If anti-inflammatory drugs can aggravate COVID-19, would the same be the case for anti-inflammatory foods and supplements?

Outside of the US they are proposing and trying many things. There are multiple case reports from China showing the effective treatment of the serious symptoms by addressing the inflammatory and pro-oxidant mechanisms I am talking about.

High-dose intravenous vitamin C treatment for COVID-19

While immune effector cells are dependent on glycolysis for their bioenergetic functions, lung epithelial cells use mitochondrial oxidative phosphorylation to produce ATP. Therefore, high-dose vitamin C treatment acts as a prooxidant for immune cells, but as an antioxidant for lung epithelial cells. Furthermore, vitamin c treatmentmay protect innate immunity of ATII through the inhibition ofthe lactatesecretion,produced by the activated immune cells.

COVID-19: combining antiviral and anti-inflammatory treatments30132-8/fulltext)

Both coronavirus disease 2019 (COVID-19) and severe acute respiratory syndrome (SARS) are characterised by an overexuberant inflammatory response and, for SARS, viral load is not correlated with the worsening of symptoms.

To take this work further in a short timescale, a necessity when dealing with a new human pathogen, we re-examined the affinity and selectivity of all the approved drugs in our knowledge graph to identify those with both antiviral and anti-inflammatory properties. Such drugs are predicted to be of particular importance in the treatment of severe cases of COVID-19, when the host inflammatory response becomes a major cause of lung damage and subsequent mortality.

the potential for combination therapy with baracitinib is high because of its low plasma protein binding and minimal interaction with CYP enzymes and drug transporters. Furthermore, there is the potential for combining baricitinib with the direct-acting antivirals (lopinavir or ritonavir and remdesivir) currently being used in the COVID-19 outbreak, since it has a minimal interaction with the relevant CYP drug-metabolising enzymes. Combinations of baricitinib with these direct-acting antivirals could reduce viral infectivity, viral replication, and the aberrant host inflammatory response.

Breakthrough: Chloroquine phosphate has shown apparent efficacy in treatment of COVID-19 associated pneumonia in clinical studies

In the early in vitro studies, chloroquine was found to block COVID-19 infection at low-micromolar concentration, with a half-maximal effective concentration (EC50) of 1.13 μM and a half-cytotoxic concentration (CC50) greater than 100 μM (4). A number of subsequent clinical trials (ChiCTR2000029939, ChiCTR2000029935, ChiCTR2000029899, ChiCTR2000029898, ChiCTR2000029868, ChiCTR2000029837, ChiCTR2000029826, ChiCTR2000029803, ChiCTR2000029762, ChiCTR2000029761, ChiCTR2000029760, ChiCTR2000029740, ChiCTR2000029609, ChiCTR2000029559, and ChiCTR2000029542) have been quickly conducted in China to test the efficacy and safety of chloroquine or hydroxychloroquine in the treatment of COVID-19 associated pneumonia in more than 10 hospitals in Wuhan, Jingzhou, Guangzhou, Beijing, Shanghai, Chongqing, and Ningbo (5). Thus far, results from more than 100 patients have demonstrated that chloroquine phosphate is superior to the control treatment in inhibiting the exacerbation of pneumonia, improving lung imaging findings, promoting a virus-negative conversion, and shortening the disease course according to the news briefing.

Chloroquine is used to prevent and treat malaria and is efficacious as an anti-inflammatory agent for the treatment of rheumatoid arthritis and lupus erythematosus. Studies revealed that it also has potential broad-spectrum antiviral activities by increasing endosomal pH required for virus/cell fusion, as well as interfering with the glycosylation of cellular receptors of SARS-CoV (6,7). The anti-viral and anti-inflammatory activities of chloroquine may account for its potent efficacy in treating patients with COVID-19 pneumonia.

MESOBLAST TO EVALUATE ANTI-INFLAMMATORY CELL THERAPY REMESTEMCEL-L FOR TREATMENT OF COVID-19 LUNG DISEASE

Mortality in COVID-19 infected patients with the inflammatory lung condition acute respiratory distress syndrome (ARDS) is reported to approach 50%,and is associated with older age, co-morbidities such as diabetes, higher disease severity, and elevated markers of inflammation.1 Current therapeutic interventions do not appear to be improving in-hospital survival.

Remestemcel-L has potential for use in the treatment of ARDS, which is the principal cause of death in COVID-19 infection.1 This is supported by recently published results from an investigator-initiated clinical study conducted in China which reportedthat allogeneic MSCs cured or significantly improved functional outcomes in all seven treated patients with severe COVID-19 pneumonia

Additionally, in post-hoc analyses of a 60-patient randomized controlled study in chronic obstructive pulmonary disease (COPD), remestemcel-L infusions were well tolerated, significantly reduced inflammatory biomarkers, and significantly improved pulmonary function in those patients with elevated inflammatory biomarkers. Since the same inflammatory biomarkers are also elevated in COVID-19, these data suggest that remestemcel-L could be useful in the treatment of patients with ARDS due to COVID-19. The COPD study results have been submitted for presentation at an international conference, with full results to be submitted for publication shortly.

Remestemcel-L is being studied in numerous clinical trials across several inflammatory conditions, including in elderly patients with lung disease and adults and children with steroid-refractory acute graft versus host disease(aGVHD).3-5 This product candidate is currently being reviewed by the United States Food and Drug Administration (FDA) for potential approval in the treatment of children with steroid-refractory aGVHD.

Thalidomide Combined with Low-dose Glucocorticoid in the Treatment of COVID-19 Pneumonia

A novel coronavirus strain (severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) first appeared in December 2019 and can cause acute respiratory distress syndrome and death. However, there are only limited therapy choices and no vaccine for SARS-CoV-2 is currently available. Here we report about a case of a SARS-CoV-2 caused pneumonia successfully treated with thalidomide. Thalidomide is an immunomodulatory and anti-inflammatory agent and was combined with a low-dose glucocorticoid. We suggest, that the effects of thalidomide might be related to regulating immunity, inhibiting the inflammatory cytokine surge, alleviating anxiety to reduce oxygen consumption, relieving vomit and lung exudation.

It has been well documented that host immune responses are important factors leading to life-threatening ARDS in COVID-19 patients 6 . Given the reported anti-inflammatory and immunomodulatory effects of thalidomide, we sought to treat this patient who had developed a severe COVID-19 pneumonia with thalidomide in combination with low-dose glucocorticoid. We report here that this therapeutic strategy had a beneficial outcome in this patient with severe COVID-19 pneumonia.

In the current case, acute pulmonary effusion was observed due to markedly elevated inflammatory cytokine profiles in the serum including IL-6, IL-10 and IFN-γ, manifesting as a cytokine surge. The cytokine surge is an inappropriate (exaggerated) immune response that is caused by rapidly proliferating and highly activated T cells. In this process, more than 100 inflammatory mediators are released, and subsequently lead to tissues damage and organs failure. High doses of Glucocorticoid are usually used for suppressing cytokine surge. For instance, glucocorticoids were widely applied during the outbreaks of Severe Acute Respiratory Syndrome (SARS) and Middle East Respiratory Syndrome (MERS) corona virus (CoV) infections to suppress lung inflammation and immune responses 8-10 . However, it appeared to be associated with treatment side effects, such as secondary bacterial infection, osteoporosis and others. Therefore, glucocorticoid was not recommended for severe COVID-19 as used in SARS-CoV or MERS-CoV infections 11 , also due to its inhibition of immune responses and pathogen clearance. Interestingly, we found that after combined treatment of thalidomide with low-dose glucocorticoid, the pulmonary effusion symptoms and elevated inflammatory cytokines in the present patient were substantially reduced without any side effect. Simultaneously, the number of lymphocytes recovered. These results indicated that thalidomide could be used in conjunction with low-dose steroids to treat a COVID-19 pneumonia, likely based on its known anti-inflammatory and immunoregulatory effects.