Fig. 1.

Gut/Lung axis: the hypothesis that the intestinal microbiota can modulate the immunological activity of the lung and vice versa: Lipopolysaccharides (LPSs) promote the activation of nuclear factor kappa-light chain-enhancer (NFkb) and plasma cells with various T cells, in particular regulatory T or suppressor T cells (T_reg cells), T helper 17 (T-h17), T helper 1 (Th1) migrating later to the lung through the bloodstream. The bacterial metabolites, in particular short chain fatty acids (SCFAs) act directly on the nuclear factor kappa-light-chain-enhancer of activated B cells (NFkB), reducing production of tumor necrosis factor alpha (TNF-α) and the downregulation of the pattern recognition receptors (PRRs). This will lead to the reduction of the inflammatory cytokines and lung immunomodulation. Then, interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), interferon gamma (IFNγ) and lymphocytes migrate to the gut .