Diesel exhaust particulates upregulate histamine receptor mRNA and increase histamine‐induced IL‐8 and GM‐CSF production in nasal epithelial cells and endothelial cells

Terada, Nobuhisa; Hamano, Nanako; Maesako, Ken-ichi; Hiruma, Kiyoshi; Hohki, Gen; Suzuki, Kazuo; Ishikawa, Kazuo; Konno, Akiyoshi

doi:10.1046/j.1365-2222.1999.00406.x

Cited by 83 publications

(48 citation statements)

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“…Up-regulation of H1R was also observed in patients with allergic rhinitis (6, 7). Terada et al (36) reported that H1R mRNA was increased in human nasal epithelial cells after stimulation with diesel exhaust particles that are known to cause chronic airway diseases. They also showed that histamine stimulation induced production of granulocyte macrophage-colony stimulating factor and interleukin-8 (IL-8) in human nasal epithelial cells.…”

Section: Discussionmentioning

confidence: 99%

Involvement of Protein Kinase Cδ/Extracellular Signal-regulated Kinase/Poly(ADP-ribose) Polymerase-1 (PARP-1) Signaling Pathway in Histamine-induced Up-regulation of Histamine H1 Receptor Gene Expression in HeLa Cells

Mizuguchi

Terao

Kitai

et al. 2011

Journal of Biological Chemistry

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The histamine H 1 receptor (H1R) gene is up-regulated in patients with allergic rhinitis. However, the mechanism and reason underlying this up-regulation are still unknown. Recently, we reported that the H1R expression level is strongly correlated with the severity of allergic symptoms. Therefore, understanding the mechanism of this up-regulation will help to develop new anti-allergic drugs targeted for H1R gene expression. Here we studied the molecular mechanism of H1R up-regulation in HeLa cells that express H1R endogenously in response to histamine and phorbol 12- Histamine is a major chemical mediator of allergic reactions, and its action is mainly mediated by the histamine H 1 receptor (H1R), 2 which is one of the four histamine receptor isoforms. H1R, which is a G protein-coupled receptor, is coupled to the G q protein. The stimulation of H1R activates inositol phospholipid hydrolysis and intracellular Ca 2ϩ mobilization. Typically, the activation of G protein-coupled receptors by their agonists induces down-regulation of the receptors. However, to date, a few reports have demonstrated up-regulation of G proteincoupled receptors by their agonists (1-4). Previously, we found that histamine stimulation up-regulated H1R at both the mRNA and protein level via activation of H1R in HeLa cells that express H1R endogenously (5). Up-regulation of H1R has been observed in patients with allergic rhinitis (6, 7). The strength of H1R signaling depends on the H1R expression level (8). Our recent studies have demonstrated that the level of H1R gene expression is strongly correlated with the severity of allergic symptoms in model rats and patients with pollinosis (9, 10), and compounds that suppress H1R gene up-regulation alleviate allergic symptoms (11-16). These findings suggest that the H1R gene is an allergy-sensitive gene, i.e. its expression level affects the severity of symptoms. Hence, understanding the molecular mechanism of H1R up-regulation may be useful for developing new anti-allergic drugs that target H1R gene expression. However, the mechanism of H1R up-regulation in response to histamine is unknown.Previously, we demonstrated that PKC-dependent signaling is involved in up-regulation of H1R gene expression in HeLa cells (5). PKC consists of at least 11 isoforms, and based on their structures and cofactor requirements, the PKC isoforms are divided into three subgroups; that is, conventional PKC (␣, ␤, and ␥), novel PKC (␦, ⑀, , and ), and atypical PKC ( and /) (17). It has been reported that PKC ␣, ␤, ␦, ⑀, and isoforms are expressed in HeLa cells (18 -20).Coupling of H1R signaling with PKC␣ has been reported in H1R-overexpressing CHO cells (21) and native human epidermal keratinocytes (22). In these cells, however, no up-regulation of H1R gene expression was observed. In addition, NF-B (23), the cAMP response element-binding protein (CREB) (24)), the nuclear factor of activated T-cell (25), and the serumresponsive element (26)

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Section: Discussionmentioning

confidence: 99%

Involvement of Protein Kinase Cδ/Extracellular Signal-regulated Kinase/Poly(ADP-ribose) Polymerase-1 (PARP-1) Signaling Pathway in Histamine-induced Up-regulation of Histamine H1 Receptor Gene Expression in HeLa Cells

Mizuguchi

Terao

Kitai

et al. 2011

Journal of Biological Chemistry

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“…Histamine H 1 receptor (H 1 R) is expressed in both central and peripheral tissues [1], and its expression level is dynamically regulated under various physiological and pathological conditions: upregulation of H 1 Rs or H 1 R mRNA in the electrical foci in the temporal cortex of epileptic patients [2] and in the nasal mucosa of patients with allergic rhinitis [3,4], downregulation of H 1 Rs in the frontal cortex of patients with chronic schizophrenia [5] and in the frontal and temporal areas of patients with Alzheimer's disease [6]. The H 1 R level may be regulated under these conditions by various processes as indicated for other types of G protein-coupled receptors (GPCRs), including modulation of receptor gene transcription [7], mRNA stability [8] and receptor degradation [9], and agonist-induced receptor degradation or receptor downregulation seems to play an important role among these processes.…”

Section: Introductionmentioning

confidence: 99%

Two threonine residues and two serine residues in the second and third intracellular loops are both involved in histamine H₁ receptor downregulation

et al. 2004

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“…Terada et al (41) demonstrated that DEPs upregulate the expression of histamine-1 receptor mRNA in human airway epithelial and endothelial cells, and enhance histamine induced increase in IL-8 and granulocyte-macrophage colony-stimulating factor (GM-CSF) production in vitro. Histamine-1 receptor mRNA is markedly increased in patients with allergic rhinitis (42), and a further up-regulation induced by DEP may further enhance the effects of histamine.…”

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confidence: 99%

Adverse respiratory effects and allergic susceptibility in relation to particulate air pollution: flirting with disaster

Cacciola

Sarvà

Polosa

2002

Allergy

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The prevalence of allergic conditions such as asthma, rhinoconjunctivitis and atopic eczema/dermatitis has steadily increased in recent decades. Elicitation of an IgE-mediated allergic trait appears to be determined by the complex interplay of multiple genetic and environmental factors. However, although genetic factors in addition to allergen exposure are important, the observed rise in the prevalence of allergic conditions is likely to be ensuing from modifications occurring in the environment (1-3). The remarkable expansion in motor vehicle traffic and its associated emissions has paralleled the world-wide increase in the prevalence of respiratory tract conditions (4). Over the last 40 years the global vehicular fleet has expanded ten-fold and the number of vehicles are predicted to increase even further over the next 20-30 years (5). Estimates by the United Nations indicate that over 600 million people living in cities and towns world-wide are exposed to unhealthy and dangerous levels of motor vehicle generated air pollutants (6).Although the health effects of urban air pollution on the respiratory tract has been the focus of much research in recent times, it appears that less attention has been given to the potential role of pollutants emitted from motor vehicle exhausts in the elicitation of allergic conditions. Several laboratory based studies have demonstrated that particulate air pollutants emitted from motor vehicles can induce mucosal inflammation, enhance IgE responses, and heighten airway hyperresponsivenss which could provide an explanation for the increasing prevalence of respiratory symptoms and allergic diseases (7). The present article reviews our current understanding of the mechanisms by which pollutants such as diesel exhaust particles (DEP) enhance the underlying allergic inflammatory response, and the evidence that supports the causative link between particulate air pollution from motor vehicles and increasing allergic diseases. This article will comply with the recently revised nomenclature of allergic disorders proposed by an EAACI task force (8).Particulate air pollutants and respiratory symptoms: epidemiological evidence A number of epidemiological studies in several countries support the view that exposure to traffic-related pollutants is associated with a broad spectrum of adverse short-term respiratory effects in vulnerable individuals. Studies in Japan (9-11) have shown that people living close to main roads with heavy traffic suffered more respiratory symptoms and allergies than those living further away. Similar studies carried out in the UK (12) and in the Netherlands (13, 14) reported increased respiratory symptoms and reduced lung function in those children living in close proximity of roads with high traffic intensity, which positively correlated with the levels of particulate matter in the

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Diesel exhaust particulates upregulate histamine receptor mRNA and increase histamine‐induced IL‐8 and GM‐CSF production in nasal epithelial cells and endothelial cells

Abstract: These results strongly suggest that DEP accelerates the inflammatory change by not only directly upregulating H1R expression but also increasing histamine-induced IL-8 and GM-CSF production.

Cited by 83 publications

References 36 publications

Involvement of Protein Kinase Cδ/Extracellular Signal-regulated Kinase/Poly(ADP-ribose) Polymerase-1 (PARP-1) Signaling Pathway in Histamine-induced Up-regulation of Histamine H1 Receptor Gene Expression in HeLa Cells

Involvement of Protein Kinase Cδ/Extracellular Signal-regulated Kinase/Poly(ADP-ribose) Polymerase-1 (PARP-1) Signaling Pathway in Histamine-induced Up-regulation of Histamine H1 Receptor Gene Expression in HeLa Cells

Two threonine residues and two serine residues in the second and third intracellular loops are both involved in histamine H₁ receptor downregulation

Adverse respiratory effects and allergic susceptibility in relation to particulate air pollution: flirting with disaster

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Diesel exhaust particulates upregulate histamine receptor mRNA and increase histamine‐induced IL‐8 and GM‐CSF production in nasal epithelial cells and endothelial cells

Abstract: These results strongly suggest that DEP accelerates the inflammatory change by not only directly upregulating H1R expression but also increasing histamine-induced IL-8 and GM-CSF production.

Cited by 83 publications

References 36 publications

Involvement of Protein Kinase Cδ/Extracellular Signal-regulated Kinase/Poly(ADP-ribose) Polymerase-1 (PARP-1) Signaling Pathway in Histamine-induced Up-regulation of Histamine H1 Receptor Gene Expression in HeLa Cells

Involvement of Protein Kinase Cδ/Extracellular Signal-regulated Kinase/Poly(ADP-ribose) Polymerase-1 (PARP-1) Signaling Pathway in Histamine-induced Up-regulation of Histamine H1 Receptor Gene Expression in HeLa Cells

Two threonine residues and two serine residues in the second and third intracellular loops are both involved in histamine H1 receptor downregulation

Adverse respiratory effects and allergic susceptibility in relation to particulate air pollution: flirting with disaster

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Two threonine residues and two serine residues in the second and third intracellular loops are both involved in histamine H₁ receptor downregulation