Long-Chain Polyunsaturated Fatty Acids Modulate Lung Inflammatory Response Induced by Pseudomonas aeruginosa in Mice

Auvin, Stéphane; François, Clément; Gottrand, Frédéric; Husson, Marie-Odile; Leroy, Xavier; Beermann, Christopher; Guery, Benoît

doi:10.1203/01.pdr.0000169979.27641.40

Cited by 11 publications

(5 citation statements)

References 24 publications

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“…We previously demonstrated that feeding C57BL/6 mice for 5 wk with EPA/DHA improved the outcomes of acute and chronic P. aeruginosa lung infections by reducing mortality and lung injury, evaluated by measuring the permeability of the alveolar-capillary barrier (27,28). This benefit was correlated with the beneficial suppressive effects on mucin overexpression (29) and better control of the proinflammatory response together with limited neutrophil recruitment and faster clearance of bacteria during the first 24 h of infection (30).…”

Section: Introductionmentioning

confidence: 99%

(n-3) Long-Chain PUFA Differentially Affect Resistance toPseudomonas aeruginosaInfection of Male and FemalecftrMice

Tiesset

Bernard

Bartke³

et al. 2011

The Journal of Nutrition

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The aim of this study was to determine whether oral supplementation with EPA/DHA (10.5 and 5.1% of fat, respectively) could improve the outcome of pulmonary P. aeruginosa infection in cftr(-/-) mice compared with wild-type (Wt) mice similarly treated. Because gender could influence the susceptibility of cftr-deficient mice, results were analyzed by gender. Wt and (-/-) mice were randomized for 6 wk to consume a control or EPA/DHA diet, infected with endotracheal injection of 5 × 10(7) CFU/mouse of P. aeruginosa, and killed 24 h later. Cftr(-/-) mice were more susceptible to infection than were Wt mice; (-/-) males had more neutrophils (P < 0.01) and a higher keratinocyte-derived chemokine (KC) level (P < 0.05), and (-/-) females had greater lung injury and mortality (P < 0.05). Female (-/-) mice were more susceptible than (-/-) males with a higher mortality and lung injury (P < 0.05). The EPA/DHA diet reduced neutrophil numbers and KC and IL-6 levels (P < 0.05) in (-/-) males and reduced mortality rate (P < 0.001), lung permeability, and IL-6 level (P < 0.05) in (-/-) females compared with (-/-) mice fed the control diet. These results were associated with a reduction in the pulmonary bacterial load (P < 0.05), an increase in the EPA/DHA concentration in cell membranes of (-/-) males and females (P < 0.01), and an increased weight gain only in males compared with (-/-) mice fed the control diet (P < 0.01). In conclusion, EPA/DHA improves the host resistance of (-/-) mice, although the beneficial effect differed in males and females.

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Section: Introductionmentioning

confidence: 99%

(n-3) Long-Chain PUFA Differentially Affect Resistance toPseudomonas aeruginosaInfection of Male and FemalecftrMice

Tiesset

Bernard

Bartke³

et al. 2011

The Journal of Nutrition

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“…In in vivo experiments using a rat model of P. aeruginosa pneumonia, it was observed that several oxidative metabolites of arachidonic acid, including 20-HETE, contributed to pulmonary vascular hypo reactivity (94). Finally, Auvin and colleagues showed that dietary supplementation of arachidonic acid in a mouse model of P. aeruginosa infection led to an increased mortality rate (95). The results from all of these studies point to an important interaction between P. aeruginosa and arachidonic acid and its metabolites.…”

Section: Discussionmentioning

confidence: 99%

Pseudomonas aeruginosa cytochrome P450 CYP168A1 is a fatty acid hydroxylase that metabolizes arachidonic acid to the vasodilator 19-HETE

Tooker¹,

Kandel²,

Work

et al. 2022

Journal of Biological Chemistry

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This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

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“…Upon infection of the airway, pseudomonads infect alveolar epithelial cells and resident macrophages, eliciting release of pro-inflammatory cytokines to recruit immune cells into the lung parenchyma and airspaces [17,19–22]. Subsequent damage to the alveolar epithelial barrier allows direct infection of lung endothelial cells that, along with the deleterious effects of endotoxin and cytokines, precipitate vascular endothelial barrier disruption [2,20,23–27].…”

Section: Introductionmentioning

confidence: 99%

In the Absence of Effector Proteins, the Pseudomonas aeruginosa Type Three Secretion System Needle Tip Complex Contributes to Lung Injury and Systemic Inflammatory Responses

et al. 2013

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Herein we describe a pathogenic role for the Pseudomonas aeruginosa type three secretion system (T3SS) needle tip complex protein, PcrV, in causing lung endothelial injury. We first established a model in which P. aeruginosa wild type strain PA103 caused pneumonia-induced sepsis and distal organ dysfunction. Interestingly, a PA103 derivative strain lacking its two known secreted effectors, ExoU and ExoT [denoted PA103 (ΔU/ΔT)], also caused sepsis and modest distal organ injury whereas an isogenic PA103 strain lacking the T3SS needle tip complex assembly protein [denoted PA103 (ΔPcrV)] did not. PA103 (ΔU/ΔT) infection caused neutrophil influx into the lung parenchyma, lung endothelial injury, and distal organ injury (reminiscent of sepsis). In contrast, PA103 (ΔPcrV) infection caused nominal neutrophil infiltration and lung endothelial injury, but no distal organ injury. We further examined pathogenic mechanisms of the T3SS needle tip complex using cultured rat pulmonary microvascular endothelial cells (PMVECs) and revealed a two-phase, temporal nature of infection. At 5-hours post-inoculation (early phase infection), PA103 (ΔU/ΔT) elicited PMVEC barrier disruption via perturbation of the actin cytoskeleton and did so in a cell death-independent manner. Conversely, PA103 (ΔPcrV) infection did not elicit early phase PMVEC barrier disruption. At 24-hours post-inoculation (late phase infection), PA103 (ΔU/ΔT) induced PMVEC damage and death that displayed an apoptotic component. Although PA103 (ΔPcrV) infection induced late phase PMVEC damage and death, it did so to an attenuated extent. The PA103 (ΔU/ΔT) and PA103 (ΔPcrV) mutants grew at similar rates and were able to adhere equally to PMVECs post-inoculation indicating that the observed differences in damage and barrier disruption are likely attributable to T3SS needle tip complex-mediated pathogenic differences post host cell attachment. Together, these infection data suggest that the T3SS needle tip complex and/or another undefined secreted effector(s) are important determinants of P. aeruginosa pneumonia-induced lung endothelial barrier disruption.

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Long-Chain Polyunsaturated Fatty Acids Modulate Lung Inflammatory Response Induced by Pseudomonas aeruginosa in Mice

Cited by 11 publications

References 24 publications

(n-3) Long-Chain PUFA Differentially Affect Resistance toPseudomonas aeruginosaInfection of Male and FemalecftrMice

(n-3) Long-Chain PUFA Differentially Affect Resistance toPseudomonas aeruginosaInfection of Male and FemalecftrMice

Pseudomonas aeruginosa cytochrome P450 CYP168A1 is a fatty acid hydroxylase that metabolizes arachidonic acid to the vasodilator 19-HETE

In the Absence of Effector Proteins, the Pseudomonas aeruginosa Type Three Secretion System Needle Tip Complex Contributes to Lung Injury and Systemic Inflammatory Responses

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