N-Acetylcysteine to Combat COVID-19: An Evidence Review.

The novel coronavirus disease (COVID-19) is caused by a virus (SARS-Cov-2) and is known for inducing multisystem organ dysfunction associated with significant morbidity and mortality. Current therapeutic strategies for COVID-19 have failed to effectively reduce mortality rate, especially for elderly patients. A newly developed vaccine against SARS-Cov-2 has been reported to induce the production of neutralizing antibodies in young volunteers.

Endotracheal intubation results in acute tracheal damage induced by mtDNA/TLR9/NF-κB activity.

Tracheitis secondary to placement of an endotracheal tube (ETT) is characterized by neutrophil accumulation in the tracheal lumen, which is generally associated with epithelial damage. Mitochondrial DNA (mtDNA), has been implicated in systemic inflammation and organ dysfunction following trauma; however, less is known about the effects of a foreign body on local trauma and tissue damage. We hypothesized that tracheal damage secondary to the ETT will result in local release of mtDNA at sufficient levels to induce TLR9 and NF-κB activation.

Mitochondrial DNA induces Foley catheter related bladder inflammation via Toll-like receptor 9 activation.

Bladder instrumentation engages the innate immune system via neutrophil activation, promoting inflammation and pain. Elevated levels of mitochondrial DNA (mtDNA) have been associated with tissue damage and organ dysfunction. We hypothesized that local bladder trauma induced by a Foley catheter (FC) will result in mtDNA release, migration of neutrophils into the bladder lumen, and activation of the Toll-like receptor 9 (TLR9) and nuclear factor kappa B (NF-κB) pathway leading to bladder tissue damage.

Endotracheal tube-induced sore throat pain and inflammation is coupled to the release of mitochondrial DNA.

In the absence of infection, the pathophysiology of endotracheal tube-induced sore throat pain is unclear. Activated neutrophils release elastase, reactive oxygen species, and inflammatory cytokines known to contribute to neuropathic pain. Sterile tissue injury can cause the release of damage-associated molecular patterns such as mitochondrial DNA that promote neutrophil activation.

Human recombinant apyrase therapy protects against canine pulmonary ischemia-reperfusion injury.

Background: There is accumulating evidence that extracellular adenosine triphosphate (eATP) promotes many of the underlying mechanisms that exacerbate acute lung injury. However, much of these data are from inbred rodent models, indicating the need for further investigation in higher vertebrates to better establish clinical relevance. To this end we evaluated a human recombinant apyrase therapy in a canine warm pulmonary ischemia-reperfusion injury (IRI) model and measured eATP levels in human lung recipients with or without primary lung graft dysfunction (PGD).

Innate immunity mediating inflammation secondary to endotracheal intubation.

Objective: To investigate the inflammatory markers associated with short-term endotracheal intubation in healthy surgical patients.

Design: An observational and prospective study of subjects scheduled for same-day surgery procedures.

Setting: Level I trauma center.

Early biochemical markers of inflammation in a swine model of endotracheal intubation.

Background: A common complaint after endotracheal tube use is sore throat, which may be due to abrasion, ischemia-reperfusion injury, or an inflammatory reaction. Few studies have evaluated localized tracheal inflammation as part of the response to intubation.

Methods: Inflammation of the trachea due to intubation was assessed in a swine model by following indicators of inflammation over time in the tracheal lumen.