Mouse Subcutaneous BCG Vaccination and Mycobacterium tuberculosis Infection Alter the Lung and Gut Microbiota

Silva, Fabiola; Enaud, Raphaël; Creissen, Elizabeth; Henao-Tamayo, Marcela; Delhaès, Laurence; Izzo, Angelo A.

doi:10.1128/spectrum.01693-21

Cited by 13 publications

(9 citation statements)

References 84 publications

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“…Of importance, mild colitis is self-limited as by 8 weeks it is largely resolved. Although two recent reports show the changes in intestinal microbiome following parenteral BCG vaccination 50 , 51 , there have not been any clinical reports on parenteral BCG-related colitis, let alone its linkage to metabolomic shifts in the gut and TII induction in the lung. The mild/transient nature of BCG vaccination-related colitis could explain its clinical insignificance.…”

Section: Discussionmentioning

confidence: 99%

Parenteral BCG vaccine induces lung-resident memory macrophages and trained immunity via the gut–lung axis

et al. 2022

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Aside from centrally induced trained immunity in the bone marrow (BM) and peripheral blood by parenteral vaccination or infection, evidence indicates that mucosal-resident innate immune memory can develop via a local inflammatory pathway following mucosal exposure. However, whether mucosal-resident innate memory results from integrating distally generated immunological signals following parenteral vaccination/infection is unclear. Here we show that subcutaneous Bacillus Calmette–Guérin (BCG) vaccination can induce memory alveolar macrophages (AMs) and trained immunity in the lung. Although parenteral BCG vaccination trains BM progenitors and circulating monocytes, induction of memory AMs is independent of circulating monocytes. Rather, parenteral BCG vaccination, via mycobacterial dissemination, causes a time-dependent alteration in the intestinal microbiome, barrier function and microbial metabolites, and subsequent changes in circulating and lung metabolites, leading to the induction of memory macrophages and trained immunity in the lung. These data identify an intestinal microbiota-mediated pathway for innate immune memory development at distal mucosal tissues and have implications for the development of next-generation vaccine strategies against respiratory pathogens.

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Section: Discussionmentioning

confidence: 99%

Parenteral BCG vaccine induces lung-resident memory macrophages and trained immunity via the gut–lung axis

et al. 2022

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“…Riboflavin derivatives produced by Bifidobacterium, Bacteroides thetaiotaomicron, Lactobacillus casei, and Enterobacter cloacae activated mucosa-associated T cells through restricted major histocompatibility complex-associated protein-1 [ 25 ]. In addition, short-chain fatty acids produced by gut bacterial metabolism could pass through the bloodstream, induce immune cell development in the bone marrow, and affect lung immune responses [ 26 ]. Segmented filamentous bacteria attached to the epithelial cells of the lower small intestine could not only stimulate IgA response, but also activate lamina propria dendritic cells and macrophages to secrete IL-1β, IL-6, and IL-23, and induce the generation of intestinal mucosal specific Th17 cell population, which has the potential to differentiate into RORgt subset cells [ 27 ].…”

Section: Gut Microbiota Affects Vaccine Efficacy By Modulating the Im...mentioning

confidence: 99%

Recent five-year progress in the impact of gut microbiota on vaccination and possible mechanisms

Huang¹,

Wang²,

Li³

2023

Gut Pathog

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Vaccine is the most effective way to prevent the spread of communicable diseases, but the immune response induced by it varies greatly between individuals and populations in different regions of the world. Current studies have identified the composition and function of the gut microbiota as key factors in modulating the immune response to vaccination. This article mainly reviews the differences in gut microbiota among different groups of vaccinated people and animals, explores the possible mechanism of vaccine immunity affected by gut microbiota, and reviews the strategies for targeting gut microbiota to improve vaccine efficacy.

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“…It is not surprising that there is a high incidence of chronic M. tuberculosis infection in AHF patients because patients with HLA-DR15 have weaker responses to M. tuberculosis ( 379 , 380 ), and AHF patients have a high frequency of HLA-DR15 phenotype ( 52 , 53 ). Gastrointestinal and even isolated pulmonary tuberculosis can induce pathological processes in the gastrointestinal tract, not only alone but also in combination with gut dysbiosis, which results in diffuse gut inflammatory lesions ( 181 , 381 , 382 ). In this setting, both pathogenic and commensal ( 185 , 186 ) microbes, in addition to M. tuberculosis infection ( 315 , 316 ), become exogenous antigens to sustain deranged immune responses.…”

Section: Particular Attention Should Be Given To Gut Inflammatory Dis...mentioning

confidence: 99%

When inflammatory stressors dramatically change, disease phenotypes may transform between autoimmune hematopoietic failure and myeloid neoplasms

Zhao,

Ju,

Xiu

et al. 2024

Front. Immunol.

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Aplastic anemia (AA) and hypoplastic myelodysplastic syndrome are paradigms of autoimmune hematopoietic failure (AHF). Myelodysplastic syndrome and acute myeloid leukemia are unequivocal myeloid neoplasms (MNs). Currently, AA is also known to be a clonal hematological disease. Genetic aberrations typically observed in MNs are detected in approximately one-third of AA patients. In AA patients harboring MN-related genetic aberrations, a poor response to immunosuppressive therapy (IST) and an increased risk of transformation to MNs occurring either naturally or after IST are predicted. Approximately 10%–15% of patients with severe AA transform the disease phenotype to MNs following IST, and in some patients, leukemic transformation emerges during or shortly after IST. Phenotypic transformations between AHF and MNs can occur reciprocally. A fraction of advanced MN patients experience an aplastic crisis during which leukemic blasts are repressed. The switch that shapes the disease phenotype is a change in the strength of extramedullary inflammation. Both AHF and MNs have an immune-active bone marrow (BM) environment (BME). In AHF patients, an inflamed BME can be evoked by infiltrated immune cells targeting neoplastic molecules, which contributes to the BM-specific autoimmune impairment. Autoimmune responses in AHF may represent an antileukemic mechanism, and inflammatory stressors strengthen antileukemic immunity, at least in a significant proportion of patients who have MN-related genetic aberrations. During active inflammatory episodes, normal and leukemic hematopoieses are suppressed, which leads to the occurrence of aplastic cytopenia and leukemic cell regression. The successful treatment of underlying infections mitigates inflammatory stress-related antileukemic activities and promotes the penetration of leukemic hematopoiesis. The effect of IST is similar to that of treating underlying infections. Investigating inflammatory stress-powered antileukemic immunity is highly important in theoretical studies and clinical practice, especially given the wide application of immune-activating agents and immune checkpoint inhibitors in the treatment of hematological neoplasms.

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Mouse Subcutaneous BCG Vaccination and Mycobacterium tuberculosis Infection Alter the Lung and Gut Microbiota

Cited by 13 publications

References 84 publications

Parenteral BCG vaccine induces lung-resident memory macrophages and trained immunity via the gut–lung axis

Parenteral BCG vaccine induces lung-resident memory macrophages and trained immunity via the gut–lung axis

Recent five-year progress in the impact of gut microbiota on vaccination and possible mechanisms

When inflammatory stressors dramatically change, disease phenotypes may transform between autoimmune hematopoietic failure and myeloid neoplasms

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