Potential role for interferon gamma in the treatment of recurrent ventilator-acquired pneumonia in patients with COVID-19: a hypothesis

Nguyen, Lee S.; Hamou, Zakaria Ait; Gastli, Nabil; Chapuis, Nicolas; Pène, Frédéric

doi:10.1007/s00134-021-06377-3

Cited by 25 publications

(26 citation statements)

References 6 publications

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“…MicroRNAs and microRNA network targeting might be a useful technology to develop faster and effective therapeutic approaches to treat hyperinflammatory responses generated during SARS-CoV-2 infection [160]. In addition to the use of anti-inflammatory therapeutics to treat pneumonia associated with COVID-19, immunostimulant drugs offer additional advantages to manage recurrent bacterial superinfections that can occur in the later course of the disease [161]. Lethal forms of COVID-19 can be attributed to the insufficient and/or inefficient immune responses associated with the hyperinflammatory syndrome/cytokine storm.…”

Section: Regulation Of Pro-and Anti-inflammatory Cytokines Via Immunomodulatory Drugs and Immunotherapeuticsmentioning

confidence: 99%

Role of Inflammatory Cytokines in COVID-19 Patients: A Review on Molecular Mechanisms, Immune Functions, Immunopathology and Immunomodulatory Drugs to Counter Cytokine Storm

et al. 2021

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Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is a severe pandemic of the current century. The vicious tentacles of the disease have been disseminated worldwide with unknown complications and repercussions. Advanced COVID-19 syndrome is characterized by the uncontrolled and elevated release of pro-inflammatory cytokines and suppressed immunity, leading to the cytokine storm. The uncontrolled and dysregulated secretion of inflammatory and pro-inflammatory cytokines is positively associated with the severity of the viral infection and mortality rate. The secretion of various pro-inflammatory cytokines such as TNF-α, IL-1, and IL-6 leads to a hyperinflammatory response by recruiting macrophages, T and B cells in the lung alveolar cells. Moreover, it has been hypothesized that immune cells such as macrophages recruit inflammatory monocytes in the alveolar cells and allow the production of large amounts of cytokines in the alveoli, leading to a hyperinflammatory response in severely ill patients with COVID-19. This cascade of events may lead to multiple organ failure, acute respiratory distress, or pneumonia. Although the disease has a higher survival rate than other chronic diseases, the incidence of complications in the geriatric population are considerably high, with more systemic complications. This review sheds light on the pivotal roles played by various inflammatory markers in COVID-19-related complications. Different molecular pathways, such as the activation of JAK and JAK/STAT signaling are crucial in the progression of cytokine storm; hence, various mechanisms, immunological pathways, and functions of cytokines and other inflammatory markers have been discussed. A thorough understanding of cytokines’ molecular pathways and their activation procedures will add more insight into understanding immunopathology and designing appropriate drugs, therapies, and control measures to counter COVID-19. Recently, anti-inflammatory drugs and several antiviral drugs have been reported as effective therapeutic drug candidates to control hypercytokinemia or cytokine storm. Hence, the present review also discussed prospective anti-inflammatory and relevant immunomodulatory drugs currently in various trial phases and their possible implications.

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Section: Regulation Of Pro-and Anti-inflammatory Cytokines Via Immunomodulatory Drugs and Immunotherapeuticsmentioning

confidence: 99%

Role of Inflammatory Cytokines in COVID-19 Patients: A Review on Molecular Mechanisms, Immune Functions, Immunopathology and Immunomodulatory Drugs to Counter Cytokine Storm

et al. 2021

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“…Although in COVID-19, mHLA-DR level seems not as low as what is seen in septic shock (< 8000 AB/C), in our study, profile kinetics seen in cluster 2 (PID) and cluster 3 (TID) were differentially associated with the development of secondary infection, which is in line with published experience in sepsis [ 16 ]. A decrease in mHLA-DR in severe COVID-19 was shown in both adults and children [ 17 – 21 ]. Spinetti et al .…”

Section: Discussionmentioning

confidence: 99%

“…The limited number of patients in the three clusters and their association with outcome warrant further confirmation. Nevertheless, the phenotypic characterization of the three clusters and their reciprocal differences are clear enough to suggest association with specific clinical courses and may be of some utility to select patients for innovative therapy [ 21 , 25 , 39 ].…”

Section: Discussionmentioning

confidence: 99%

Myeloid phenotypes in severe COVID-19 predict secondary infection and mortality: a pilot study

Morin

Barreault

Beggaz³

et al. 2021

Ann. Intensive Care

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Background De-regulated host response to severe coronavirus disease 2019 (COVID-19), directly referring to the concept of sepsis-associated immunological dysregulation, seems to be a strong signature of severe COVID-19. Myeloid cells phenotyping is well recognized to diagnose critical illness-induced immunodepression in sepsis and has not been well characterized in COVID-19. The aim of this study is to review phenotypic characteristics of myeloid cells and evaluate their relations with the occurrence of secondary infection and mortality in patients with COVID-19 admitted in an intensive care unit. Methods Retrospective analysis of the circulating myeloid cells phenotypes of adult COVID-19 critically ill patients. Phenotyping circulating immune cells was performed by flow cytometry daily for routine analysis and twice weekly for lymphocytes and monocytes subpopulations analysis, as well as monocyte human leukocyte antigen (mHLA)-DR expression. Results Out of the 29 critically ill adult patients with severe COVID-19 analyzed, 12 (41.4%) developed secondary infection and six patients died during their stay. Monocyte HLA-DR kinetics was significantly different between patients developing secondary infection and those without, respectively, at day 5–7 and 8–10 following admission. The monocytes myeloid-derived suppressor cells to total monocytes ratio was associated with 28- and 60-day mortality. Those myeloid characteristics suggest three phenotypes: hyperactivated monocyte/macrophage is significantly associated with mortality, whereas persistent immunodepression is associated with secondary infection occurrence compared to transient immunodepression. Conclusions Myeloid phenotypes of critically ill COVID-19 patients may be associated with development of secondary infection, 28- and 60-day mortality.

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“…In critically ill patients, in the absence of effective antivirals and efficient antibodies, an alternative would lie in boosting immune responses as presently assessed in sepsis ( 36 , 37 , 38 ). Preliminary results in COVID-19 with IFN-γ ( 39 ) or IL-7 ( 40 , 41 ) are already published and would deserve additional trials.…”

Section: Discussionmentioning

confidence: 99%

Seroconversion in septic ICU patients presenting with COVID-19: necessary but not sufficient

Conti

Oriol

Cheynet

et al. 2021

Archives of Medical Research

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Background As COVID-19 pandemic and vaccination effects progress, research now focuses on adaptive immunological response to SARS-CoV-2. Few studies specifically investigated intensive care unit (ICU) patients, and little is known about kinetics of humoral response in such critically ill patients. In this context, the main objective of the present work was to perform a longitudinal analysis of the humoral response in critically ill COVID-19 patients with prolonged ICU stays in regard with initial inflammatory response, disease severity and mortality. Methods Over a 3 week period, circulating immunoglobulins (Ig) against SARS-CoV-2 along with several immunological and clinical parameters were measured in 64 ICU COVID-19 patients. Results Critically ill COVID-19 patients mounted a dynamic and sustained antibody response of both IgM and IgG as soon as the first day of ICU hospitalization. This serological response was not associated with any of the classical immunological parameters measured at ICU admission or with initial severity clinical scores. IgM and IgG levels and seroconversion trajectories were not associated with unfavourable outcome. Conclusion Despite rapid seroconversion and elevated humoral response, COVID-19 patients are still characterized by elevated mortality. Additional studies, including cytotoxic T cell functions, are mandatory to understand the immunological mechanisms contributing to long stay of COVID-19 patients in ICU.

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Potential role for interferon gamma in the treatment of recurrent ventilator-acquired pneumonia in patients with COVID-19: a hypothesis

Cited by 25 publications

References 6 publications

Role of Inflammatory Cytokines in COVID-19 Patients: A Review on Molecular Mechanisms, Immune Functions, Immunopathology and Immunomodulatory Drugs to Counter Cytokine Storm

Role of Inflammatory Cytokines in COVID-19 Patients: A Review on Molecular Mechanisms, Immune Functions, Immunopathology and Immunomodulatory Drugs to Counter Cytokine Storm

Myeloid phenotypes in severe COVID-19 predict secondary infection and mortality: a pilot study

Seroconversion in septic ICU patients presenting with COVID-19: necessary but not sufficient

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