Bacterial communities and metabolites impact multiple stages in the well-established pathway of allergic inflammation, both offering potentially protective effects (blue arrows) and exacerbating allergic inflammation (red arrows).

(A) SCFAs produced by gut microbiota enhance bone marrow production of dendritic cells and macrophages with increased phagocytic capacity but reduced ability to stimulate Th2 responses in the lung [33]. (B) Bacteria found in the airway have been associated with increased markers of Th17 inflammation [20,21,24]. (C) Microbially derived metabolites may directly stimulate or inhibit [35] Th2 development [31]. (D) Microbially derived SCFAs found in the healthy gut promote Treg differentiation [34], whereas metabolites like DiHOME produced by asthmatic gut microbiota inhibit Treg proliferation [31]. (E) Viral respiratory tract infections are associated with increased risk for asthma and exacerbations [8]. (F) S. aureus colonizes the skin of AD patients depleted of antimicrobial peptides by allergic inflammation and carries virulence factors that influence the host immune system to sustain the inflamed state. S. aureus delta toxin, for example, acts on pathways not associated with immunoglobulin E to stimulate mast-cell degranulation near the site of colonization [3]. Investigating the precise mechanisms by which bacteria can worsen or mitigate asthma and allergic inflammation will offer novel probiotic candidates and biomarkers with therapeutic potential. AD, atopic dermatitis; DiHOME, 12,13-dihydroxy-9Z-octadecenoic acid; IL, interleukin; SCFA, short-chain fatty acid; Th2, T-helper 2; Th17, T-helper 17; Treg, T regulatory cell.