The healing process for chronic lung damage, which can arise from initial respiratory viral infections or subsequent bacterial complications, is often lengthy and may ultimately result in the formation of permanent scarring. Once damaged, it is difficult to rebuild the damaged lung structure. Recent interest in the effects of respiratory viruses on lung function has been fueled in large part by the impact of past pandemic coronaviruses, SARS-CoV-2 and MERS-CoV, which suppress innate immunity and promote inflammatory responses. Studies indicate that fucoidan can improve the body’s inherent defense mechanisms and lessen inflammatory responses.
The blog will delve into the following study, known as “Fucoidan and Lung Function: Value in Viral Infection,” conducted by J Helen Fitton et al. A review of current research into fucoidan’s impact on viral lung infections and associated lung injury was conducted by the researchers.
The potential contribution of seaweed metabolites to influenza infection has been re-evaluated lately. A more relevant role specific to fucoidan may be as either an immunomodulator or a tissue-sparing anti-inflammatory agent. Respiratory virus infections, including influenza strains, are inhibited by orally administered fucoidan in vitro and in vivo. Indirectly, oral fucoidan appears to have the ability to enhance innate immunity and vaccine response in elderly individuals. Daily administration of 300 mg of wakame-derived fucoidan improved immune reactions to vaccinations.
A key feature of SARS-CoV-2 is a low initial innate immune response, allowing viral infection to progress until a cytokine response becomes dominant. High proinflammatory signaling is a key factor in COVID-19 and can progress to a cytokine storm. Even without a cytokine storm, the immune response to the pathogen can cause persistent fibrotic changes in the lungs. Oral fucoidan may be an appropriate dietary treatment to alleviate this inflammatory damage early. Richards et al. recently observed a significant reduction in gross lung lesions, although no reduction in virus transmission, using orally administered fucoidan in a mouse model of severe influenza.
Influenza, coronaviruses, and respiratory syncytial viruses are among the respiratory viruses that gain entry into 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. Coronaviruses attach to the ACE2 receptor and collaborate with the heparin sulfate receptor using their S protein spike, in contrast to influenza viruses which use hemagglutinin and neuraminidase for cell entry. SARS-CoV-2 also appears to intervene in the innate immune response in the gut, suppressing the autocrine effects of interferon. The virus’s action in this manner leads to the suppression of the intestinal immune response and the formation of its own sanctuary.
The restorative effect of fucoidan on impaired gut lysozyme function has been observed in recent studies, which proposes it could mitigate this issue at the intestinal level. Richards and Hayashi reported that further research into orally administered fucoidan indicates it may lessen virus-induced lung damage.
Research indicates that fucoidan and similar polysaccharides from marine algae can directly block the entry of influenza viruses into host cells. This activity has been demonstrated for fucoidans of various origins, as shown in Table 1.
A key feature of COVID-19 infection is micro coagulation, and the anticoagulant properties of heparin have proven lifesaving. Furthermore, heparin has been shown to directly inhibit SARS-CoV-2 in vitro, raising the possibility of its efficacy as a therapeutic agent. The fucoidan fractions tested so far—laboratory samples of galactofucans rather than commercial formulations—have shown intriguing activity by inhibiting the binding of the viral spike protein to heparin but not to ACE2. However, recent testing of unfractionated fucoidans from Fucus vesiculosus and Undaria pinnatifida did not reveal any activity in in vitro infection models. Currently, there are no clinical studies of fucoidans in this area.
COPD, or chronic obstructive pulmonary disease, encompasses irreversible lung damage stemming from chronic conditions like asthma and bronchitis, as well as factors such as smoking and air pollution. Fibrosis caused by COPD leaves scar tissue instead of functional lung tissue.
Fucoidan acts as both an anti-inflammatory and an inhibitor of epithelial-mesenchymal transition (EMT), potentially ameliorating 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. In unrelated cell types, fucoidan inhibits EMT, preserving tissue function. Fucoidan has demonstrated the ability to lessen bleomycin-induced damage in mouse models. A recent review by Chen et al. demonstrated that fucoidan reduces lung injury.
In addition to stimulating significant inflammation, the SARS-CoV-2 coronavirus is also responsible for inhibiting the effectiveness of the innate immune system. Fucoidan preparations have potential as adjuncts to reduce the damage associated with respiratory viral infections by restoring innate immune function and suppressing inflammation, but further research is needed. The direct inhibition of infection in vitro by fucoidan fractions is not observed in all cases. Staying informed about public health recommendations is a critical step in the ongoing effort to stop the proliferation of infectious agents.
Source： Mar Drugs. 2020 Dec 24;19(1):4. doi: 10.3390/md19010004