Resident Pleural Macrophages Are Key Orchestrators of Neutrophil Recruitment in Pleural Inflammation

Cailhier, Jean François; Sawatzky, Deborah A.; Kipari, Tiina; Houlberg, Kris; Walbaum, Dave; Watson, Sandra; Lang, Richard A.; Clay, Spike; Kluth, David; Savill, John; Hughes, Jeremy

doi:10.1164/rccm.200504-538oc

Cited by 63 publications

(45 citation statements)

References 39 publications

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“…DT (10 ng/g) (18,19) was administered 6 and 24 hours after intratracheal LPS. For adoptive cell add-back experiments, age-, strain-, and sex-matched animals were used as controls, and DT was administered at the same intervals as described above.…”

Section: Monocyte Depletionmentioning

confidence: 99%

“…Delineating the role of the PBM independently from its tissue descendents in the mononuclear phagocyte system (MPS) has been difficult. The majority of published models investigating depletion in the MPS system in vivo affect PBMs and tissue-resident macrophages (17)(18)(19). Indeed, studies have highlighted the role played by the resident alveolar macrophage (AM) in eliciting the inflammatory response in ALI through orchestration of early chemokine responses (20,21).…”

mentioning

confidence: 99%

“…Indeed, studies have highlighted the role played by the resident alveolar macrophage (AM) in eliciting the inflammatory response in ALI through orchestration of early chemokine responses (20,21). In contrast to models used to study anatomical compartments such as the peritoneum and pleura (18,19), it is possible to selectively ablate the PBM compartment without affecting resident AMs in murine models of lung inflammation (22). We used three independent techniques to deplete PBMs: systemic liposomal clodronate (sLC), diphtheria toxin (DT) administration in CD11b diphtheria toxin receptor (DTR) mice, and targeted antibody-dependent cell-mediated cytotoxic (ADCC) depletion of monocytes (Table 1).…”

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confidence: 99%

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Monocytes Control Second-Phase Neutrophil Emigration in Established Lipopolysaccharide-induced Murine Lung Injury

Dhaliwal

Scholefield

Ferenbach

et al. 2012

Am J Respir Crit Care Med

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108

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Rationale: Acute lung injury (ALI) is an important cause of morbidity and mortality, with no currently effective pharmacological therapies. Neutrophils have been specifically implicated in the pathogenesis of ALI, and there has been significant research into the mechanisms of early neutrophil recruitment, but those controlling the later phases of neutrophil emigration that characterize disease are poorly understood. Objectives: To determine the influence of peripheral blood monocytes (PBMs) in established ALI. Methods: In a murine model of LPS-induced ALI, three separate models of conditional monocyte ablation were used: systemic liposomal clodronate (sLC), inducible depletion using CD11b diphtheria toxin receptor (CD11b DTR) transgenic mice, and antibodydependent ablation of CCR2 hi monocytes. Measurements and Main Results: PBMs play a critical role in regulating neutrophil emigration in established murine LPS-induced lung injury. Gr1 hi and Gr1 lo PBM subpopulations contribute to this process. PBM depletion is associated with a significant reduction in measures of lung injury. The specificity of PBM depletion was demonstrated by replenishment studies in which the effects were reversed by systemic PBM infusion but not by systemic or local pulmonary infusion of mature macrophages or lymphocytes. Conclusions: These results suggest that PBMs, or the mechanisms by which they influence pulmonary neutrophil emigration, could represent therapeutic targets in established ALI. Keywords: acute lung injury; LPS; monocytes; neutrophilsThe innate inflammatory response is geared to the clearance of pathogens, but excessive and persistent granulocyte accumulation is detrimental to the host (1). Acute lung injury (ALI) and its severe form, acute respiratory distress syndrome (ARDS), are characterized by neutrophil-mediated lung injury, the most common etiology being severe sepsis (2). Neutrophil-mediated lung injury of the epithelial/endothelial interface and consequent vascular leak are the hallmarks of ALI/ARDS (2-4). There are 200,000 cases per year of ALI in the United States, with a mortality of approximately 40% (2). No pharmacological agents have been shown convincingly to affect mortality. There is thus a pressing need to define critical mediators of neutrophil recruitment and to implement specific, mechanismbased therapeutic interventions.The neutrophilic response in ALI has been described as occurring in two distinct phases (5): an initial "recruitment phase" mediated by chemokines followed by a "persistent phase" of neutrophil recruitment, possibly mediated in part by stromal-derived factor-1 (SDF-1/CXCL12) (5). Patients often present with established lung inflammation, and interventions must therefore be guided toward this second phase of neutrophil recruitment to reduce lung injury and ventilator dependence. The underlying cellular mechanisms driving this second phase of neutrophil recruitment remain to be fully characterized.Peripheral blood monocytes (PBMs) are recruited alongside neutrophils in acute inflammati...

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Section: Monocyte Depletionmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Monocytes Control Second-Phase Neutrophil Emigration in Established Lipopolysaccharide-induced Murine Lung Injury

Dhaliwal

Scholefield

Ferenbach

et al. 2012

Am J Respir Crit Care Med

Self Cite

108

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“…24,25 In this context, previous studies [11][12][13] had also shown that these two cytokines are the prior mediators involved in the inflammatory response as well as the inflammation caused by carrageenan in the mouse model of pleurisy and the leukocytes are targets of TNFα and IL-1β. …”

Section: Discussionmentioning

confidence: 96%

“…9 These cytokines profoundly affect structural and functional cells, promoting cellular chemotaxis and other responses. 10 Further, studies from Fröde et al 11 as well as from Cailhier et al 12 and Mazzon and Cuzzocrea 13 had shown that these two cytokines (TNFα and IL-1β) are the prior mediators involved in the inflammatory response, and the leukocytes are known to be both the source and the target of these cytokines in the mouse model of pleurisy induced by carrageenan.…”

Section: Introductionmentioning

confidence: 99%

Cyclosporin A inhibits CD11a/CD18 adhesion molecules due to inhibition of TNF-α and IL-1β levels in the mouse model of pleurisy induced by carrageenan

Dalmarco

Medeiros

Fröde

2008

Cell Adhesion & Migration

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The mouse model of pleurisy induced by carrageenan is characterized by a significant enhancement of cell migration due to neutrophils 4 h after pleurisy induction. Forty-eight hours after pleurisy induction, a significant increase in cell migration due to mononuclear cells occurs. Recently, studies in our laboratory have demonstrated that cyclosporine A (CsA) inhibits leukocyte migration in the pleural cavity and lungs in the mouse model of pleurisy induced by carrageenan. In the present work we evaluated whether CsA was able to downregulate CD11a/CD18 adhesion molecule in the lungs, as well as TNFα and IL-1β levels in the fluid leakage of the pleural cavity in this model. Our results showed that CsA significantly decreased CD11a/CD18 in the lungs, as well as TNFα and IL-1β levels in the fluid leakage of the pleural cavity 4 h and 48 h after pleurisy induction. It is our hypothesis that the inhibitory effect elicited by CsA upon these adhesion molecules may be also be attributed to the downregulation of TNFα and IL-1β cytokines.

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Pharmacoengineering of Lipid Nanoarchitectonics in Modulating Particle Uptake by Lung Macrophages

Thalla¹,

Banerjee²

2021

Nanoengineering of Biomaterials

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Resident Pleural Macrophages Are Key Orchestrators of Neutrophil Recruitment in Pleural Inflammation

Abstract: These studies indicate a critical role for resident pleural macrophages in sensing perturbation to the local microenvironment and orchestrating subsequent neutrophil infiltration.

Cited by 63 publications

References 39 publications

Monocytes Control Second-Phase Neutrophil Emigration in Established Lipopolysaccharide-induced Murine Lung Injury

Monocytes Control Second-Phase Neutrophil Emigration in Established Lipopolysaccharide-induced Murine Lung Injury

Cyclosporin A inhibits CD11a/CD18 adhesion molecules due to inhibition of TNF-α and IL-1β levels in the mouse model of pleurisy induced by carrageenan

Pharmacoengineering of Lipid Nanoarchitectonics in Modulating Particle Uptake by Lung Macrophages

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