Modulation of the Rat Alveolar Macrophage Respiratory Burst by Hydroperoxides Is Calcium Dependent

Hoyal, Carolyn R.; Gozal, Evelyne; Zhou, Huanfang; Foldenauer, Kim; Forman, Henry Jay

doi:10.1006/abbi.1996.0061

Cited by 43 publications

(32 citation statements)

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“…Macrophages express three classes of phospholipase A 2 (PLA 2 ) and two of these are activated in a Ca 2+ -dependent manner [1]. Several agonists have been shown to elicit an increase 2+ ] i in macrophages [7,12,31]. In mouse intestinal resident macrophages, we have already shown that agonists such as ATP, PAF and LPS increased [Ca 2+ ] i [20].…”

Section: Discussionmentioning

confidence: 99%

Phagocytotic Activation of Muscularis Resident Macrophages Inhibits Smooth Muscle Contraction in Rat Ileum

Sato

Torihashi

Hori

et al. 2007

The Journal of Veterinary Medical Science

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ABSTRACT. Intestinal muscularis resident macrophages distributed in myenteric region may play an important role in the immunological host defense against infection. In this study, we investigated the phagocytic stimulation of resident macrophages on cyclooxygenase-2 (COX-2) expression and smooth muscle contraction in the small intestine of rat. After the injection of FITC-dextran to rat, phagocytosed macrophages could be detected in the myenteric plexus. FITC-positive macrophages were also immunostained with COX-2 antibody. The number of COX-2 immunopositive cells increased in a time-dependent manner reaching its maximum at 4 hr after the injection, which then decreased gradually but considerable number of cells were still remained on 7 days. The injection of FITC-dextran, however, did not change the population of ED2-positive resident macrophages even on 7 days. Production of PGE 2 was significantly higher in the dextran treated tissue as compared to control tissue. In the smooth muscle tissue phagocytosed dextran, carbachol-induced contraction was significantly decreased. The suppression of the carbachol-induced contraction was completely restored by COX inhibitor, indomethacin. Finally we demonstrated that, in freshly isolated macrophage cells, addition of dextran induced a slow and sustained increase in intracellular Ca 2+ concentration. These results indicate that phagocytotic activation of muscularis resident macrophages induces COX-2 gene expression and then results in production of PGE 2 to suppress the smooth muscle contractile activity. KEY WORDS: intestinal smooth muscle, phagocytosis, prostaglandin, resident macrophage.

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Section: Discussionmentioning

confidence: 99%

Phagocytotic Activation of Muscularis Resident Macrophages Inhibits Smooth Muscle Contraction in Rat Ileum

Sato

Torihashi

Hori

et al. 2007

The Journal of Veterinary Medical Science

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“…For example, hydroperoxides increase the concentration of intracellular calcium (75,76). Some studies suggest that H202 treatment induces inositol-1,4,5-triphosphate (IP3) production, which allows IP3 to bind to receptors on the endoplasmic reticulum and provoke release of intracellularly stored calcium (72).…”

Section: Introductionmentioning

confidence: 99%

“…Some studies suggest that H202 treatment induces inositol-1,4,5-triphosphate (IP3) production, which allows IP3 to bind to receptors on the endoplasmic reticulum and provoke release of intracellularly stored calcium (72). It may be this increase in calcium that then stimulates phospholipase activity resulting in proteolytic events that have direct effects on the activation of transcription factors such as NF-icB (61,76).…”

Section: Introductionmentioning

confidence: 99%

The role of reactive oxygen and nitrogen species in airway epithelial gene expression.

Martin

Krunkosky

Voynow

et al. 1998

Environ Health Perspect

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The body first encounters deleterious inhaled substances, such as allergens, industrial particles, pollutants, and infectious agents, at the airway epithelium. When this occurs, the epithelium and its resident inflammatory cells respond defensively by increasing production of cytokines, mucus, and reactive oxygen and nitrogen species (ROS/RNS). As inflammation in the airway increases, additional infiltrating cells increase the level of these products. Recent interest has focused on ROS/RNS as potential modulators of the expression of inflammation-associated genes important to the pathogenesis of various respiratory diseases. ROS/RNS appear to play a variety of roles that lead to changes in expression of genes such as interleukin-6 and intercellular adhesion molecule 1. By controlling this regulation, the reactive species can serve as exogenous stimuli, as intercellular signaling molecules, and as modulators of the redox state in epithelial cells. Unraveling the molecular mechanisms affected by ROS/RNS acting in these capacities should aid in the understanding of how stimulated defense mechanisms within the airway can lead to disease.

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“…Pretreatment with thapsigargin, an inhibitor of the e.r. Ca 2C pump, did not affect the ROOH-stimulated Ca 2C release (34), ruling out the e.r. as the source of Ca 2C .…”

Section: Signaling By Ros In Macrophagesmentioning

confidence: 79%

Signaling by the Respiratory Burst in Macrophages

Forman

Torrès²

2001

IUBMB Life

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SummaryDuring phagocytosis or stimulation with a wide variety of agents, macrophages and other phagocytic cells produce reactive oxygen species (ROS) through activation of a multicomponent NADPH oxidase. ROS production through related NADPH oxidases has recently been demonstrated in several other cell types. Furthermore, the physiological generation of ROS production has now been clearly implicated in activating signaling pathways resulting in a broad array of physiological responses from cell proliferation to gene expression and apoptosis. This brief review suggests that: 1) hydrogen peroxide and superoxide, but not the hydroxyl radical, function as second messengers; 2) antioxidant enzymes function in the "turn-off" phase of signal transduction; 3) the chemistry of thiols is critical in redox signaling; and 4) the primary physiological role of the respiratory burst in macrophages may be in redox signaling rather than microbicidal activity. IUBMB INTRODUCTIONOxygen is essential to life and reactive oxygen species (ROS), which include superoxide anion (O :¡ 2 ), hydroxyl radical ( : OH), hydrogen peroxide (H 2 O 2 ), and lipid peroxides (ROOH), which are produced in cells under aerobic conditions. Studies done around 20 years ago had hinted at a role for ROS as second messengers when it was revealed that exogenous H 2 O 2 could mimic the action of the insulin growth factor (1) and that insulin and nerve growth factor stimulated endogenous H 2 O 2 production (2). At that time, the role of ROS in pathology took center stage and researchers focused their attention on the role of phosphorylation of small molecules and proteins as the principal means of transmitting signaling events, pushing signaling by ROS into the background. The more recent discoveries of the activation of several transcription factors by ROS, the role of nitric oxide, a free radical, as a signaling molecule that activates cyclic GMP production (3), and the discovery in many tissues of speci c enzymes as a source of ROS (4-8) stimulated a renaissance in redox signaling studies (see [9][10][11][12][13][14][15] for reviews). Here, we focus on signaling by ROS in macrophages, cells that produce ROS and are exposed to ROS during in ammation.

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Modulation of the Rat Alveolar Macrophage Respiratory Burst by Hydroperoxides Is Calcium Dependent

Cited by 43 publications

References 0 publications

Phagocytotic Activation of Muscularis Resident Macrophages Inhibits Smooth Muscle Contraction in Rat Ileum

Phagocytotic Activation of Muscularis Resident Macrophages Inhibits Smooth Muscle Contraction in Rat Ileum

The role of reactive oxygen and nitrogen species in airway epithelial gene expression.

Signaling by the Respiratory Burst in Macrophages

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