Pro‐inflammatory effects of hydrogen sulphide on substance P in caerulein‐induced acute pancreatitis

Bhatia, Madhav; Sidhapuriwala, Jenab N.; Ng, Siaw Wei; Tamizhselvi, Ramasamy; Moochhala, Shabbir

doi:10.1111/j.1582-4934.2007.00131.x

Cited by 57 publications

(34 citation statements)

References 37 publications

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“…In the exocrine pancreas, H 2 S was initially demonstrated to be a pro-inflammatory factor involved in caerulein-induced pancreatitis (5,53). Later, however, anti-inflammatory effects were also reported (50,54).…”

Section: Discussionmentioning

confidence: 99%

Hydrogen Sulfide Regulates Ca²⁺ Homeostasis Mediated by Concomitantly Produced Nitric Oxide via a Novel Synergistic Pathway in Exocrine Pancreas

Moustafa

Habara

2014

Antioxidants & Redox Signaling

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Aim: The present study was designed to explore the effects of hydrogen sulfide (H 2 S) on Ca 2+ homeostasis in rat pancreatic acini. Results: Sodium hydrosulfide (NaHS; an H 2 S donor) induced a biphasic increase in the in- ] i increase was markedly inhibited in the presence of NG-monomethyl L-arginine or 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO), and diaminofluorescein-2/diaminofluorescein-2 triazole (DAF-2/DAF-2T) fluorometry demonstrated that nitric oxide (NO) was also produced by H 2 S in a dose-dependent manner with an EC 50 of 64.8 lM, indicating that NO was involved in the H 2 S effect. The H 2 S-induced [Ca 2+ ] i increase was inhibited by pretreatment with U73122, xestospongin C, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one, KT5823, and GP2A, indicating that phospholipase C (PLC), the inositol 1,4,5-trisphosphate (IP 3 ) receptor, soluble guanylate cyclase (sGC), protein kinase G (PKG), and G q -protein play roles as intermediate components in the H 2 S-triggered intracellular signaling. Innovation: To our knowledge, our study is the first one highlighting the effect of H 2 S on intracellular Ca 2+ dynamics in pancreatic acinar cells. Moreover, a novel cascade was presumed to function via the synergistic interaction between H 2 S and NO. Conclusion: We conclude that H 2 S affects [Ca 2+ ] i homeostasis that is mediated by H 2 S-evoked NO production via an endothelial nitric oxide synthase (eNOS)-NO-sGC-cyclic guanosine monophosphate-PKG-G q -protein-PLC-IP 3 pathway to induce Ca 2+ release, and this pathway is identical to the one we recently proposed for a sole effect of NO and the two gaseous molecules synergistically function to regulate Ca 2+ homeostasis. Antioxid. Redox Signal. 20, 747-758.

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Section: Discussionmentioning

confidence: 99%

Hydrogen Sulfide Regulates Ca²⁺ Homeostasis Mediated by Concomitantly Produced Nitric Oxide via a Novel Synergistic Pathway in Exocrine Pancreas

Moustafa

Habara

2014

Antioxidants & Redox Signaling

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“…To induce mild acute pancreatitis, we gave AQP12-KO mice and their WT littermates seven hourly intraperitoneal injections of the CCK-8 analog caerulein (50 g/kg body wt; Sigma-Aldrich) as previously described (1,2). Blood was collected at both 9 and 24 h after the first caerulein injection to examine the serum amylase and lipase levels.…”

Section: Methodsmentioning

confidence: 99%

Pancreas-specific aquaporin 12 null mice showed increased susceptibility to caerulein-induced acute pancreatitis

Ohta

Itoh

Nemoto

et al. 2009

American Journal of Physiology-Cell Physiology

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Aquaporin 12 (AQP12) is the most recently identified member of the mammalian AQP family and is specifically expressed in pancreatic acinar cells. In vitro expression studies have revealed that AQP12 is localized at intracellular sites. To determine the physiological roles of AQP12 in the pancreas, we generated knockout mice for this gene (AQP12-KO). No obvious differences were observed under normal conditions between wild-type (WT) and AQP12-KO mice in terms of growth, blood chemistry, pancreatic fluid content, or histology. However, when we induced pancreatitis through the administration of a cholecystokinin-8 (CCK-8) analog, the AQP12-KO mice showed more severe pathological damage to this organ than WT mice. Furthermore, when we analyzed exocytosis in the pancreatic acini using a two-photon excitation imaging method, the results revealed larger exocytotic vesicles (vacuoles) in the acini of AQP12-KO mice at a high CCK-8 dose (100 nM). From these results, we conclude that AQP12 may function in the mechanisms that control the proper secretion of pancreatic fluid following rapid and intense stimulation.

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“…In addition to its known effects in nociception, it also has proinflammatory roles [85], and absence or inhibition of this receptor is protective against ALI [86][87][88]. Hydrogen sulfide (H 2 S) has also recently been shown to be an important mediator of inflammatory responses and may induce the production or release of substance P [89,90]. Although H 2 S may be proinflammatory, in certain models of ALI, H 2 S production is decreased, and administration of the H 2 S donor sodium hydrosulfide decreased proinflammatory cytokines IL-6 and IL-8, and the resultant ALI [91].…”

Section: Release Of Other Proinflammatory Mediatorsmentioning

confidence: 99%

Role of the pulmonary epithelium and inflammatory signals in acute lung injury

Manicone¹

2009

Expert Review of Clinical Immunology

118

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Acute lung injury (ALI) is a clinical disease marked by respiratory failure due to disruption of the epithelial and endothelial barrier, flooding of the alveolar compartment with protein-rich fluid and recruitment of neutrophils into the alveolar space. ALI affects approximately 200,000 patients annually in the USA and results in approximately 75,000 deaths. It is associated with prolonged mechanical ventilation, intensive medical care, high morbidity and mortality, and rising healthcare costs. Owing to its impact on public health, great strides have been made towards understanding the pathobiology of ALI to affect outcome. This review will focus on the role of the epithelial cell in the pathogenesis and resolution of ALI and the role of various inflammatory mediators in ALI. Keywordsβ2-agonist; acute lung injury; acute respiratory distress syndrome; chemokine; cytokine; epithelial cell; inflammation; methylprednisolone; neutrophil; salbutamol; steroid; ventilator-induced lung injuryAcute lung injury/acute respiratory distress syndrome (ALI/ARDS) was first described in 1967 by Ashbaugh and colleagues in a group of 12 patients who shared a constellation of clinical symptoms including acute respiratory distress, hypoxemia refractory to supplemental oxygen, decreased lung compliance and diffuse pulmonary infiltrates [1]. Since this first description, the clinical criteria have evolved to include acute onset of respiratory distress, bilateral pulmonary infiltrates seen on chest radiographs, absence of left-sided heart failure and hypoxemia, with the severity of hypoxemia distinguishing ALI and ARDS (Box 1) [2]. Extrapolating from recent epidemiologic studies using these criteria, ALI affects about 200,000 patients annually in the USA and results in approximately 75,000 deaths [3]. This disease, which can be caused by common events such as pneumonia, sepsis and trauma, results in high morbidity, mortality and healthcare expenditures associated with prolonged mechanical ventilation and intensive care. Because of its impact on public health and patient outcomes, great strides have been made towards understanding the pathobiology of ALI.When defined broadly to include all processes related to defense against microbes, other environmental insults and injury, a wide variety of cell types and proteins participate in inflammation and immunity. Leukocytes are the paradigmatic inflammatory cell type, but they are not the only cells that function in defense and immunity. The epithelial lining of all tissues forms a continuous barrier to the environment and is the first line of defense against infectious agents and toxins. Though specialized to serve distinct functions among tissues, epithelial cells respond similarly to injury and infection, and regulate leukocyte influx through the production of proinflammatory cytokines, chemokines and other factors that modulate chemokine gradients and effect leukocyte migration. This review will focus on the role of the pulmonary epithelium and inflammatory mediators in ALI. More s...

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Pro‐inflammatory effects of hydrogen sulphide on substance P in caerulein‐induced acute pancreatitis

Cited by 57 publications

References 37 publications

Hydrogen Sulfide Regulates Ca²⁺ Homeostasis Mediated by Concomitantly Produced Nitric Oxide via a Novel Synergistic Pathway in Exocrine Pancreas

Hydrogen Sulfide Regulates Ca²⁺ Homeostasis Mediated by Concomitantly Produced Nitric Oxide via a Novel Synergistic Pathway in Exocrine Pancreas

Pancreas-specific aquaporin 12 null mice showed increased susceptibility to caerulein-induced acute pancreatitis

Role of the pulmonary epithelium and inflammatory signals in acute lung injury

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Pro‐inflammatory effects of hydrogen sulphide on substance P in caerulein‐induced acute pancreatitis

Cited by 57 publications

References 37 publications

Hydrogen Sulfide Regulates Ca2+ Homeostasis Mediated by Concomitantly Produced Nitric Oxide via a Novel Synergistic Pathway in Exocrine Pancreas

Hydrogen Sulfide Regulates Ca2+ Homeostasis Mediated by Concomitantly Produced Nitric Oxide via a Novel Synergistic Pathway in Exocrine Pancreas

Pancreas-specific aquaporin 12 null mice showed increased susceptibility to caerulein-induced acute pancreatitis

Role of the pulmonary epithelium and inflammatory signals in acute lung injury

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Hydrogen Sulfide Regulates Ca²⁺ Homeostasis Mediated by Concomitantly Produced Nitric Oxide via a Novel Synergistic Pathway in Exocrine Pancreas

Hydrogen Sulfide Regulates Ca²⁺ Homeostasis Mediated by Concomitantly Produced Nitric Oxide via a Novel Synergistic Pathway in Exocrine Pancreas