The Role of Endogenous Histamine on the Pathogenesis of the Lipopolysaccharide (LPS)-Induced, Acute Lung Injury: A Pilot Study

Kim, Tae-Hyung; Yoon, Ho Joo; Lim, Chae Man; Kim, Min Jung; Kim, Mi Jung; Koh, Younsuck

doi:10.1007/s10753-006-9001-3

Cited by 19 publications

(8 citation statements)

References 28 publications

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“…The involvement of histamine via H 1 -receptors in lung vascular hyperpermeability in sepsis has been documented [9, 31]. H 2 -receptors have also been shown to be involved in the recruitment of neutrophils and protein leaks in LPS-induced acute lung injury [32]. These adverse effects of histamine mediated by H 1 - and H 2 -receptors could be responsible for liver injury in sepsis.…”

Section: Discussionmentioning

confidence: 99%

Critical role of endogenous histamine in promoting end-organ tissue injury in sepsis

Hattori

Yamazaki

Ohashi

et al. 2016

ICMx

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BackgroundHistamine assumes an important role as a major mediator in various pathologic disorders associated with inflammation and immune reactions. However, the involvement of histamine in the pathological conditions and symptoms of sepsis remains entirely unknown. In this study, we establish that histamine is identified as a contributory mediator to promoting the development of organ injury in sepsis.MethodsHistidine decarboxylase (HDC) gene knockout (HDC−/−) mice, histamine H1-/H2-receptor gene-double knockout (H1R−/−/H2R−/−) mice, and their littermate wild-type (WT) C57BL/6J mice underwent cecal ligation and puncture (CLP) or sham operation. Some WT mice were injected intraperitoneally with d-chlorpheniramine and famotidine 60 min before CLP to block H1- and H2-receptors, respectively.ResultsIn mice rendered septic by CLP, tissue histamine levels were elevated in association with increased HDC expression. Sepsis-induced abnormal cytokine production and multiple organ injury (lung, liver, and kidney) were significantly less pronounced in HDC−/− mice as compared with WT controls, and HDC deficiency had improved survival in sepsis. This benefit corresponded with a significant reduction in activation levels of the nuclear factor (NF)-κB signaling pathway. H1R−/−/H2R−/− mice apparently behaved similar to HDC knockout mice in reducing sepsis-related pathological changes. Pharmacological interventions with H1- and H2-receptor antagonists indicated that both H1- and H2-receptors were involved in septic lung and liver injury, whereas only H2-receptors contributed to septic kidney injury.ConclusionsIn the setting of sepsis, histamine, through activation of H1- and H2-receptors, serves as an aggravating mediator to contribute to the development of sepsis-driven major end-organ failure.Electronic supplementary materialThe online version of this article (doi:10.1186/s40635-016-0109-y) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Critical role of endogenous histamine in promoting end-organ tissue injury in sepsis

Hattori

Yamazaki

Ohashi

et al. 2016

ICMx

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“…When organs with the galactosyltransferase gene knocked out (GalTKO) also express one or more human complement pathway regulatory proteins (hCPRPs), xenograft failure is typically associated with coagulation cascade activation in the recipient, and an inflammatory response in the xenogeneic organ, particularly during human blood perfusion of pig pulmonary xenografts . Platelet sequestration as well as thromboxane and histamine elaboration are identified as early events during GalTKO.hCD46 as well as wild‐type (WT), GalTKO, and other hCPRP‐expressing porcine lung xenograft rejection, and have been implicated in elevated pulmonary vascular resistance (PVR), loss of lung vascular barrier function, and subsequent organ failure in these circumstances and in other lung models …”

Section: Introductionmentioning

confidence: 99%

Thromboxane and histamine mediate PVR elevation during xenogeneic pig lung perfusion with human blood

Burdorf

Harris

Dahi

et al. 2018

Xenotransplantation

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Combined thromboxane and histamine pathway blockade prevents PVR elevation and significantly inhibits loss of vascular barrier function when GalTKO.hCD46 lungs are perfused with human blood. Platelet activation and platelet and neutrophil sequestration persist in all groups despite efficient complement regulation, and appear to occur independent of thromboxane and histamine antagonism. Our work identifies thromboxane and histamine as key mediators of xenolung injury and defines those pathways as therapeutic targets to achieve successful xenolung transplantation.

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“…LPS is a structural part of endotoxin in the outer membrane of Gram-negative bacteria, which is one of the most potent stimuli to organism (Shin et al, 2004 ). It has been shown that LPS plays an important role in inducing the inflammatory response and leading to various inflammatory diseases (Brigham and Meyrick, 1986 ; Kim T. H. et al, 2005 ). In order to create a ideal model for studying systemic inflammation, LPS administration has been extensively used in chicken to induce inflammatory response (Munyaka et al, 2012 ).…”

Section: Introductionmentioning

confidence: 99%

Baicalin Alleviates Lipopolysaccharide-Induced Liver Inflammation in Chicken by Suppressing TLR4-Mediated NF-κB Pathway

et al. 2017

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As a kind of potent stimulus, lipopolysaccharide (LPS) has the ability to cause cell damage by activating toll-like receptor(TLR)4, then nuclear factor kappa B (NF-κB) translocates into the nucleus and changes the expression of related inflammatory genes. Baicalin is extracted from Radix Scutellariae, which possesses anti-inflammation, antioxidant and antibacterial properties. However, the effects of it on LPS-induced liver inflammation have not been fully elucidated. This study aims to investigate the anti-inflammatory effects of Baicalin on the LPS-induced liver inflammation and its underlying molecular mechanisms in chicken. The results of histopathological changes, serum biochemical analysis, NO levels and myeloperoxidase activity showed that Baicalin pretreatment ameliorated LPS-induced liver inflammation. ELISA and qPCR assays showed that Baicalin dose-dependently suppressed the production of IL-1β, IL-6, and TNF-α. Furthermore, the mRNA expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) were significantly decreased by Baicalin. TLR4 is an important sensor in LPS infection. Molecular studies showed that the expression of TLR4 was inhibited by Baicalin pretreatment. In addition, Baicalin pretreatment inhibited NF-kB signaling pathway activation. All results demonstrated the protective effects of Baicalin pretreatment against LPS-induced liver inflammation in chicken via negative regulation of inflammatory mediators through the down-regulation of TLR4 expression and the inhibition of NF-kB activation.

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The Role of Endogenous Histamine on the Pathogenesis of the Lipopolysaccharide (LPS)-Induced, Acute Lung Injury: A Pilot Study

Cited by 19 publications

References 28 publications

Critical role of endogenous histamine in promoting end-organ tissue injury in sepsis

Critical role of endogenous histamine in promoting end-organ tissue injury in sepsis

Thromboxane and histamine mediate PVR elevation during xenogeneic pig lung perfusion with human blood

Baicalin Alleviates Lipopolysaccharide-Induced Liver Inflammation in Chicken by Suppressing TLR4-Mediated NF-κB Pathway

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