Acute ethanol intoxication regulates f-met-leu-phe-induced chemotaxis and superoxide release by neutrophils and Kupffer cells through modulation of the formyl peptide receptor in the rat

Bautista, Abraham P.; Elliott, Kirk E.

doi:10.1016/0024-3205(94)90161-9

Cited by 26 publications

(10 citation statements)

References 23 publications

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“…Ethanol administration has been shown to affect immune cells directly to inhibit chemotaxis and proliferation and to modulate the production of some cytokines (12,15,32,49). Recent studies have further shown that ethanol intoxication suppresses pulmonary inflammation (50,51) and impairs neutrophil chemotaxis, thereby exposing the host to increased subsequent infection (52,53). This is consistent with our earlier observation that burn ϩ ethanol-treated mice are less likely to survive a Pseudomonas aeruginosa infection than are burn ϩ vehicle-treated mice (32).…”

Section: Discussionsupporting

confidence: 88%

Elevation in Pulmonary Neutrophils and Prolonged Production of Pulmonary Macrophage Inflammatory Protein-2 after Burn Injury with Prior Alcohol Exposure

Patel

Faunce

Gregory

et al. 1999

Am J Respir Cell Mol Biol

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Various studies have shown that alcohol exposure before thermal injury leads to increased morbidity and mortality. Pulmonary failure is a major complication seen in these patients. This study examines the effects of prior alcohol exposure on lung pathology after burn injury. There is a marked increase in neutrophil recruitment in the lung after thermal injury, and herein we show that this appears to be significantly elevated in animals given alcohol before burn injury. Consequently, we chose to determine whether there is a difference in pulmonary production of macrophage inflammatory protein (MIP)-2, a potent neutrophil chemoattractant, in mice subjected to a 15% total body surface area scald (or sham) injury with or without prior ethanol treatment. Lung tissue was obtained at various time points after injury and homogenates were assayed for MIP-2 by enzyme-linked immunosorbent assay. At 2 h after injury, peak levels of the chemokine were produced in both burn and burn + alcohol-treated mice. This represents a 7-fold increase above baseline. In mice exposed to burn injury alone, the level of MIP-2 returned to baseline within 8 h. In contrast, mice given alcohol before burn injury continued to show elevated levels of the chemokine at 8 h, after which MIP-2 decreased. This study may provide a basis for understanding the mechanism responsible for the increased neutrophil presence in the lung after thermal injury in individuals who have consumed alcohol. Subsequently, this may lead to the enhanced neutrophil-mediated pulmonary damage observed in these patients.

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Section: Discussionsupporting

confidence: 88%

Elevation in Pulmonary Neutrophils and Prolonged Production of Pulmonary Macrophage Inflammatory Protein-2 after Burn Injury with Prior Alcohol Exposure

Patel

Faunce

Gregory

et al. 1999

Am J Respir Cell Mol Biol

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“…The possibility that ethanol could enhance the NADPH oxidase system or the assay used to measure O − 2 was examined, and has been ruled out due to the following observations: (a) under our experimental conditions ethanol decreased by 70% the fMet‐Leu‐Phe‐induced oxidative response, as described in other studies [34,35]; by contrast, ethanol increased the oxidative response in PMA‐stimulated PMNs. (b) The production of O − 2 in a cell‐free system generating O − 2 was unaffected in the presence of ethanol showing no effect of ethanol on the assay itself.…”

Section: Discussionmentioning

confidence: 77%

Ethanol increases superoxide anion production stimulated with 4β‐phorbol 12‐myristate 13‐acetate in human polymorphonuclear leukocytes

Raddassi¹,

Murray

2000

European Journal of Biochemistry

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Stimulation of human polymorphonuclear leukocytes (PMNs) with PMA initiates a cascade of events leading to the production and release of superoxide anion (O 2 2 ), a major component in anti-bacterial defense. Generation of O 2 2 by PMA-stimulated PMNs occurs through the translocation and activation of protein kinase C (PKC). In this study, using freshly isolated PMNs, we examined the effect of ethanol on this response to PMA. Our results show that the basal production of O 2 2 was not affected by ethanol. In contrast, the response induced by PMA was potentiated by ethanol. This potentiation was observed even at high doses of PMA (200 nm) which alone had stimulated the O 2 2 response maximally. This enhanced response was not due to an increase of PMA uptake by PMNs. The maximal effect was obtained when the cells were preincubated with 80 mm of ethanol before PMA stimulation. Measurement of PKC activity in the cytosolic and membrane fractions showed that pretreatment of PMNs with ethanol increased twofold the PMA-stimulated PKC activity in the membrane fraction. Furthermore, Western blot analysis verified that this increase in PKC activity in the membrane fraction was linked to an increase in the translocation of PKC-a and -b isoforms to the membrane. These results suggest that ethanol potentiates PMA-induced O 2 2 production through increasing PKC translocation and activity in PMNs.

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“…A few reports propose that the impaired phagocytosis by neutrophils in alcohol-treated animals may be due to lower expression levels of important receptors involved in phagocytosis [135,136,155]. Interestingly, reports show that both chronic and binge alcohol exposure boosts the production of ROS by neutrophils [121,149,150,156]; yet, the ability of neutrophils to kill pathogens is lessened after both binge and chronic alcohol exposure, which may partially be due to their aforementioned compromised phagocytic capacity [150,157,158]. There are no reports to date regarding the effect of alcohol consumption on NET formation, but NET formation is blunted with advanced age, possibly because of poorer ROS production in neutrophils from aged humans and mice [88,89].…”

Section: Neutrophilsmentioning

confidence: 99%

Alcohol, aging, and innate immunity

Boule

Kovacs

2017

Journal of Leukocyte Biology

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The global population is aging: in 2010, 8% of the population was older than 65 y, and that is expected to double to 16% by 2050. With advanced age comes a heightened prevalence of chronic diseases. Moreover, elderly humans fair worse after acute diseases, namely infection, leading to higher rates of infection-mediated mortality. Advanced age alters many aspects of both the innate and adaptive immune systems, leading to impaired responses to primary infection and poor development of immunologic memory. An often overlooked, yet increasingly common, behavior in older individuals is alcohol consumption. In fact, it has been estimated that >40% of older adults consume alcohol, and evidence reveals that >10% of this group is drinking more than the recommended limit by the National Institute on Alcohol Abuse and Alcoholism. Alcohol consumption, at any level, alters host immune responses, including changes in the number, phenotype, and function of innate and adaptive immune cells. Thus, understanding the effect of alcohol ingestion on the immune system of older individuals, who are already less capable of combating infection, merits further study. However, there is currently almost nothing known about how drinking alters innate immunity in older subjects, despite innate immune cells being critical for host defense, resolution of inflammation, and maintenance of immune homeostasis. Here, we review the effects of aging and alcohol consumption on innate immune cells independently and highlight the few studies that have examined the effects of alcohol ingestion in aged individuals.

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Acute ethanol intoxication regulates f-met-leu-phe-induced chemotaxis and superoxide release by neutrophils and Kupffer cells through modulation of the formyl peptide receptor in the rat

Cited by 26 publications

References 23 publications

Elevation in Pulmonary Neutrophils and Prolonged Production of Pulmonary Macrophage Inflammatory Protein-2 after Burn Injury with Prior Alcohol Exposure

Elevation in Pulmonary Neutrophils and Prolonged Production of Pulmonary Macrophage Inflammatory Protein-2 after Burn Injury with Prior Alcohol Exposure

Ethanol increases superoxide anion production stimulated with 4β‐phorbol 12‐myristate 13‐acetate in human polymorphonuclear leukocytes

Alcohol, aging, and innate immunity

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