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Respiratory diseases | Alterations in the gut microbiota | Possible mechanisms | References |
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Asthma | Gut microbiota disrupted by antibiotics | Exacerbate Th2 responses by increasing the infiltration of inflammatory cells and the production of inflammatory cytokines (IL-4 and IL-13). | [117, 118] |
Reduce Treg abundance in the lung. | [119] |
Exaggerate Th1/Th17 adaptive immune responses in the lung. | [120] |
GF mice | Elevate the total number of eosinophils, number of CD4+ T cells, and level of Th2 cytokines and alter the number and phenotype of conventional DCs in the airways. | [114] |
Increase CXCL16 expression and accumulate iNKT cells in the gut and lungs. | [121] |
Probiotics | Reverse the Th1/Th2 imbalance: increase the levels of the anti-inflammatory cytokine IL-10 while reduce the levels of proinflammatory cytokines such as IL-4, IL-5, and IL-13. | [122–125] |
Increase PPARγ expression of DCs in the lung. | [126] |
Increase lung CD4+ T cell and CD4+Foxp3+ Treg abundance while decrease activated CD11b+ DC abundance. | [37] |
Decrease MMP9 expression in the BALF and serum and inhibit inflammatory cell infiltration into the lung. | [36] |
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COPD | Cigarette smoke | Alter mucin gene expression and cytokine production in the gut; increase Muc2, Muc3, and Muc4 expression; and increase CXCL2 and IL-6 expression while decrease IFN-γ and TGF-β expression. | [54] |
Inhibit the NK-κB pathway by reducing p65 phosphorylation and IκBα in the gut. | [127] |
Probiotics | Suppress macrophage inflammation by inducing the expression of IL-1β, IL-6, IL-10, IL-23, TNF-α, CXCL-8, and HMGB1. | [58] |
Increase NK cell activity and the number of CD16+ cells. | [128] |
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CF | Probiotics | Reduce IL-8 production by intestinal cells. | [129] |
Reduce the level of the gut inflammatory marker calprotectin. | [68] |
Antibiotic treatment | Augment the proportions of Th17, CD8+ IL-17+, and CD8+ IFNγ+ lymphocytes and IL-17-producing γδ T cells. | [130] |
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Lung cancer | Gut microbiota disrupted by antibiotics | Upregulate the expression of VEGFA and downregulate the expression of BAX and CDKN1B while reduce IFN-γ, GZMB, and PRF1 produced by CD8+ T cells. | [131] |
Suppress CTX-induced Th17 responses and reduce the abundance of tumor-infiltrating CD3+ T cells and Th1 cells. | [132] |
FMT | Accumulate CCR9+CXCR3+CD4+ T cells into the tumor microenvironment. | [79] |
Probiotics | Upregulate the mRNA levels of IFN-γ, GZMB, and PRF1. | [131] |
Boost CTX-induced anticancer Th1 and Tc1 responses and promote the infiltration of IFN-γ+γδT cells into cancer lesions. | [80] |
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Respiratory infection | Commensal gut microbiota | SFB promotes pulmonary Th17 immunity as demonstrated by increased IL-22 and IL-22+ TCRβ+ cell levels. | [133] |
Protect against Mtb infection by improving the activity of MAIT cells in the lungs. | [89] |
Regulate virus-specific CD4 and CD8 T cell and antibody responses. | [134] |
Contribute to the accumulation of IL-22-producing ILC3s in newborn lung. | [81] |
Induce NF-κB activation in the lung through TLR4. | [135, 136] |
Gut microbiota disrupted by antibiotics | Reduce pulmonary GM-CSF production through IL-17A signaling. | [115] |
Reduce MAIT cell and IL-17A levels. | [89] |
Reduce mincle expression on lung DCs. | [95] |
Decrease bacterial killing activity of alveolar macrophages while increase the levels of proinflammatory cytokines such as IL-6 and IL-1β in the lung. | [136] |
GF mice | Decrease proinflammatory cytokine (TNF-α and CXCL1) levels and neutrophil influx while produce large amounts of IL-10 in the lungs. | [137] |
FMT | Normalize the pulmonary TNF-α and IL-10 levels. | [82] |
Probiotics | Activate the TLR-signaling pathway through the protein Mal. | [85] |
Enhance the mRNA expression of IFN-γ, IL-12a, IL-2rb, IL-12rb1, PRF1, Klrk1, CD247, and TNF-α in the lung. | [138] |
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ALI | FMT | Reduce TNF-α, IL-1β, and IL-6 levels by downregulating the TGF-β1/Smads/ERK signaling pathway. | [102] |
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