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Lectins as a source of unproductive inflammation
Modulation of immune function by dietary lectins in rheumatoid arthritis:
https://pubmed.ncbi.nlm.nih.gov/10884708/
Despite the almost universal clinical observation that inflammation of the gut is frequently associated with inflammation of the joints and vice versa, the nature of this relationship remains elusive. In the present review, we provide evidence for how the interaction of dietary lectins with enterocytes and lymphocytes may facilitate the translocation of both dietary and gut-derived pathogenic antigens to peripheral tissues, which in turn causes persistent peripheral antigenic stimulation. In genetically susceptible individuals, this antigenic stimulation may ultimately result in the expression of overt rheumatoid arthritis (RA) via molecular mimicry, a process whereby foreign peptides, similar in structure to endogenous peptides, may cause antibodies or T-lymphocytes to cross-react with both foreign and endogenous peptides and thereby break immunological tolerance. By eliminating dietary elements, particularly lectins, which adversely influence both enterocyte and lymphocyte structure and function, it is proposed that the peripheral antigenic stimulus (both pathogenic and dietary) will be reduced and thereby result in a diminution of disease symptoms in certain patients with RA.
Plant lectins are novel Toll-like receptor agonists (TLR receptor agonists are toxins like mercury, endotoxin, etc)
https://pubmed.ncbi.nlm.nih.gov/21420389/
The T cell mitogen and plant glycoprotein, phytohaemagglutinin (PHA), is commonly used to stimulate peripheral blood mononuclear cell (PBMC) preparations to produce IL-2, IL-5, GM-CSF and IFN-γ and so provide an assay to detect immunosuppressants like FK506 and anti-inflammatories such as PDE IV inhibitors. During the early discovery of novel TLR agonists for the treatment of asthma we initially showed that PHA-L is a specific human TLR4 agonist, devoid of effects on equivalent TLR4 null cells. This TLR4 agonism was not due to LPS contamination of PHA-L, as polymyxin B was ineffective and unlike PHA-L, LPS did not stimulate TLR5 or TLR2/6. Also this specific PHA-L agonism of TLR4 was shown for different PHA forms, for example, PHA-P. This TLR lectin pharmacology finding was further explored by testing a broader panel of plant lectin representatives for agonism against a suite of hrTLR cell reporter assays (2/6, 3, 4, 5, 7, 8 and 9). Soybean agglutinin (SBA), concanavalin A (ConA) and PHA lectin family members only stimulated extracellular TLRs (2/6, 4 and 5) probably due to lack of intracellular access, whilst other lectins were either pan-active (WGA) or inactive (AIL). Interestingly SBA only stimulated TLR4, ConA, TLR2/6 and PHA-L, TLR2/6, 4 and 5. As each lectin family exhibits different sugar ligand specificity for interaction, these results suggest that the pharmacology of this TLR agonism is encoded by the lectin's carbohydrate recognition motifs and the appropriate surface presentation of these motifs on different TLRs.
In mice, administration of lectins aids IgG and IgA production(inflammation, allergic/autoimmune reactions):
Mucosal immunogenicity of plant lectins in mice
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2327126/
How to Remove Arsenic, Lectins and Phytic Acid From Rice:
https://www.youtube.com/watch?v=4AISEnGISyI
The truth about rice: Why brown rice isn't always better:
https://www.euronews.com/2018/12/07/truth-about-rice-brown-rice-really-better-you-t144165
Other veg-based stuff with a potential to mess with our bodies:
Phytosterols Suppress Phagocytosis and Inhibit Inflammatory Mediators via ERK Pathway on LPS-Triggered Inflammatory Responses in RAW264.7 Macrophages and the Correlation with Their Structure
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6915509/
Results showed that the phagocytic activity was significantly inhibited by the tested phytosterol compounds, which demonstrated that the administration of phytosterol compounds may have a certain effect on the immune response caused by inflammation. To detect the phagocytosis of RAW264.7 cells, two methods were chosen, the FITC-dextran method and neutral red method, which were widely used in previous studies [51]. The results of these two methods were comparable, and the FITC-dextran method contributed more to the comparison of inhibitory effects on phagocytosis between β-sitosterol and campesterol, showing a more definitive result, i.e., the inhibitory effects of β-sitosterol were stronger than those of campesterol. Similarly, the NO and TNF-α production in LPS-induced RAW264.7 cells treated with ergosterol, β-sitosterol, stigmasterol, campesterol, and ergosterol acetate was significantly reduced (p < 0.05), which means that the inflammatory response stimulated by LPS was recovered by these phytosterols. In other words, phytosterol compounds could relieve the inflammatory reaction induced by LPS.
Keep Your Cholesterol in Check with Foods High in Phytosterols
https://www.verywellhealth.com/which-foods-contain-the-highest-amount-of-phytosterols-697742
Present-day (2016) dietary intake of phytosterol ranges between 150 to 450 per day, even with food manufacturers enriching many common food products with the compound
[1997] A randomized placebo-controlled trial of the efficacy of beta-sitosterol and its glucoside as adjuvants in the treatment of pulmonary tuberculosis.
https://pubmed.ncbi.nlm.nih.gov/9487449/
[..]This is a double-blind study of 43 persons positively infected with pulmonary tuberculosis receiving conventional multi-antibiotic treatment to ascertain if the addition of a plant sterol/sterolin mixture could improve the clinical outcome. The study took place over 6 months and the patients were closely monitored with a variety of lab and radiographic tests. The groups receiving the sterol/sterolin mixture showed a significant weight gain over the placebo group. As well, the treatment group showed a significant increase in lymphocytes and eosinophils. The increase in lymphocytes is consistent with previous experiments indicating a T-cell proliferative effect with the oral intake of phytosterols. The increase in eosinophils is difficult to explain, since no previous allergic response has been attributable to the ingestion of the phytosterols. However, other data indicate there may be a relationship between the rise of CD4 lymphocytes and eosinophils. Plant sterols/sterolins have been demonstrated elsewhere to selectively increase CD4 lymphocyte counts. Other lab parameters remained the same between the two groups including hemoglobin, hematocrit, neutrophil count, serum globulin, creatinine, and urea.[..]
https://en.wikipedia.org/wiki/Phytosterol
The richest naturally occurring sources of phytosterols are vegetable oils and products made from them. Sterols can be present in the free form and as fatty acid esters and glycolipids. The bound form is usually hydrolyzed in the small intestines by pancreatic enzymes. Some of the sterols are removed during the deodorization step of refining oils and fats, without, however, changing their relative composition. Sterols are therefore a useful tool in checking authenticity.
As common sources of phytosterols, vegetable oils have been developed as margarine products highlighting phytosterol content. Cereal products, vegetables, fruit and berries, which are not as rich in phytosterols, may also be significant sources of phytosterols due to their higher intakes.
The intake of naturally occurring phytosterols ranges between ~200–300 mg/day depending on eating habits. Specially designed vegetarian experimental diets have been produced yielding upwards of 700 mg/day. The most commonly occurring phytosterols in the human diet are β-sitosterol, campesterol and stigmasterol, which account for about 65%, 30% and 3% of diet contents, respectively. The most common plant stanols in the human diet are sitostanol and campestanol, which combined make up about 5% of dietary phytosterol.
Does anyone else remember the blood type diet, it was all about lectins? Gosh I forgot I tried this one, LOL. It actually wasn't so bad really, for me when I tried my blood type version of it.
https://www.healthline.com/nutrition/the-blood-type-diet-review
Green tea polyphenols mitigate the plant lectins-induced liver inflammation:
https://www.sciencedirect.com/science/article/abs/pii/S027869152030466X
Imagine drinking green tea only to mitigate lectins toxic effects.