Histaminase activity in rat lung and its comparison with intestinal mucosal diamine oxidase

Ignesti, G.; Banchelli, G.; Raimondi, Laura; Pirisino, R.; Buffoni, F.

doi:10.1007/bf01997499

Cited by 14 publications

(4 citation statements)

References 18 publications

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“…Separation of these subtypes by plating on plastic culture plates, to facilitate macrophage adherence, showed that gene expression for HDC was predominately in the neutrophil population, although there was significant upregulation in the macrophage population from LPS-treated mice versus those from PBS-treated mice (Figure 1C). The relatively higher levels of histamine observed after cell isolation, compared to the whole lung homogenates, might reflect greater degradation in the presence of the lung epithelium, which has high expression of the histamine-degrading enzymes diamine oxidase and histamine N-methyltransferase [18,19]. …”

Section: Resultsmentioning

confidence: 99%

TLR-induced activation of neutrophils promotes histamine production via a PI3 kinase dependent mechanism

2011

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Histamine is a bioactive amine that exerts immunomodulatory functions, including many allergic symptoms. It is preformed and stored in mast cells and basophils but recent evidence suggests that other cell types produce histamine in an inducible fashion. During infection, it has been suggested that neutrophils may produce histamine. We also observed that histamine is released in a neutrophil-mediated LPS-induced model of acute lung injury. Therefore, we sought to examine whether innate signals promote histamine production by neutrophils. Bone marrow-derived neutrophils stimulated with a range of TLR agonists secreted histamine in response to LPS or R837, suggesting TLR4 or TLR7 are important. LPS-driven histamine was enhanced by coculture with GM-CSF and led to a transient release of histamine that peaked at 8 hours post stimulation. This was dependent upon de novo synthesis of histamine, since cells derived from histidine decarboxylase (HDC) deficient mice were unable to produce histamine but did generate reactive oxygen species upon stimulation. Using pharmacological inhibitors, we show that histamine production requires PI3 kinase, which has been shown to regulate other neutrophil functions, including activation and selective granule release. However, unlike mast cells, HDC deficiency did not alter the granule structure of neutrophils, suggesting that histamine does not participate in granule integrity in these cells. Consequently, our findings establish that neutrophils generate histamine in response to a select panel of innate immune triggers and that this might contribute to acute lung injury responses.

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Section: Resultsmentioning

confidence: 99%

TLR-induced activation of neutrophils promotes histamine production via a PI3 kinase dependent mechanism

2011

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“…In contrast, a 30-min exposure to hay and straw did not result in a significant increase in BALF histamine concentration (26). However, histaminase activity in the lung (22) may have resulted in the degradation of histamine released during an early-phase response by the time the 30-min sample was collected. Mast cells that contain chymase rather than tryptase appear to play a role in RAO, with the number of chymasepositive mast cells correlating with the severity of neutrophil infiltration (41).…”

mentioning

confidence: 92%

Early onset airway obstruction in response to organic dust in the horse

Deaton

Deaton²,

Jose‐Cunilleras³

et al. 2007

Journal of Applied Physiology

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Deaton CM, Deaton L, Jose-Cunilleras E, Vincent TL, Baird AW, Dacre K, Marlin DJ. Early onset airway obstruction in response to organic dust in the horse. J Appl Physiol 102: [1071][1072][1073][1074][1075][1076][1077] 2007. First published December 7, 2006; doi:10.1152/japplphysiol.00264.2006.-Equine recurrent airway obstruction (RAO) has been used as a naturally occurring model of human asthma. However, it is unknown whether there is an early-phase response in RAO. The aim of this study was to determine whether exposure to organic dust induces immediate changes in lung function in RAO-affected horses, which could be mediated by airway mast cells. Six RAO-affected horses in remission and six control horses were challenged with hay-straw dust suspension by nebulization. Total respiratory resistance at 1 Hz, measured by forced oscillation, was increased from 0.62 Ϯ 0.09 cmH 2O ⅐ l Ϫ1 ⅐ s (mean Ϯ SE) to 1.23 Ϯ 0.20 cmH2O ⅐ l Ϫ1 ⅐ s 15 min after nebulization in control horses (P ϭ 0.023) but did not change significantly in the RAO group. Total respiratory reactance at 1 Hz (P ϭ 0.005) was significantly lower in the control horses (Ϫ0.77 Ϯ 0.07 cmH2O ⅐ l Ϫ1 ⅐ s) than in the RAO group (Ϫ0.49 Ϯ 0.04 cmH2O ⅐ l Ϫ1 ⅐ s) 15 min after nebulization. Bronchoalveolar lavage fluid (BALF) histamine concentration was significantly elevated 10 and 20 min postnebulization in control horses but not in RAO horses. Minimum reactance at 1 Hz in the early postnebulization period significantly correlated with both prechallenge BALF mast cell numbers (r ϭ Ϫ0.65, P ϭ 0.02) and peak BALF histamine concentration postnebulization (r ϭ Ϫ0.61, P ϭ 0.04). In conclusion, RAO horses, unlike human asthmatic patients, do not exhibit an early-phase response. However, healthy control horses do demonstrate a mild but significant early (Ͻ20 min) phase response to inhaled organic dust. This response may serve to decrease the subsequent dose of dust inhaled and as such provide a protective mechanism, which may be compromised in RAO horses. equine; lung function; allergen HUMAN ASTHMATIC PATIENTS develop an early-phase bronchoconstriction within minutes of exposure to inhaled allergens.

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“…The mucosa was scraped off'with a spatula, suspended 1:4 (w/v), homogenized and centrifuged as for the liver. The radioisotopic assay, H2Oz production and the spectrophotometric assay of 81-pyrroline formation were performed as previously described [10]. Protein determinations were performed by the method of Lowry et al [11] with bovine serum albumin as the standard.…”

Section: Methodsmentioning

confidence: 99%

Some problems with the diamine oxidase (DAO) assay using putrescine as substrate in rat liver

et al. 1993

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Determination of diamine oxidase (DAO) activity in rat liver preparations by measuring the formation of radioactive delta 1-pyrroline from 14C-putrescine is complicated by the complexity of competing metabolic pathways. This can lead to complete masking of the DAO activity present when rat liver homogenates are used as the enzyme source. However, subcellular fractionation of rat liver homogenates makes it possible to detect some putrescine oxidizing activity in the microsomal fraction when assayed at pH 8.5. When 1 mM putrescine was used as the substrate, over 90% of this activity was inhibited by 6 x 10(-4) M selegiline (deprenyl), indicating that monoamine oxidase (MAO) rather than DAO activity was being measured. The observed activity was also interfered with by agents that reduced acetylation processes and polyamine synthesis. A different picture appears when microM concentrations of putrescine are used: in these conditions all interference is strongly reduced and DAO activity can be measured in rat liver microsomes. Furthermore, kinetic studies on deaminative oxidation of 14C-putrescine at concentrations from 1 microM to 5 mM confirm the existence of two enzymes: one with a high affinity for the substrate and similar to intestinal mucosa DAO in its sensitivity to alpha-aminoguanidine, and the other one with a low affinity and selegiline-sensitive.

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Histaminase activity in rat lung and its comparison with intestinal mucosal diamine oxidase

Cited by 14 publications

References 18 publications

TLR-induced activation of neutrophils promotes histamine production via a PI3 kinase dependent mechanism

TLR-induced activation of neutrophils promotes histamine production via a PI3 kinase dependent mechanism

Early onset airway obstruction in response to organic dust in the horse

Some problems with the diamine oxidase (DAO) assay using putrescine as substrate in rat liver

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