Ticks Resist Skin Commensals with Immune Factor of Bacterial Origin.
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ABSTRACT:
SUBMITTER: Hayes BM
PROVIDER: S-EPMC8034492 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:The adaptive immune system provides critical defense against pathogenic bacteria. Commensal bacteria have begun to receive much attention in recent years, especially in the gut where there is growing evidence of complex interactions with the adaptive immune system. In the present study, we observed that commensal skin bacteria are recognized by major populations of T cells in skin-draining lymph nodes of mice. Recombination activating gene 1 (Rag1)(-/-) mice, which lack adaptive immune cells, contained living skin-derived bacteria and bacterial sequences, especially mycobacteria, in their skin-draining lymph nodes. T cells from skin-draining lymph nodes of normal mice were shown, in vitro, to specifically recognize bacteria of several species that were grown from Rag1(-/-) lymph nodes. T cells from skin-draining lymph nodes, transferred into Rag1(-/-) mice proliferated in skin-draining lymph nodes, expressed a restricted T-cell receptor spectrotype and produced cytokines. Transfer of T cells into Rag1(-/-) mice had the effect of reducing bacterial sequences in skin-draining lymph nodes and in skin itself. Antibacterial effects of transferred T cells were dependent on IFNγ and IL-17A. These studies suggest a previously unrecognized role for T cells in controlling skin commensal bacteria and provide a mechanism to account for cutaneous infections and mycobacterial infections in T-cell-deficient patients.
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Project description:All bacterial infections occur within a polymicrobial environment, from which a pathogen population emerges to establish disease within a host. Emphasis has been placed on prevention of pathogen dominance by competing microflora acting as probiotics1. Here we show that the virulence of the human pathogen Staphylococcus aureus is augmented by native, polymicrobial, commensal skin flora and individual species acting as 'proinfectious agents'. The outcome is pathogen proliferation, but not commensal. Pathogenesis augmentation can be mediated by particulate cell wall peptidoglycan, reducing the S. aureus infectious dose by over 1,000-fold. This phenomenon occurs using a range of S. aureus strains and infection models and is not mediated by established receptor-mediated pathways including Nod1, Nod2, Myd88 and the NLPR3 inflammasome. During mouse sepsis, augmentation depends on liver-resident macrophages (Kupffer cells) that capture and internalize both the pathogen and the proinfectious agent, leading to reduced production of reactive oxygen species, pathogen survival and subsequent multiple liver abscess formation. The augmented infection model more closely resembles the natural situation and establishes the role of resident environmental microflora in the initiation of disease by an invading pathogen. As the human microflora is ubiquitous2, its role in increasing susceptibility to infection by S. aureus highlights potential strategies for disease prevention.
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Project description:Intestinal commensal bacteria induce protective and regulatory responses that maintain host-microbial mutualism. However, the contribution of tissue-resident commensals to immunity and inflammation at other barrier sites has not been addressed. We found that in mice, the skin microbiota have an autonomous role in controlling the local inflammatory milieu and tuning resident T lymphocyte function. Protective immunity to a cutaneous pathogen was found to be critically dependent on the skin microbiota but not the gut microbiota. Furthermore, skin commensals tuned the function of local T cells in a manner dependent on signaling downstream of the interleukin-1 receptor. These findings underscore the importance of the microbiota as a distinctive feature of tissue compartmentalization, and provide insight into mechanisms of immune system regulation by resident commensal niches in health and disease.
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Project description:Introduction: As therapies for atopic dermatitis (AD) based on live biotherapeutic products (LBP) are developed, the potential displacement of biotherapeutic strains, and species to mucosal sites where they are not naturally found is of investigative interest. However, formal assessment of the toxicity potential of healthy skin commensal organisms has not been reported in the literature. Our previous research indicates that topical application of live Roseomonas mucosa to treat AD was associated with clinical benefit on the skin, but the effects of exposure via inhalation, eye inoculation, and ingestion were unknown. Methods: Herein we report our findings from mice inoculated with commensal strains of R. mucosa, coagulase negative Staphylococci (CNS), and Pseudomonas aeruginosa. Bacterial isolates were collected under clinical trial NCT03018275, however these results do not represent an interventional clinical trial. Results: Our tested R. mucosa isolates did not display significant infection or inflammation. However, neutropenic mice inoculated with CNS had infection without major inflammation in pulmonary models. In contrast, systemic infection generated hepatic and splenic pathology for P. aeruginosa and CNS, which was worsened by the presence of neutropenia. Discussion: Our results suggest that LBP derived from bacteria without significant infectivity histories, such as R. mucosa, may represent safer options than known pathobionts like P. aeruginosa and Staphylococcus spp. Overall, these results suggest that topically applied LBP from select skin commensals are likely to present safe therapeutic options and reinforce our prior clinical findings.
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Project description:In nature, roots of healthy plants are colonized by multikingdom microbial communities that include bacteria, fungi, and oomycetes. A key question is how plants control the assembly of these diverse microbes in roots to maintain host-microbe homeostasis and health. Using microbiota reconstitution experiments with a set of immunocompromised Arabidopsis thaliana mutants and a multikingdom synthetic microbial community (SynCom) representative of the natural A. thaliana root microbiota, we observed that microbiota-mediated plant growth promotion was abolished in most of the tested immunocompromised mutants. Notably, more than 40% of between-genotype variation in these microbiota-induced growth differences was explained by fungal but not bacterial or oomycete load in roots. Extensive fungal overgrowth in roots and altered plant growth was evident at both vegetative and reproductive stages for a mutant impaired in the production of tryptophan-derived, specialized metabolites (cyp79b2/b3). Microbiota manipulation experiments with single- and multikingdom microbial SynComs further demonstrated that 1) the presence of fungi in the multikingdom SynCom was the direct cause of the dysbiotic phenotype in the cyp79b2/b3 mutant and 2) bacterial commensals and host tryptophan metabolism are both necessary to control fungal load, thereby promoting A. thaliana growth and survival. Our results indicate that protective activities of bacterial root commensals are as critical as the host tryptophan metabolic pathway in preventing fungal dysbiosis in the A. thaliana root endosphere.
| S-EPMC8670527 | biostudies-literature
Project description:Human settlers transported chickens (Gallus gallus domesticus) to most East Polynesian archipelagos between AD 1000 and 1300; however, it has long been assumed that New Zealand was an exception. Despite the fact that chicken bones have been recovered from localities of early archaeological middens in New Zealand, their age and genetic relationships have never been critically assessed. Here, we test the assumption that chickens were not introduced to New Zealand during prehistory through ancient DNA and radiocarbon analyses of chicken bones from sites of M?ori middens containing prehistoric material. The chickens belong to the widespread mitochondrial control region haplogroup E. Radiocarbon dating reveals that the bones are not prehistoric, but are still the earliest chicken remains known from New Zealand. Two of the bones pre-date permanent European settlement (ca 1803s onwards) but overlap with the arrival of James Cook's second voyage (1773-1774), and, therefore, they are likely to be chickens, or progeny thereof, liberated during that voyage. Our results support the idea that chickens were first introduced to New Zealand by Europeans, and provide new insights into M?ori uptake and integration of resources introduced during the early post-European period.
| S-EPMC5108951 | biostudies-literature
Project description:The aim of this work was to access the early immune response triggered by R. microplus larvae attachment in previously selected resistant and susceptible animals in a bovine F2 population derived from Gyr (Bos indicus) × Holstein (Bos taurus) crosses. We used microarray data both to access the changes in gene expression over the course of the first 48 hours after tick infestation as constrasting the phenotypically diferent groups.
2014-05-23 | GSE57907 | GEO
Project description:BackgroundThe intestinal microbiota fundamentally guides the development of a normal intestinal physiology, the education, and functioning of the mucosal immune system. The Citrobacter rodentium-carrier model in germ-free (GF) mice is suitable to study the influence of selected microbes on an otherwise blunted immune response in the absence of intestinal commensals.ResultsHere, we describe that colonization of adult carrier mice with 14 selected commensal microbes (OMM12 + MC2) was sufficient to reestablish the host immune response to enteric pathogens; this conversion was facilitated by maturation and activation of the intestinal blood vessel system and the step- and timewise stimulation of innate and adaptive immunity. While the immature colon of C. rodentium-infected GF mice did not allow sufficient extravasation of neutrophils into the gut lumen, colonization with OMM12 + MC2 commensals initiated the expansion and activation of the visceral vascular system enabling granulocyte transmigration into the gut lumen for effective pathogen elimination.ConclusionsConsortium modeling revealed that the addition of two facultative anaerobes to the OMM12 community was essential to further progress the intestinal development. Moreover, this study demonstrates the therapeutic value of a defined consortium to promote intestinal maturation and immunity even in adult organisms. Video Abstract.
| S-EPMC9520927 | biostudies-literature
Project description:The aim of this work was to access the early immune response triggered by R. microplus larvae attachment in previously selected resistant and susceptible animals in a bovine F2 population derived from Gyr (Bos indicus) x Holstein (Bos taurus) crosses. We used microarray data both to access the changes in gene expression over the course of the first 48 hours after tick infestation as constrasting the phenotypically diferent groups. From a bovine F2 population, six tick-resistant (R) and seven tick-susceptible (S) animals were used in this experiment. Skin biopses were taken at the feeding sites before infestation (0 hour), 24 and 48 hours after tick infestation in each animal.
2014-05-23 | E-GEOD-57907 | biostudies-arrayexpress
Project description:Bacteria that use electron transport proteins in the membrane to produce electricity in the gut microbiome have been identified recently. However, the identification of electrogenic bacteria in the skin microbiome is almost completely unexplored. Using a ferric iron-based ferrozine assay, we have identified the skin Staphylococcus epidermidis (S. epidermidis) as an electrogenic bacterial strain. Glycerol fermentation was essential for the electricity production of S. epidermidis since the inhibition of fermentation by 5-methyl furfural (5-MF) significantly diminished the bacterial electricity measured by voltage changes in a microbial fuel cell (MFC). A small-scale chamber with both anode and cathode was fabricated in order to study the effect of ultraviolet-B (UV-B) on electricity production and bacterial resistance to UV-B. Although UV-B lowered bacterial electricity, a prolonged incubation of S. epidermidis in the presence of glycerol promoted fermentation and elicited higher electricity to suppress the effect of UV-B. Furthermore, the addition of glycerol into S. epidermidis enhanced bacterial resistance to UV-B. Electricity produced by human skin commensal bacteria may be used as a dynamic biomarker to reflect the UV radiation in real-time.
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