The presence of a viral infection is frequently associated with the occurrence of pneumonia. Infants and the elderly, in particular, are susceptible to various influenza viruses, including SARS-CoV-2. Additionally, infants are prone to respiratory syncytial virus, adenovirus, human metapneumovirus, and other similar infections. Furthermore, individuals with weakened immune systems are at risk of contracting cytomegalovirus, while those residing in regions like the Middle East may be exposed to MERS coronavirus due to endemic conditions. Measles virus and varicella virus can also cause pneumonia.
The recovery period for chronic lung damage caused by respiratory viral infections and subsequent bacterial infections is prolonged, and it may result in permanent scarring. Once compromised, it is difficult to rebuild damaged lung structures. Hence, if we can sufficiently preserve lung function and decrease lung damage after hospitalization and chronic infection, it will have considerable positive implications for both patients and society. Seaweed-derived polysaccharides are gaining interest due to their potential in preventing or improving viral infections.
Therefore, I would like to discuss the study titled “Fucoidan and Lung Function: Value in Viral Infection” by J. Helen Fitton et al. in this blog.
Respiratory viral infections, including influenza strains, are inhibited in vitro and in vivo by orally delivered fucoidan. Oral fucoidan has the potential to indirectly strengthen the immune system and enhance vaccine responses in older adults. A modest oral dose of 300 mg of fucoidan from Undaria pinnatifida per day, enhanced the vaccine response.
A key feature of SARS-CoV-2 is the low initial innate immune response, allowing viral infection to progress until cytokine responses become prevalent. COVID-19 infection is often triggered by heightened pro-inflammatory cues, which can subsequently escalate into a dangerous cytokine storm. Even in the absence of an extreme cytokine storm, inflammatory damage resulting from the immune response to pathogens can cause persistent fibrotic changes in the lungs. In a recent study conducted by Richards and his colleagues, they discovered that orally administering fucoidan to a mouse model of severe influenza resulted in a significant reduction in overall lung pathology, despite no reduction in virus levels.
Respiratory viruses such as influenza, coronaviruses, and RSV enter the respiratory system through receptor-mediated mechanisms. Certain viruses bind to receptors in the upper respiratory tract, while others have a preference for attaching to the bronchi or lower lungs, depending on the specific cell surface receptors they express. Influenza viruses use hemagglutinin and neuraminidase to enter cells, while coronaviruses use S protein spikes that attach via ACE2 receptors, apparently in coordination with additional heparin sulfate receptors. It is worth noting that SARS-CoV-2 seems to affect the immune response in the gut, suppressing the self-regulating effects of interferon, as previously mentioned by Blanco-Melo. In this way, the virus suppresses the immune response in the gut and creates a reservoir for itself.
Moreover, it has been discovered through recent studies that fucoidan can effectively reverse the decline in lysozyme function that occurs in the intestine. This suggests that the compound may have the ability to alleviate this specific effect at the intestinal level. Research has indicated that Fucoidan and other polysaccharides obtained from marine algae can effectively prevent the entry of influenza virus into cells.
The recent pandemic caused by the coronavirus variant SARS-CoV-2 was evaluated in vitro using various fucan, fucoidan, and heparin compounds. Microcoagulation is a crucial characteristic of COVID-19, and the life-saving effects of heparin as an anticoagulant have been established. Heparin has also been shown to directly inhibit SARS-CoV-2 in vitro, further increasing its efficacy as a therapeutic agent. The fucoidan fraction that has been tested thus far, although not a commercially available product but rather a lab sample of galactofucan, displayed intriguing potential in inhibiting the attachment of the viral spike protein to heparin. However, it did not exhibit the same effect on ACE2.
Fucoidan acts as both an anti-inflammatory agent and an inhibitor of epithelial-to-mesenchymal transformation and may ameliorate some of the damage. The effectiveness of Fucoidan in preventing the activation of MUC5 and inhibiting Toll-like receptor-mediated cytokine release in bronchial cells has been demonstrated. In unrelated cell types, fucoidan prevents epithelial-mesenchymal transition and preserves tissue function. In a mouse model, bleomycin-induced damage is attenuated by fucoidan. In a recent review, Chen et al delved into the potential contribution of plant polysaccharides in mitigating pulmonary fibrosis, paying special attention to the aftermath of viral infections.
Viral infections affecting the respiratory system can lead to both short-term and long-term lung damage. By restoring innate immune function and suppressing inflammation, fucoidan formulations show promise as adjuvants to limit damage after respiratory viral infections. Nonetheless, additional research is needed to delve deeper into this hypothesis. Also, following public health information remains essential to prevent the spread of SARS-CoV-2 and other pathogens.
Source: Mar Drugs. 2021 Jan; 19(1): 4. doi: 10.3390/md19010004