Increased MerTK expression in circulating innate immune cells of patients with septic shock

Guignant, Caroline; Venet, Fabienne; Planel, Séverine; Demaret, Julie; Gouel-Cheron, Aurélie; Nougier, Christophe; Friggeri, Arnaud; Allaouchiche, Bernard; Lepape, Alain; Monneret, Guillaume

doi:10.1007/s00134-013-3006-9

Cited by 30 publications

(23 citation statements)

References 31 publications

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“…Patients who received macrolides more often had chronic obstructive pulmonary diseases. Length of ICU stay in survivors was not significantly different in patients who received macrolides compared to patients who did not [10][11][12][13][14][15][16][17][18][19][20] vs. [10][11][12][13][14][15][16][17][18][19][20], p = 0.9]. ICU mortality was 24.1 % (n = 177).…”

Section: Community-acquired Pneumoniamentioning

confidence: 92%

“…MerTK is a protein tyrosine kinase that with Tyro-3 and Axl comprises the TAM receptor family. In their very interesting and elegant study, Guignant et al [10] prospectively evaluated 98 patients with septic shock and severe trauma to investigate the expression patterns of TAM receptors in circulating white blood cells. They observed that the evolution of MerTK expression in circulating monocytes over time is associated with adverse outcome in patients with septic shock.…”

Section: Immune Dysfunction During Sepsis and Antimicrobial Dose Varimentioning

confidence: 99%

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Year in review in Intensive Care Medicine 2013: III. Sepsis, infections, respiratory diseases, pediatrics

et al. 2014

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Section: Community-acquired Pneumoniamentioning

confidence: 92%

Section: Immune Dysfunction During Sepsis and Antimicrobial Dose Varimentioning

confidence: 99%

Year in review in Intensive Care Medicine 2013: III. Sepsis, infections, respiratory diseases, pediatrics

et al. 2014

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“…Although inhibition of innate inflammation is essential to prevent autoimmunity during apoptotic cell clearance, prolonged engagement of TAM receptors may cause a state of unresponsiveness in antigen presenting cells required to clear pathogenic micro-organisms. To support this hypothesis, elevated GAS-6 plasma levels are observed in patients with severe sepsis [41,42], and MerTK is elevated on monocytes from patients with septic shock, and is linked to an adverse outcome [43]. The consequences of these observations remain as yet unexplored.…”

Section: Mechanisms Of Susceptibility To Infectionsmentioning

confidence: 99%

Macrophage adaptation in airway inflammatory resolution

et al. 2015

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Bacterial and viral infections (exacerbations) are particularly problematic in those with underlying respiratory disease, including post-viral infection, asthma, chronic obstructive pulmonary disease and pulmonary fibrosis. Patients experiencing exacerbations tend to be at the more severe end of the disease spectrum and are often difficult to treat. Most of the unmet medical need remains in this patient group. Airway macrophages are one of the first cell populations to encounter airborne pathogens and, in health, exist in a state of reduced responsiveness due to interactions with the respiratory epithelium and specific factors found in the airway lumen. Granulocyte-macrophage colony-stimulating factor, interleukin-10, transforming growth factor-β, surfactant proteins and signalling via the CD200 receptor, for example, all raise the threshold above which airway macrophages can be activated. We highlight that following severe respiratory inflammation, the airspace microenvironment does not automatically re-set to baseline and may leave airway macrophages more restrained than they were at the outset. This excessive restraint is mediated in part by the clearance of apoptotic cells and components of extracellular matrix. This implies that one strategy to combat respiratory exacerbations would be to retune airway macrophage responsiveness to allow earlier bacterial recognition. @ERSpublications Re-educating airway macrophages that do not reset to baseline following severe inflammation

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“…Monocytes expressing MERTK bore enhanced migratory capacity and hence accumulated in diverse sites of inflammation, that is, liver, lymph nodes, the peritoneum and the circulatory compartment [26]. MERTK has also been found activated in nonhepatic conditions of prolonged anti-inflammatory responses such as septic shock [29].…”

Section: Infection Related Mortality In Acute-on-chronic Liver Failurementioning

confidence: 99%

Immunotherapy in the Treatment and Prevention of Infection in Acute-on-chronic Liver Failure

et al. 2015

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Chronic liver disease, depicted by gradual destruction and fibrosis of the liver, is a condition with high and probably increasing prevalence worldwide. Its deterioration, acute-on-chronic liver failure (ACLF), is characterized by an in-hospital mortality of up to 65%. Infectious complications are the main precipitants eliciting ACLF and concurrently the main cause of death from ACLF. Patients have a marked susceptibility to bacterial infections, which is thought to arise a consequence of an inadequate immune response to microbial challenge, termed immuneparesis. The pathophysiologic mechanisms remain poorly understood. Treatments aimed at restoring the patients' immune function may prevent onset of ACLF and death from secondary infections. A number of drugs approved for patients with liver disease bear immunomodulatory potential such as albumin, glucocorticoids, N-acetylcysteine. Specific targets have been defined that may lead to development of new immunotherapeutic agents. Here, we summarize the pathophysiology of immuneparesis in ACLF and drug candidates to restore immune function and improve survival in the future.

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Increased MerTK expression in circulating innate immune cells of patients with septic shock

Cited by 30 publications

References 31 publications

Year in review in Intensive Care Medicine 2013: III. Sepsis, infections, respiratory diseases, pediatrics

Year in review in Intensive Care Medicine 2013: III. Sepsis, infections, respiratory diseases, pediatrics

Macrophage adaptation in airway inflammatory resolution

Immunotherapy in the Treatment and Prevention of Infection in Acute-on-chronic Liver Failure

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