Helicobacter hepaticus infection in BALB/c mice abolishes subunit-vaccine-induced protection against M. tuberculosis

Arnold, Isabelle C.; Hutchings, Claire; Kondova, Ivanela; Hey, Ariann; Powrie, Fiona; Beverley, Peter C. L.; Tchilian, Elma

doi:10.1016/j.vaccine.2015.02.041

Cited by 44 publications

(46 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…43 Interestingly, these CIP effects were not influenced by the microbiome as the same effect was seen in germ-free mice. 43 While the microbiome and its metabolites can enhance or dysregulate the immune system, 44,45 CIP directly decreases immune strength and causes dysbiosis, while its metabolites enhance phagocytosis (macrophages) and reduce antimicrobial action. 42,43 These complex relationships require further study.…”

Section: Antimicrobials: the Major Enemy Of The Microbiomementioning

confidence: 99%

Mycobacterium tuberculosis, antimicrobials, immunity, and lung–gut microbiota crosstalk: current updates and emerging advances

Sekyere

Maningi

Fourie

2020

Annals of the New York Academy of Sciences

View full text Add to dashboard Cite

Increasingly, gut microbiota distortions are being implicated in the pathogenesis of several infectious and noninfectious diseases. Specifically, in the absence of an eubiotic microbiota, mice are more prone to colonization and infection by Mycobacterium tuberculosis (Mtb). In this qualitative analysis, the following were observed: (1) antimicrobials cause long-term gut microbiota perturbations; (2) Mtb causes limited and transient disturbances to the lung-gut microbiota; (3) pathogens (e.g., Helicobacter hepaticus) affect microbiota integrity and reduce resistance to Mtb; (4) dysbiosis depletes bacterial species regulating proper immune functioning, reducing resistance to Mtb; (5) dysregulated immune cells fail to express important pathogen-recognition receptors (e.g., macrophageinducible C-type lectin; MINCLE) and Mtb-killing cytokines (e.g., IFN-γ, TNF-α, and IL-17), with hampered phagocytic capability; (6) autophagy is central to the immune system's clearance of Mtb, control of inflammation, and immunity-microbiome balance; (7) microbiota-produced short-chain fatty acids, which are reduced by dysbiosis, affect immune cells and increase Mtb proliferation; (8) commensal species (e.g., Lactobacillus plantarum) and microbiota metabolites (e.g., indole propionic acid) reduce tuberculosis progression; and (9) fecal transplants mostly restored eubiosis, increased immune resistance to Mtb, restricted dissemination of Mtb, and reduced tuberculosis-associated organ pathologies. Overuse of antimicrobials, as shown in mice, is a risk factor for reactivating latent or treated tuberculosis.

show abstract

Section: Antimicrobials: the Major Enemy Of The Microbiomementioning

confidence: 99%

Mycobacterium tuberculosis, antimicrobials, immunity, and lung–gut microbiota crosstalk: current updates and emerging advances

Sekyere

Maningi

Fourie

2020

Annals of the New York Academy of Sciences

View full text Add to dashboard Cite

show abstract

“…Cells were diluted to a final density of 1 ϫ 10 6 cells ml Ϫ1 in cRPMI, and cells were dispensed in propylene tubes for fluorescence-activated cell sorting (FACS) staining. Following removal of epithelial cells and collagenase VIII/DNase I (Roche) digestion of the tissue, lamina propria mononuclear cells were isolated as described previously (29). At the end of the process, cells were counted using the Scepter cell counter (Millipore) and diluted to a final concentration of 1 ϫ 10 6 cells ml Ϫ1 in cRPMI in propylene FACS staining tubes.…”

mentioning

confidence: 99%

The Surface-Associated Exopolysaccharide of Bifidobacterium longum 35624 Plays an Essential Role in Dampening Host Proinflammatory Responses and Repressing Local T _H 17 Responses

Schiavi

Gleinser

Molloy

et al. 2016

Appl Environ Microbiol

134

View full text Add to dashboard Cite

The immune-modulating properties of certain bifidobacterial strains, such as Bifidobacterium longum subsp. longum 35624 (B. longum 35624), have been well described, although the strain-specific molecular characteristics associated with such immuneregulatory activity are not well defined. It has previously been demonstrated that B. longum 35624 produces a cell surface exopolysaccharide (sEPS), and in this study, we investigated the role played by this exopolysaccharide in influencing the host immune response. B. longum 35624 induced relatively low levels of cytokine secretion from human dendritic cells, whereas an isogenic exopolysaccharide-negative mutant derivative (termed sEPS neg ) induced vastly more cytokines, including interleukin-17 (IL-17), and this response was reversed when exopolysaccharide production was restored in sEPS neg by genetic complementation. Administration of B. longum 35624 to mice of the T cell transfer colitis model prevented disease symptoms, whereas sEPS neg did not protect against the development of colitis, with associated enhanced recruitment of IL-17 ؉ lymphocytes to the gut. Moreover, intranasal administration of sEPS neg also resulted in enhanced recruitment of IL-17 ؉ lymphocytes to the murine lung. These data demonstrate that the particular exopolysaccharide produced by B. longum 35624 plays an essential role in dampening proinflammatory host responses to the strain and that loss of exopolysaccharide production results in the induction of local T H 17 responses. IMPORTANCEParticular gut commensals, such as B. longum 35624, are known to contribute positively to the development of mucosal immune cells, resulting in protection from inflammatory diseases. However, the molecular basis and mechanisms for these commensalhost interactions are poorly described. In this report, an exopolysaccharide was shown to be decisive in influencing the immune response to the bacterium. We generated an isogenic mutant unable to produce exopolysaccharide and observed that this mutation caused a dramatic change in the response of human immune cells in vitro. In addition, the use of mouse models confirmed that lack of exopolysaccharide production induces inflammatory responses to the bacterium. These results implicate the surfaceassociated exopolysaccharide of the B. longum 35624 cell envelope in the prevention of aberrant inflammatory responses. T he gut microbiota contributes significantly to host health via multiple mechanisms, including the digestion of foods, competitive exclusion of pathogens, enhancement of epithelial cell differentiation, and promotion of mucosa-associated lymphoid tissue proliferation (1, 2). Furthermore, accumulating evidence suggests that the composition and metabolic activity of the gut microbiota has profound effects on proinflammatory activity and the induction of immune tolerance within mucosal tissue (3-5). Certain microbes induce regulatory responses, while others induce effector responses, resulting in the case of healthy individuals in a balanced homeostatic...

show abstract

“…Two case‐contact studies in Gambia and Pakistan revealed association of the commensal opportunist, Helicobacter ( H.) pylori with protection to active tuberculosis, which was confirmed in experimentally infected cynomolgus macaques . In contrast, H. hepaticus conferred increased susceptibility of Balb/c mice to experimental tuberculosis . Dysbiosis in mice induced by antibiotic treatment promoted M. tuberculosis growth .…”

Section: Microbiome Guided Treatment Perspectivesmentioning

confidence: 97%

“…suggested that bacterial LPS augments liver‐toxicity of isoniazid . Vaccination efficacy to tuberculosis can also be influenced by commensals as shown for Helicobacter hepaticus in Balb/c mice and Bifidobacterium in infants .…”

Section: Microbiome Guided Treatment Perspectivesmentioning

confidence: 99%

“…Su et al suggested that bacterial LPS augments liver-toxicity of isoniazid [168]. Vaccination efficacy to tuberculosis can also be influenced by commensals as shown for Helicobacter hepaticus in Balb/c mice [159] and Bifidobacterium in infants [169]. Significant changes in intestinal microbiota compositions have been observed in M. tuberculosis infected mice, such as lower overall diversity and abundance of Clostridiales [170].…”

Section: Microbiome Guided Treatment Perspectivesmentioning

confidence: 99%

See 1 more Smart Citation

Perspectives for personalized therapy for patients with multidrug‐resistant tuberculosis

et al. 2018

View full text Add to dashboard Cite

According to the World Health Organization (WHO), tuberculosis is the leading cause of death attributed to a single microbial pathogen worldwide. In addition to the large number of patients affected by tuberculosis, the emergence of Mycobacterium tuberculosis drug-resistance is complicating tuberculosis control in many high-burden countries. During the past 5 years, the global number of patients identified with multidrug-resistant tuberculosis (MDR-TB), defined as bacillary resistance at least against rifampicin and isoniazid, the two most active drugs in a treatment regimen, has increased by more than 20% annually. Today we experience a historical peak in the number of patients affected by MDR-TB. The management of MDR-TB is characterized by delayed diagnosis, uncertainty of the extent of bacillary drug-resistance, imprecise standardized drug regimens and dosages, very long duration of therapy and high frequency of adverse events which all translate into a poor prognosis for many of the affected patients. Major scientific and technological advances in recent years provide new perspectives through treatment regimens tailor-made to individual needs. Where available, such personalized treatment has major implications on the treatment outcomes of patients with MDR-TB. The challenge now is to bring these adances to those patients that need them most.

show abstract

Helicobacter hepaticus infection in BALB/c mice abolishes subunit-vaccine-induced protection against M. tuberculosis

Cited by 44 publications

References 30 publications

Mycobacterium tuberculosis, antimicrobials, immunity, and lung–gut microbiota crosstalk: current updates and emerging advances

Mycobacterium tuberculosis, antimicrobials, immunity, and lung–gut microbiota crosstalk: current updates and emerging advances

The Surface-Associated Exopolysaccharide of Bifidobacterium longum 35624 Plays an Essential Role in Dampening Host Proinflammatory Responses and Repressing Local T _H 17 Responses

Perspectives for personalized therapy for patients with multidrug‐resistant tuberculosis

Contact Info

Product

Resources

About

Helicobacter hepaticus infection in BALB/c mice abolishes subunit-vaccine-induced protection against M. tuberculosis

Cited by 44 publications

References 30 publications

Mycobacterium tuberculosis, antimicrobials, immunity, and lung–gut microbiota crosstalk: current updates and emerging advances

Mycobacterium tuberculosis, antimicrobials, immunity, and lung–gut microbiota crosstalk: current updates and emerging advances

The Surface-Associated Exopolysaccharide of Bifidobacterium longum 35624 Plays an Essential Role in Dampening Host Proinflammatory Responses and Repressing Local T H 17 Responses

Perspectives for personalized therapy for patients with multidrug‐resistant tuberculosis

Contact Info

Product

Resources

About

The Surface-Associated Exopolysaccharide of Bifidobacterium longum 35624 Plays an Essential Role in Dampening Host Proinflammatory Responses and Repressing Local T _H 17 Responses