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Table 2 Immune factors influencing gut microbes

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).