It is well-established that reduced lung function is a characteristic of both infectious and non-infectious pathologies; however, it is crucial to recognize that viral infections affecting the lungs can lead to both immediate and chronic damage that persists over time. For example, SARS-CoV-2 infection suppresses innate immunity and promotes inflammatory responses. Clinical and animal studies have shown that fucoidan enhances innate immunity and reduces inflammation. In addition, dietary fucoidan has been shown to reduce lung injury in acute viral infection models. Direct inhibition of SARS-CoV-2 in vitro has been reported, but it is not universal. This is to bring your attention to the study, “Fucoidan and Lung Function: Value in Viral Infection” by J Helen Fitton et al. The research provides a review and summary of the most recent findings regarding the use of fucoidan in cases of viral lung infections and lung damage.
Restoring damaged lung tissue is challenging, and direct antiviral medications have not been shown to lessen the severity of the illness. Even after recovering from COVID-19, some individuals continue to experience health issues for months afterward, a condition known as “long COVID”. SARS-CoV-2 suppresses the innate immune response and promotes robust inflammatory expression.
Fucoidan from foods has been shown to enhance innate immunity in various models. Seaweed-derived polysaccharides have attracted attention for their potential to prevent or mitigate viral infections. In vitro and in vivo data have demonstrated efficacy against influenza virus infection. However, commercially available fucoidans from Fucus vesiculosus and Undaria pinnatifida showed no activity in vitro. Research into lung injury reduction and antiviral activity is ongoing. This brief review summarizes recent studies on fucoidan’s effects on the lungs.
Recent reviews have examined seaweed metabolites for their potential in treating influenza. However, regarding the ongoing coronavirus pandemic, a more relevant role for fucoidan could be as an immunomodulator or an anti-inflammatory agent that protects tissues. Respiratory virus infections, including influenza strains, are inhibited by orally administered fucoidan in vitro and in vivo. Indirectly, an oral fucoidan appears to have the ability to enhance innate immunity in the elderly and boost vaccine response. For example, one study showed that oral intake of 300 mg of wakame-derived fucoidan per day enhanced vaccine response.
A key feature of SARS-CoV-2 is the low initial innate immune response, which allows viral infection to progress until a cytokine response dominates, which can cause persistent fibrotic changes in the lungs. Oral fucoidan may be a suitable dietary treatment to reduce this inflammatory damage at an early stage. In a recent study, Richards and his colleagues discovered that fucoidan taken orally significantly lessened the overall lung lesions in a mouse model of severe influenza, but did not reduce the presence of the virus.
Influenza, coronaviruses, and respiratory syncytial virus are examples of respiratory viruses that access the respiratory system through a receptor-mediated process. Some viruses attach to receptors in the upper gastrointestinal tract, while others tend to attach to the bronchi or lower lungs, depending on the expression of cell surface receptors. Previous studies have shown that variations in how ACE2 receptors are expressed in children and smokers are factors in the disparity in infection rates. SARS-CoV-2 also appears to interfere with the intrinsic immune response in the gut, suppressing the autocrine action of interferon. In this way, the virus suppresses the immune response in the intestinal tract and forms its reservoir.
Recent studies have shown that fucoidan can restore reduced lysozyme function in the intestine, suggesting that it may attenuate this effect at the intestinal level. Additional data on orally administered fucoidan suggest a potential attenuating effect on viral lung injury.
Heparin has also been shown to directly inhibit SARS-CoV-2 in in vitro studies, raising the possibility of its efficacy as a therapeutic agent. While not commercially available, the fucoidan fractions, specifically laboratory-made galactofucan, have displayed promising results by hindering the viral spike protein’s connection to heparin, unlike its interaction with ACE2.
Chronic obstructive pulmonary disease (COPD) is a collective term for irreversible lung damage caused by chronic diseases such as asthma and bronchitis, smoking, and air pollution. In cases of COPD, fibrosis results in the formation of scars, which then replace the normally functioning lung tissue.
Fucoidan has both anti-inflammatory and epithelial-mesenchymal transition inhibitory effects and may alleviate some of the damage. Fucoidan has been shown to suppress cigarette smoke-induced MUC5 activation in bronchial cells and inhibit Toll-like receptor-mediated cytokine release. Fucoidan prevents epithelial-mesenchymal transition and maintains tissue function in different cell types. In mouse models, bleomycin-induced damage is attenuated by fucoidan. A recent review by Chen et al. has shown that fucoidan reduces lung injury. The potential role of various plant polysaccharides in reducing pulmonary fibrosis is also discussed, with a particular focus on the damage that follows viral infection.
In conclusion, this review demonstrates that lung damage, both sudden and persistent, can be caused by respiratory viral infections. The current pandemic coronavirus SARS-CoV-2, inhibits innate immune responses and promotes robust inflammatory expression. Additional studies are necessary; however, Fucoidan formulations hold potential as adjuvants in the effort to inhibit damage linked to respiratory viral infections by reviving innate immune function and also suppressing inflammation. Direct inhibition of infection in vitro by fucoidan fractions is not necessarily universal. It’s crucial to follow public health guidelines to stop the spread of SARS-CoV-2 and other germs.
Source: Mar Drugs. 2020 Dec 24;19(1):4. doi: 10.3390/md19010004