Beyond a Gasotransmitter: Hydrogen Sulfide and Polysulfide in Cardiovascular Health and Immune Response

Yuan, Shuai; Shen, Xinggui; Kevil, Christopher G.

doi:10.1089/ars.2017.7096

Cited by 90 publications

(74 citation statements)

References 210 publications

(271 reference statements)

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“…In mammals, H 2 S is important for a wide range of important biological functions, including cellular bioenergetics and cardiovascular and neuronal functions (1). Additionally, H 2 S has been reported to have both pro-and anti-inflammatory effects (23,24). Therefore, these inhibitors are not suitable for the treatment of bacterial infections due to their inhibitory effects on host enzymes.…”

Section: Discussionmentioning

confidence: 99%

H ₂ S, a Bacterial Defense Mechanism against the Host Immune Response

et al. 2019

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The biological mediator hydrogen sulfide (H2S) is produced by bacteria and has been shown to be cytoprotective against oxidative stress and to increase the sensitivity of various bacteria to a range of antibiotic drugs. Here we evaluated whether bacterial H2S provides resistance against the immune response, using two bacterial species that are common sources of nosocomial infections, Escherichia coli and Staphylococcus aureus. Elevations in H2S levels increased the resistance of both species to immune-mediated killing. Clearances of infections with wild-type and genetically H2S-deficient E. coli and S. aureus were compared in vitro and in mouse models of abdominal sepsis and burn wound infection. Also, inhibitors of H2S-producing enzymes were used to assess bacterial killing by leukocytes. We found that inhibition of bacterial H2S production can increase the susceptibility of both bacterial species to rapid killing by immune cells and can improve bacterial clearance after severe burn, an injury that increases susceptibility to opportunistic infections. These findings support the role of H2S as a bacterial defense mechanism against the host response and implicate bacterial H2S inhibition as a potential therapeutic intervention in the prevention or treatment of infections.

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Section: Discussionmentioning

confidence: 99%

H ₂ S, a Bacterial Defense Mechanism against the Host Immune Response

et al. 2019

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“…In oxidized low density lipoprotein (ox-LDL)-treated macrophage, the levels of CSE mRNA and protein expression, as well as H2S production are remarkably decreased, thus, this finding indicates that alterations of the CSE/H2S pathway plays an important role in ox-LDL-stimulated m acrophage infl am ma tion a nd atherosclerosis (Wang et al, 2013b). It is worth noting that CBS deficiency may cause hyperhomocysteinemia, which is an independent risk factor for the development of atherosclerosis (Zhang et al, 2012a;Yuan et al, 2017). In transgenic CBSdeficient mice, the emegence of hypercholesterolemia accelerates atherosclerotic lesions via oxidative stress and inflammatory monocyte generation (Zhang et al, 2009).…”

Section: H 2 S-related Endothelial Dysfunction In Atherosclerosismentioning

confidence: 97%

Role of Endothelial Dysfunction in Cardiovascular Diseases: The Link Between Inflammation and Hydrogen Sulfide

et al. 2020

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Endothelial cells are important constituents of blood vessels that play critical roles in cardiovascular homeostasis by regulating blood fluidity and fibrinolysis, vascular tone, angiogenesis, monocyte/leukocyte adhesion, and platelet aggregation. The normal vascular endothelium is taken as a gatekeeper of cardiovascular health, whereas abnormality of vascular endothelium is a major contributor to a plethora of cardiovascular ailments, such as atherosclerosis, aging, hypertension, obesity, and diabetes. Endothelial dysfunction is characterized by imbalanced vasodilation and vasoconstriction, elevated reactive oxygen species (ROS), and proinflammatory factors, as well as deficiency of nitric oxide (NO) bioavailability. The occurrence of endothelial dysfunction disrupts the endothelial barrier permeability that is a part of inflammatory response in the development of cardiovascular diseases. As such, abrogation of endothelial cell activation/inflammation is of clinical relevance. Recently, hydrogen sulfide (H 2 S), an entry as a gasotransmitter, exerts diverse biological effects through acting on various targeted signaling pathways. Within the cardiovascular system, the formation of H 2 S is detected in smooth muscle cells, vascular endothelial cells, and cardiomyocytes. Disrupted H 2 S bioavailability is postulated to be a new indicator for endothelial cell inflammation and its associated endothelial dysfunction. In this review, we will summarize recent advances about the roles of H 2 S in endothelial cell homeostasis, especially under pathological conditions, and discuss its putative therapeutic applications in endothelial inflammation-associated cardiovascular disorders.

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“…H 2 S, previously regarded primarily as an environmental hazard and toxic gas, has recently been recognized as the third gasotransmitter after carbon monoxide (CO) and nitric oxide (NO; Szabo, ). H 2 S has become a focus of researches because of its role in various biological processes, such as neuronal health (Paul & Snyder, ), cardiovascular health, immune response (Yuan, Shen, & Kevil, ), and inflammation (Luo et al, ). Besides, H 2 S has also been reported to regulate cell cycle, proliferation, autophagy, apoptosis, and oxidative stress in malignant tumors (Hellmich & Szabo, ).…”

Section: Introductionmentioning

confidence: 99%

Diallyl trisulfide, a H₂S donor, inhibits cell growth of human papillary thyroid carcinoma KTC‐1 cells through a positive feedback loop between H₂S and cystathionine‐gamma‐lyase

Pan

Cheng

et al. 2020

Phytotherapy Research

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Diallyl trisulfide (DATS), derived from garlic, is a well‐known hydrogen sulfide (H2S) donor. H2S has recently emerged as a novel gasotransmitter involved in the regulation of cancer progression. The present study demonstrated that DATS along with other two H2S donors, NaHS and GYY4137, significantly inhibited papillary thyroid carcinoma KTC‐1 cells growth. DATS treatment triggered a rapid H2S generation within 5 min in KTC‐1 cells. Iodoacetamide, a potent thiol blocker reagent, partially rescued the cell membrane damage and ultimate cell death induced by DATS, indicating H2S contributed to the apoptosis‐inducing efficacy of DATS on thyroid cancer cells. Specifically, DATS treatment significantly upregulated the expression and enzymatic activity of cystathionine gamma‐lyase (CTH), one of H2S‐producing enzymes, which was responsible for endogenous H2S generation. After DATS treatment, H2S quickly permeated cell membranes and activated NF‐κΒ/p65 signaling pathway in KTC‐1 cells. Nuclear translocated NF‐κB bound to the promoter of CTH to enhance its transcription. These evidences proved that exogenous H2S elevated CTH expression. CTH, in turn, catalytically generated a much higher level of endogenous H2S. This positive feedback sustained excess H2S production, which resulted in PTC cells growth inhibition. These findings may shed light on the development of novel H2S‐based antitumor agents.

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Beyond a Gasotransmitter: Hydrogen Sulfide and Polysulfide in Cardiovascular Health and Immune Response

Cited by 90 publications

References 210 publications

H ₂ S, a Bacterial Defense Mechanism against the Host Immune Response

H ₂ S, a Bacterial Defense Mechanism against the Host Immune Response

Role of Endothelial Dysfunction in Cardiovascular Diseases: The Link Between Inflammation and Hydrogen Sulfide

Diallyl trisulfide, a H₂S donor, inhibits cell growth of human papillary thyroid carcinoma KTC‐1 cells through a positive feedback loop between H₂S and cystathionine‐gamma‐lyase

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Beyond a Gasotransmitter: Hydrogen Sulfide and Polysulfide in Cardiovascular Health and Immune Response

Cited by 90 publications

References 210 publications

H 2 S, a Bacterial Defense Mechanism against the Host Immune Response

H 2 S, a Bacterial Defense Mechanism against the Host Immune Response

Role of Endothelial Dysfunction in Cardiovascular Diseases: The Link Between Inflammation and Hydrogen Sulfide

Diallyl trisulfide, a H2S donor, inhibits cell growth of human papillary thyroid carcinoma KTC‐1 cells through a positive feedback loop between H2S and cystathionine‐gamma‐lyase

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H ₂ S, a Bacterial Defense Mechanism against the Host Immune Response

H ₂ S, a Bacterial Defense Mechanism against the Host Immune Response

Diallyl trisulfide, a H₂S donor, inhibits cell growth of human papillary thyroid carcinoma KTC‐1 cells through a positive feedback loop between H₂S and cystathionine‐gamma‐lyase