Lack of microbiota reduces innate responses and enhances adaptive immunity against<i>Listeria monocytogenes</i>infection

Mittrücker, Hans‐Willi; Seidel, Daniel; Bland, Paul W.; Zarzycka, Agnieszka; Kaufmann, Stefan H. E.; Visekruna, Alexander; Steinhoff, Ulrich

doi:10.1002/eji.201343927

Cited by 21 publications

(17 citation statements)

References 19 publications

(19 reference statements)

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“…An example of the systemic effect of gut microbiota on granulopoiesis during infection has been provided by a research work demonstrating that early innate resistance to Klebsiella pneumoniae lung infection was impaired in microbiota-depleted mice, and that the peptidoglycan translocated from the gut was able to modulate the systemic innate immunity (28). Therefore, factors affecting the normal granulopoiesis lead to alterations in innate defenses and reduce the resistance against pathogens (23, 28, 29) (Table 1). …”

Section: Granulopoiesis and Its Regulation By The Gut Microbiotamentioning

confidence: 99%

The Role of Microbiota and Immunobiotics in Granulopoiesis of Immunocompromised Hosts

Salva

Alvarez

2017

Front. Immunol.

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The number of granulocytes is maintained by a regulated balance between granulopoiesis in the bone marrow and clearance and destruction in peripheral tissues. Granulopoiesis plays a fundamental role in the innate immune response. Therefore, factors affecting the normal granulopoiesis lead to alterations in innate defenses and reduce the resistance against infections. In this study, we give a description on recent advances regarding the molecular and cellular events that regulate steady-state and emergency granulopoiesis, which are crucial processes for the generation of protective innate immune responses. Particular attention will be given to emergency granulopoiesis alterations in immunosuppression states caused by malnutrition and chemotherapy. The role of microbiota in maintaining a steady-state granulopoiesis and the immunological mechanisms involved are also discussed. Moreover, we describe the findings of our laboratory demonstrating that the dietary supplementation with immunobiotics is an interesting alternative to improve steady-state and emergency granulopoiesis, the respiratory innate immune response, and the resistance against respiratory pathogens in immunocompromised hosts.

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Section: Granulopoiesis and Its Regulation By The Gut Microbiotamentioning

confidence: 99%

The Role of Microbiota and Immunobiotics in Granulopoiesis of Immunocompromised Hosts

Salva

Alvarez

2017

Front. Immunol.

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“…GF or antibiotics-treated mice have defective myelopoiesis and impaired neutrophil homeostasis with an increased susceptibility to late-onset sepsis (23). Defective myelopoiesis also makes GF mice unable to resist acute infection with Listeria monocytogenes , however, they have an enhanced adaptive immune response to vaccination with an attenuated L. monocytogenes strain, a result compatible with normal or heightened adaptive response to nominal antigens in GF mice (14, 24, 25). …”

Section: The Microbiota Modulates Inflammation and Immunity By Priminmentioning

confidence: 99%

Microbiota Modulation of Myeloid Cells in Cancer Therapy

Goldszmid

Dzutsev

Viaud

et al. 2015

Cancer Immunology Research

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Myeloid cells represent a major component of the tumor microenvironment where they play divergent dual roles: they can induce antitumor immune responses but mostly they promote immune evasion, tumor progression and metastases formation. Thus, strategies aiming at reprogramming the tumor microenvironment represent a promising immunotherapy approach. Myeloid cells respond to environmental factors including signals derived from commensal microbes. In this Cancer Immunology at the Crossroads overview we discuss recent advances on the effects of the commensal microbiota on myeloid-cell function and how that impacts the response to cancer therapy.

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“…For example, Clostridium difficile infection, which is the leading health care-associated illness, usually follows the disruption of the indigenous gut microbiota after antibiotic treatment, leading to the loss of colonization resistance against C. difficile (2–4). The gut microbiota also affects intestinal infections by mediating the host innate and adaptive immune responses (5, 6). For example, germ-free mice are highly susceptible to Listeria monocytogenes infection because of impaired activation and accumulation of phagocytes to the site of infection (6).…”

Section: Introductionmentioning

confidence: 99%

“…The gut microbiota also affects intestinal infections by mediating the host innate and adaptive immune responses (5, 6). For example, germ-free mice are highly susceptible to Listeria monocytogenes infection because of impaired activation and accumulation of phagocytes to the site of infection (6). …”

Section: Introductionmentioning

confidence: 99%

Intestinal Microbiota-Derived GABA Mediates Interleukin-17 Expression during Enterotoxigenic Escherichia coli Infection

et al. 2017

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Intestinal microbiota has critical importance in pathogenesis of intestinal infection; however, the role of intestinal microbiota in intestinal immunity during enterotoxigenic Escherichia coli (ETEC) infection is poorly understood. The present study tested the hypothesis that the intestinal microbiota is associated with intestinal interleukin-17 (IL-17) expression in response to ETEC infection. Here, we found ETEC infection induced expression of intestinal IL-17 and dysbiosis of intestinal microbiota, increasing abundance of γ-aminobutyric acid (GABA)-producing Lactococcus lactis subsp. lactis. Antibiotics treatment in mice lowered the expression of intestinal IL-17 during ETEC infection, while GABA or L. lactis subsp. lactis administration restored the expression of intestinal IL-17. L. lactis subsp. lactis administration also promoted expression of intestinal IL-17 in germ-free mice during ETEC infection. GABA enhanced intestinal IL-17 expression in the context of ETEC infection through activating mechanistic target of rapamycin complex 1 (mTORC1)-ribosomal protein S6 kinase 1 (S6K1) signaling. GABA–mTORC1 signaling also affected intestinal IL-17 expression in response to Citrobacter rodentium infection and in drug-induced model of intestinal inflammation. These findings highlight the importance of intestinal GABA signaling in intestinal IL-17 expression during intestinal infection and indicate the potential of intestinal microbiota-GABA signaling in IL-17-associated intestinal diseases.

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Lack of microbiota reduces innate responses and enhances adaptive immunity againstListeria monocytogenesinfection

Cited by 21 publications

References 19 publications

The Role of Microbiota and Immunobiotics in Granulopoiesis of Immunocompromised Hosts

The Role of Microbiota and Immunobiotics in Granulopoiesis of Immunocompromised Hosts

Microbiota Modulation of Myeloid Cells in Cancer Therapy

Intestinal Microbiota-Derived GABA Mediates Interleukin-17 Expression during Enterotoxigenic Escherichia coli Infection

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