scholarly journals Host-bacteria metabolic crosstalk drives S. aureus biofilm

2021 ◽  
Vol 8 (6) ◽  
pp. 106-107
Author(s):  
Kira L. Tomlinson ◽  
Sebastián A. Riquelme

Staphylococcus aureus is a prominent pathogen that can cause intractable lung infections in humans. S. aureus persists in the airway despite inflammation and immune cell recruitment by adapting to host-derived antimicrobial factors. A key component of the immune response to infection are host metabolites that regulate inflammation and bacterial survival. In our recent paper (Tomlinson et al., Nat Commun, doi: 10.1038/s41467-021-21718-y), we demonstrated that S. aureus induces the production of the immunoreglatory metabolite itaconate in airway immune cells by stimulating mitochondrial oxidant stress. Itaconate in turn inhibited S. aureus glycolysis and growth, and promoted carbon flux through bacterial metabolic pathways that support biofilm production. These itaconate-induced metabolic changes were recapitulated in a longitudinal series of clinical isolates from a patient with chronic staphylococcal lung infections, demonstrating a role for host immunometabolism in driving bacterial persistence during long-term staphylococcal lung infections.

2021 ◽  
Vol 22 (3) ◽  
pp. 1118
Author(s):  
Abdulaziz Alamri ◽  
Derek Fisk ◽  
Deepak Upreti ◽  
Sam K. P. Kung

Dendritic cells (DC) connect the innate and adaptive arms of the immune system and carry out numerous roles that are significant in the context of viral disease. Their functions include the control of inflammatory responses, the promotion of tolerance, cross-presentation, immune cell recruitment and the production of antiviral cytokines. Based primarily on the available literature that characterizes the behaviour of many DC subsets during Severe acute respiratory syndrome (SARS) and coronavirus disease 2019 (COVID-19), we speculated possible mechanisms through which DC could contribute to COVID-19 immune responses, such as dissemination of Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) to lymph nodes, mounting dysfunctional inteferon responses and T cell immunity in patients. We highlighted gaps of knowledge in our understanding of DC in COVID-19 pathogenesis and discussed current pre-clinical development of therapies for COVID-19.


2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Ruth Seelige ◽  
Robert Saddawi-Konefka ◽  
Nicholas M. Adams ◽  
Gaëlle Picarda ◽  
Joseph C. Sun ◽  
...  

2021 ◽  
Vol 7 (3) ◽  
pp. 54
Author(s):  
Tobias Plowman ◽  
Dimitris Lagos

The highly infectious severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) emerged as the causative agent of coronavirus disease 2019 (COVID-19) in late 2019, igniting an unprecedented pandemic. A mechanistic picture characterising the acute immunopathological disease in severe COVID-19 is developing. Non-coding RNAs (ncRNAs) constitute the transcribed but un-translated portion of the genome and, until recent decades, have been undiscovered or overlooked. A growing body of research continues to demonstrate their interconnected involvement in the immune response to SARS-CoV-2 and COVID-19 development by regulating several of its pathological hallmarks: cytokine storm syndrome, haemostatic alterations, immune cell recruitment, and vascular dysregulation. There is also keen interest in exploring the possibility of host–virus RNA–RNA and RNA–RBP interactions. Here, we discuss and evaluate evidence demonstrating the involvement of short and long ncRNAs in COVID-19 and use this information to propose hypotheses for future mechanistic and clinical studies.


2013 ◽  
Vol 133 (9) ◽  
pp. 2138-2140
Author(s):  
Kimberley A. Beaumont ◽  
Marcia A. Munoz ◽  
Wolfgang Weninger

2017 ◽  
Vol 16 (3) ◽  
pp. e230-e231 ◽  
Author(s):  
B. Nausch ◽  
J. Röhrl ◽  
A. Koeberle ◽  
U. Harler ◽  
M. Joannidis ◽  
...  

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