From: Gut microbiota and the human gut physiological changes
Immunity | Observations in the gut | Alteration in the gut | Alternative remedies or mechanisms |
---|---|---|---|
Absences of immunoglobulin A | Increase in mucosa-adherent segmented filamentous bacteria (SFB) from the phylum Firmicutes (Wells et al. 2011). | This is linked with autoimmune diseases such as encephalitis and arthritis. | Enriching the gut with genera such as Eubacterium, Prevetolla and Roseburia(Qiu et al., 2020a, b) |
Absence of dendritic cells-specific (DC-specific) TGF-β signaling | E. coli are enriched in the gut. | Non mediation of immune tolerance and inflammatory response is prominent (Wells et al. 2011). | The probiotic Clostridium butyricum is able to induce TGF-β signaling in DC, which in turn induces Treg cell generation (Hornung et al. 2009). |
Polymorphisms in the NOD1 gene and NOD2 gene | Changes in the levels of Enterobacteriaceae in humans (Knights et al. 2014; Elinav et al. 2011). | The resulting dysbiosis is associated with intestinal permeability and onset of inflammation (Kamada et al. 2013). | The knockout of resistant-like molecule β (RELMβ) gives abundance of Bacteroidetes, Firmicutes and Proteobacteria (Bonder et al. 2016) and hence a healthy gut. |
NOD2 knockout mice | Harbor a higher amount of Bacteroides, Firmicutes and Bacillus in the terminal ileum | Have downregulated expression of α-defensins and were more susceptible to Listeria monocytogenes infection (Dheer et al. 2016). | NLRP6 inflammasome deficient mice increased Prevotellaceae and TM7, and reductions of genus Lactobacillus in the Firmicutes phylum (Kobayashi et al. 2005) |
Mice with intestinal epithelium over expression of TLR4 | Abundance of Fusobacteria and Proteobacteria and lower abundances of Firmicutes in the colonic mucosa (Bereswill et al. 2014) | This condition is associated with the onset of colorectal cancer. | TLR2 in T cells has been proven to help the colonization of commensal Bacteroides fragilis in the gut (June et al., 2011). |
TLR9 knockout mice | Lower Enterobacteria and Bacteroidetes, whereas levels of Clostridium leptum and Bifidobacteria expand (Xiao et al. 2019). | Increased prevalence of IgG2a and accelerated renal diseases (Albert et al. 2009). | Increase Firmicutes and Proteobacteria associated with higher level of miR-200a-3p (Johansson et al. 2011). |
Mice deficient in TLR5 | Higher abundance in Bacteroidetes and Lachnospiraceae (Suzuki et al. 2004) | Spontaneous intestinal inflammation and metabolic abnormalities, however not much evidence. | TLR4 knockout in mice decreased the abundance of Bacteroidetes (Suzuki et al., 2004), The mice lacking matrix metalloproteinase 7; (MMP7 displayed a significantly higher abundances of Firmicutes and a significantly lower abundances of Bacteroidetes (Mathias et al. 2010). |
Inactivation of NLRP6 proteins | NLRP-6-deficiency affects the goblet cells in | Reduced mucus layer thereby enabling microbes to be more susceptible to dextran sulfate sodium-induced colitis and some forms of intestinal infections (Hooper, 2010). | TLR2 in T cells has been proven to help the colonization of commensal Bacteroides fragilis in the gut (June et al., 2011). |
NLRP6 protein | Mediates IL-18 secretion via caspase-1 | A pro-inflammatory cytokine that suppresses mucin production and promote ulcerative colitis among the type colitis (Hu et al. 2015). | IL-22-binding protein express antimicrobial peptides and induce tissue repair (Wells et al. 2011), hence playing an important function in intestinal homeostatic (Wang et al. 2014). |
RIG-1 knockout | Altered microbiota in comparison with wild-type mice. | Microbial change could be linked to the downregulation of IgA, REGIIIγ, and PD-1 (Schroeder et al. 2011). | AIM2 mediation of antimicrobial peptides such as C-type lectins (REGIIIβ and REGIIIγ), calprotectin (S100A8 and S100A9) and lipocalin 2 (Lcn2) in gut epithelial cells (Schneeberger et al. 2018). |
β-defensins, such as DEFB1, beta-defensin 1 (DEFB1) | Bactericidal effects against the gram-positive commensal of Bifidobacterium and Lactobacillus (Mathias et al. 2010). | Reduction in mucosal microbial community and likelihood of onset of insulin resistance. | Immunoglobulin receptor (pIgR), CD71, and CD89 on the epithelial cells may enable microbes to benefit from sIgA to build up a mucosal microbial community (Mathias et al. 2010;Vangay et al. 2018). |