Induction of endoplasmic reticulum stress under endotoxin tolerance increases inflammatory responses and decreases <i>Pseudomonas aeruginosa</i> pneumonia

Kim, Se-Na; Joe, Yeonsoo; Park, Se-Ung; Jeong, Sun Oh; Kim, Jin‐Kyung; Park, Seong Hoon; Pae, Hyun‐Ock; Surh, Young‐Joon; Shin, Jaekyoon; Chung, Hun Taeg

doi:10.1002/jlb.3a0317-106rrr

Cited by 8 publications

(7 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…NOD1 (but not NOD2) restricts C. jejuni infection in intestinal epithelial cells (90) and therefore may be involved in ER stress-mediated restriction of C. jejuni infection. Other bacteria that induce ER stress and are also inhibited by NOD1 or NOD2 include P. aeruginosa (141)(142)(143)(144)(145), Staphylococcus aureus (146,147), S. Typhimurium (148), and S. pneumoniae (149). Additional studies are necessary to determine a link between bacterium-induced ER stress and NOD1/2 antibacterial effects.…”

Section: Pathogen-induced Er Stress Sensing and Nod1/2mentioning

confidence: 99%

NOD1 and NOD2 Activation by Diverse Stimuli: a Possible Role for Sensing Pathogen-Induced Endoplasmic Reticulum Stress

Kuss-Duerkop

Keestra-Gounder

2020

Infect Immun

View full text Add to dashboard Cite

Prompt recognition of microbes by cells is critical to eliminate invading pathogens. Some cell-associated pattern recognition receptors (PRRs) recognize and respond to microbial ligands. However, others can respond to cellular perturbations, such as damage-associated molecular patterns (DAMPs). Nucleotide oligomerization domains 1 and 2 (NOD1/2) are PRRs that recognize and respond to multiple stimuli of microbial and cellular origin, such as bacterial peptidoglycan, viral infections, parasitic infections, activated Rho GTPases, and endoplasmic reticulum (ER) stress. How NOD1/2 are stimulated by such diverse stimuli is not fully understood but may partly rely on cellular changes during infection that result in ER stress. NOD1/2 are ER stress sensors that facilitate proinflammatory responses for pathogen clearance; thus, NOD1/2 may help mount broad antimicrobial responses through detection of ER stress, which is often induced during a variety of infections. Some pathogens may subvert this response to promote infection through manipulation of NOD1/2 responses to ER stress that lead to apoptosis. Here, we review NOD1/2 stimuli and cellular responses. Furthermore, we discuss pathogen-induced ER stress and how it might potentiate NOD1/2 signaling.

show abstract

Section: Pathogen-induced Er Stress Sensing and Nod1/2mentioning

confidence: 99%

NOD1 and NOD2 Activation by Diverse Stimuli: a Possible Role for Sensing Pathogen-Induced Endoplasmic Reticulum Stress

Kuss-Duerkop

Keestra-Gounder

2020

Infect Immun

View full text Add to dashboard Cite

show abstract

“…ER stress is also involved in the inflammatory response by activating GSK-3β 38 . Activation of ER stress leads to activation of GSK-3β, which in turn restores the inflammatory response in endotoxin-tolerant macrophages 39 . ER stress participated in myocardial ischemia-reperfusion injury by activating GSK-3β 40 , and inhibiting the appeal process can play a role in myocardial protection.…”

Section: Discussionmentioning

confidence: 99%

Renalase Prevents Renal Fibrosis by Inhibiting Endoplasmic Reticulum Stress and Down-Regulating GSK-3β/Snail Signaling

Wu¹,

Feng²,

Zhang³

et al. 2023

Int. J. Med. Sci.

View full text Add to dashboard Cite

Background: Treating renal fibrosis is crucial to delaying chronic kidney disease. The glycogen synthase kinase-3β (GSK-3β)/Snail pathway regulates renal fibrosis and Renalase can ameliorate renal interstitial fibrosis. However, it is not clear whether GSK-3β/Snail signaling affects Renalase action. Here, we explored the role and mechanism of GSK-3β/Snail in the anti-fibrosis action of Renalase. Materials and methods:We used mice with complete unilateral ureteral obstruction (UUO) and human proximal renal tubular epithelial (HK-2) cells with transforming growth factor-β1 (TGF-β1)-induced fibrosis to explore the role and regulatory mechanism of the GSK-3β/Snail pathway in the amelioration of renal fibrosis by Renalase. Results:In UUO mice and TGF-β1-induced fibrotic HK-2 cells, the expression of p-GSK-3β-Tyr216/p-GSK-3β-Ser9, GSK-3β and Snail was significantly increased, and endoplasmic reticulum (ER) stress was activated. After Renalase supplementation, fibrosis was alleviated, ER stress was inhibited and p-GSK-3β-Tyr216/p-GSK-3β-Ser9, GSK-3β and Snail were significantly down-regulated. The amelioration of renal fibrosis by Renalase and its inhibitory effect on GSK-3β/Snail were reversed by an ER stress agonist. Furthermore, when an adeno-associated virus or plasmid was used to overexpress GSK-3β, the effect of Renalase on delaying renal fibrosis was counteracted, although ER stress markers did not change. Conclusion:Renalase prevents renal fibrosis by down-regulating GSK-3β/Snail signaling through inhibition of ER stress. Exogenous Renalase may be an effective method of slowing or stopping chronic kidney disease progression.

show abstract

“…fumigatus antigens, respectively, and it has recently been suggested that ABPA-related symptoms may be attributed to the A. fumigatus-induced ER stress. , P. aeruginosa secretes virulence factors including PCN and TpIE that are known to induce ER stress and activate UPR via the p38 mitogen-activated protein kinase (MAPK) pathway. ,, The relative abundance of multiple proteins associated with protein processing in the ER was increased in the A.…”

Section: Discussionmentioning

confidence: 99%

“…62 In vivo and in vitro studies have demonstrated an increase in ER stress markers in murine lungs and tracheal epithelial cells challenged with A. fumigatus antigens, respectively, and it has recently been suggested that ABPA-related symptoms may be attributed to the A. fumigatus-induced ER stress. 63,64 P. aeruginosa secretes virulence factors including PCN and TpIE that are known to induce ER stress and activate UPR via the p38 mitogen-activated protein kinase (MAPK) pathway. 61,65,66 The relative abundance of multiple proteins associated with protein processing in the ER was increased in the A. fumigatus-and P. aeruginosa-exposed groups compared to that in the controls and sequentially exposed A549 cells.…”

Section: Journal Of Proteome Researchmentioning

confidence: 99%

Characterization of the Proteomic Response of A549 Cells Following Sequential Exposure to Aspergillus fumigatus and Pseudomonas aeruginosa

2019

View full text Add to dashboard Cite

Aspergillus fumigatus and Pseudomonas aeruginosa are the most prevalent fungal and bacterial pathogens associated with cystic-fibrosisrelated infections, respectively. P. aeruginosa eventually predominates as the primary pathogen, though it is unknown why this is the case. Label-free quantitative proteomics was employed to investigate the cellular response of the alveolar epithelial cell line, A549, to coexposure of A. fumigatus and P. aeruginosa. These studies revealed a significant increase in the rate of P. aeruginosa proliferation where A. fumigatus was present. Shotgun proteomics performed on A549 cells exposed to either A. fumigatus or P. aeruginosa or to A. fumigatus and P. aeruginosa sequentially revealed distinct changes to the host cell proteome in response to either or both pathogens. While key signatures of infection were retained among all pathogen-exposed groups, including changes in mitochondrial activity and energy output, the relative abundance of proteins associated with endocytosis, phagosomes, and lysosomes was decreased in sequentially exposed cells compared to cells exposed to either pathogen. Our findings indicate that A. fumigatus renders A549 cells unable to internalize bacteria, thus providing an environment in which P. aeruginosa can proliferate. This research provides novel insights into the whole-cell proteomic response of A549 cells to A. fumigatus and P. aeruginosa and highlights distinct differences in the proteome following sequential exposure to both pathogens, which may explain why P. aeruginosa can predominate.

show abstract

Induction of endoplasmic reticulum stress under endotoxin tolerance increases inflammatory responses and decreases Pseudomonas aeruginosa pneumonia

Cited by 8 publications

References 43 publications

NOD1 and NOD2 Activation by Diverse Stimuli: a Possible Role for Sensing Pathogen-Induced Endoplasmic Reticulum Stress

NOD1 and NOD2 Activation by Diverse Stimuli: a Possible Role for Sensing Pathogen-Induced Endoplasmic Reticulum Stress

Renalase Prevents Renal Fibrosis by Inhibiting Endoplasmic Reticulum Stress and Down-Regulating GSK-3β/Snail Signaling

Characterization of the Proteomic Response of A549 Cells Following Sequential Exposure to Aspergillus fumigatus and Pseudomonas aeruginosa

Contact Info

Product

Resources

About