airway obstruction. Despite aggressive treatment, most patients will have persistent disease. Manipulating the immune response in bronchiectasis may potentially have therapeutic potential.

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Long noncoding RNA MALAT1 contributes to inflammatory response of microglia following spinal cord injury via the modulation of a miR-199b/IKKβ/NF-κB signaling pathway

AJP Cell Physiology ◽

10.1152/ajpcell.00278.2017 ◽

2018 ◽

Vol 315 (1) ◽

pp. C52-C61 ◽

Cited By ~ 37

Author(s):

Heng-Jun Zhou ◽

Li-Qing Wang ◽

Duan-Bu Wang ◽

Jian-Bo Yu ◽

Yu Zhu ◽

...

Keyword(s):

Spinal Cord ◽

Spinal Cord Injury ◽

Inflammatory Response ◽

Signaling Pathway ◽

Proinflammatory Cytokines ◽

Long Noncoding Rna ◽

Noncoding Rna ◽

Tnf Α ◽

Cord Injury

Long noncoding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) was widely recognized to be implicated in human cancer, vascular diseases, and neurological disorders. This study was to explore the role and underlying mechanism of MALAT1 in acute spinal cord injury (ASCI). ASCI models in adult rats were established and demonstrated by a numerical decrease in BBB scores. Expression profile of MALAT1 and miR-199b following ASCI in rats and in vitro was determined using quantitative real-time PCR. RNA pull-down assays combined with RIP assays were performed to explore the interaction between MALAT1 and miR-199b. In the present study, MALAT1 expression was significantly increased (2.4-fold that of control) in the spinal cord of the rat contusion epicenter accompanied by activation of IKKβ/NF-κB signaling pathway and an increase in the level of proinflammatory cytokines TNF-α and IL-1β. Upon treatment with LPS, MALAT1 expression dramatically increased in the microglia in vitro, but knockdown of MALAT1 attenuated LPS-induced activation of MGs and TNF-α and IL-1β production. Next, we confirmed that LPS-induced MALAT1 activated IKKβ/NF-κB signaling pathway and promoted the production of proinflammatory cytokines TNF-α and IL-1β through downregulating miR-199b. More importantly, MALAT1 knockdown gradually improved the hindlimb locomotor activity of ASCI rats as well as inhibited TNF-α, IL-1β levels, and Iba-1 protein, the marker of activated microglia in injured spinal cords. Our study demonstrated that MALAT1 was dysregulated in ASCI rats and in LPS-activated MGs, and MALAT1 knockdown was expected to attenuate ASCI through repressing inflammatory response of MGs.

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Total polysaccharides of adlay bran (Coix lachryma-jobi L.) improve TNF-α induced epithelial barrier dysfunction in Caco-2 cells via inhibition of the inflammatory response

Food & Function ◽

10.1039/c9fo00590k ◽

2019 ◽

Vol 10 (5) ◽

pp. 2906-2913 ◽

Cited By ~ 8

Author(s):

Yanlong Li ◽

Xudong Tian ◽

Shengcai Li ◽

Lijun Chang ◽

Ping Sun ◽

...

Keyword(s):

Inflammatory Bowel Disease ◽

Irritable Bowel Syndrome ◽

Epithelial Barrier ◽

Intestinal Epithelial ◽

Barrier Dysfunction ◽

Intestinal Epithelial Barrier ◽

Tnf Α ◽

Inflammatory Bowel ◽

Irritable Bowel ◽

Epithelial Barrier Dysfunction

Dysfunction of the intestinal epithelial barrier plays an important role in the pathogenesis of several intestinal diseases, including celiac disease, inflammatory bowel disease, and irritable bowel syndrome.

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The Invasion Plasmid Antigen J (IpaJ) from Salmonella Inhibits NF-κB Activation by Suppressing IκBα Ubiquitination

Infection and Immunity ◽

10.1128/iai.00875-19 ◽

2019 ◽

Vol 88 (3) ◽

Author(s):

Qiuchun Li ◽

Lijuan Xu ◽

Chao Yin ◽

Zijian Liu ◽

Yang Li ◽

...

Keyword(s):

Inflammatory Response ◽

Proinflammatory Cytokines ◽

Hela Cells ◽

Salmonella Enterica ◽

Systemic Infection ◽

Peripheral Blood Monocyte ◽

Effector Proteins ◽

Economic Losses ◽

Necrosis Factor Alpha ◽

Content Type

ABSTRACT Salmonella enterica serovar Pullorum is the pathogen of pullorum disease, which leads to severe economic losses in many developing countries. In contrast to the strong inflammatory response induced by Salmonella enterica serovar Typhimurium and Salmonella enterica serovar Enteritidis, S. Pullorum causes systemic infection with little inflammation. The effector proteins secreted by Salmonella often play a crucial role in modulating host signal transduction and cellular processes to the pathogen’s advantage. In the present study, the invasion plasmid antigen J (IpaJ) protein specifically identified in S. Pullorum was found to significantly inhibit activation of the key proinflammatory transcription factor, NF-κB, which was induced by tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), and lipopolysaccharide (LPS). IpaJ inhibited the NF-κB pathway in cells infected with S. Pullorum through the stabilization of IκBα. Deletion of ipaJ in S. Pullorum caused a significantly increased level of ubiquitinated IκBα that was subsequently degraded by the proteasome in HeLa cells. Moreover, IpaJ was efficient in the prevention of NF-κB translocation to the nucleus and ultimately interfered with the secretion of the proinflammatory cytokines IL-1β, IL-6, and IL-8 in infected HeLa cells. Additionally, the transformation of ipaJ into S. Enteritidis decreased the secretion of proinflammatory cytokines in HeLa cells through suppression of the NF-κB pathway. The infection of chicken peripheral blood monocyte-derived macrophages (chMDM) confirmed that ipaJ-deleted S. Pullorum induced a stronger expression of proinflammatory cytokines than the wild-type and complementary strains. In summary, the present study revealed that IpaJ functions as an important anti-inflammatory protein involved in S. Pullorum infection through inhibition of the NF-κB pathway and the subsequent inflammatory response.

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