The pulmonary and hepatic immune microenvironment and its contribution to the early systemic inflammation following blunt chest trauma

Perl, Mario; Gebhard, Florian; Braumüller, Sonja; Tauchmann, Björn; Brückner, U. B.; Kinzl, L.; Knöferl, Markus W.

doi:10.1097/01.ccm.0000207343.53990.a8

Cited by 40 publications

(39 citation statements)

References 44 publications

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“…Our histological data showed marked cellular infiltration and free erythrocytes due to alveolar haemorrhage consistent with previous human and rodent reports 11,35 . Furthermore and in line with previous studies 18, 36 , we observed increased BALF levels of CXCL-1, IL-6, TNF-α and albumin -an indicator of endothelial and epithelial barrier damage. Collectively these data support the validity of the injury generated in this system resulting in PBLI.…”

Section: Modelsupporting

confidence: 80%

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CD43Lo classical monocytes participate in the cellular immune response to isolated primary blast lung injury

Barnett-Vanes

Sharrock

Eftaxiopoulou

et al. 2016

Journal of Trauma and Acute Care Surgery

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BackgroundExplosive blast trauma occurs by four mechanisms: primary injuries are due to the isolated effect of the blast wave on the human body, secondary injuries are due to damage from fragments energised from the explosion, tertiary injuries result from acceleration of the body against an object or through the explosion energising hard materials in a solid form (not fragments) and encroaching upon the person, and quaternary injuries describe other physical insults, including burns and smoke inhalation 1 .Gas-containing organs such as the lungs are particularly susceptible to barotrauma, and 'Primary Blast Lung Injury' (PBLI) is a commonly reported injury amongst blast casualties. A review of terrorist bombings worldwide found the incidence of PBLI in immediate fatalities to be as high as 47% 2 ; whilst in a review of military blast casualties that survived to emergency admission, PBLI was found in 11.2% of 648 blast casualties. In this series, 16.2% of mounted and 17.1% of dismounted injuries developed PBLI, which was significantly associated with increased mortality 3,4 .Laboratory investigations of PBLI have sought to recapitulate the injury under experimental conditions. Studies investigating the subsequent immune response have been reported most commonly in rats 5-10 , mice [11][12][13][14][15] and swine 16,17 . These studies have offered overwhelming evidence of the neutrophil response to PBLI in animal models, with increases in circulating and broncho-alveolar lavage fluid (BALF) neutrophils, increases in Myeloperoxidase (MPO) activity in the lung, and neutrophil staining by histology [9][10][11][12]14,18,19 . However, the immune response to tissue damage differs depending on the type of organ injured and their local physiology; it remains unclear what specific contribution blast injuries to different parts of the body make to the inflammatory response that ensues. Whilst most clinically blast injured patients are polytraumatised, discerning these interacting immune responses experimentally is necessary for translational studies seeking to better understand, monitor or attenuate the immune response in blast trauma.Further, knowledge of the role played by other immune cells to PBLI is limited -no study has characterised the full repertoire of immune cells in PBLI; specifically, the involvement of monocytes in PBLI remains unclear. These cells are frequently recruited to sites of inflammation; in humans they are characterised by differential CD14 and CD16 expression 20 , in mice by CCR2, CX3CR1 and Ly6C 21,22 and in rats by CD43 alone or in conjunction with His48 23 . In rats, CD43 Hi and Lo monocytes are considered to be analogous to the Ly6C Lo (Non-classical) and Ly6C Hi (Classical) murine monocytes respectively. Classical Ly6C Hi monocytes are recruited to tissues in sterile 24 and infectious 25 models of inflammation. There, they can differentiate into inflammatory macrophages and dendritic cells, amplifying or resolving inflammation. In rats, circulating monocyte subsets are activated by inflammator...

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Section: Modelsupporting

confidence: 80%

“…We saw significant increases in neutrophils in the blood across all time points, which may in part be driven by circulating chemokines and complement products previously reported to be elevated in PBLI 12,19,36,37 . Additionally, we observed a rapid increase in neutrophils in the lung at 1 and 3hr, returning to baseline by 6hr.…”

Section: Neutrophilsmentioning

confidence: 88%

CD43Lo classical monocytes participate in the cellular immune response to isolated primary blast lung injury

Barnett-Vanes

Sharrock

Eftaxiopoulou

et al. 2016

Journal of Trauma and Acute Care Surgery

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“…In our data this is mirrored by an early increase of MCP-1 at 6 h in BALF and plasma. In lung tissue however, MCP-1 levels were markedly elevated in response to Fas activation late at 18 h. The discrepancies between BALF and lung tissue levels here might be explicable by the different pulmonary compartments involved, since AM and pneumocytes present major sources for MCP-1 and mainly contribute to BALF mediator levels, whereas their influence on lung tissue mediator levels remains limited due to their numerical inferiority [140,144,150]. Finally, the aforementioned early increase of MCP-1 leads directly and indirectly (via MIP-2, KC) to neutrophil attraction and -in case of an additional trigger -to neutrophil activation with subsequent cytokine production.…”

Section: Inflammationmentioning

confidence: 76%

“…In this regard, i.t. instillation of human IL-6 lead to a dose-dependent correlation between BALF and plasma levels after blunt chest trauma, constituting a direct relationship between the local pulmonary and systemic concentration of inflammatory mediators [150]. As opposed to the plethora of consequences following blunt chest trauma, isolated pulmonary Fas-activation leads to the apoptosis of pneumocytes, which has been described as a major contributor regarding a compromise of alveolar wall permeability [73].…”

Section: Inflammationmentioning

confidence: 99%

Divergent Effects of Neutrophils on Fas-Induced Pulmonary Inflammation, Apoptosis, and Lung Damage

Bruns

Hönle

Kellermann

et al. 2017

Shock

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“…They showed for the first time a response to thorax trauma by Kupffer cells within 30 minutes. In so doing, the liver formed IL-6, TNF-alpha and IL-10 in high concentrations, without the liver itself being traumatized (38).…”

Section: "Liver Transplantation Due To Abdominal Trauma" (Discussion)mentioning

confidence: 99%

Liver Transplantation Due to Abdominal Trauma

Heuer¹,

Lendemans²,

Kaiser³

et al. 2012

Liver Transplantation - Basic Issues

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The pulmonary and hepatic immune microenvironment and its contribution to the early systemic inflammation following blunt chest trauma

Cited by 40 publications

References 44 publications

CD43Lo classical monocytes participate in the cellular immune response to isolated primary blast lung injury

CD43Lo classical monocytes participate in the cellular immune response to isolated primary blast lung injury

Divergent Effects of Neutrophils on Fas-Induced Pulmonary Inflammation, Apoptosis, and Lung Damage

Liver Transplantation Due to Abdominal Trauma

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