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Transcriptional immunogenomic analysis reveals distinct immunological clusters in pediatric nervous system tumours

To inform immunotherapy approaches in children, we performed an immunogenomic analysis of RNA-seq data from 925 treatment-naive pediatric nervous system tumours (pedNST) spanning 12 cancer types from three public data sets. Within pedNST, we uncovered four broad immune clusters: Pediatric Inflamed (10%), Myeloid Predominant (30%), Immune Neutral (43%) and Immune Excluded (17%). We validated these clusters using immunohistochemistry, methylation immune inference, and segmentation analysis of tissue images. We report shared biology of these immune clusters within and across cancer types, and characterization of specific immune-cell frequencies as well as T- and B-cell repertoires. We found no associations between immune infiltration levels and tumour mutational burden, although molecular cancer entities were enriched within specific immune clusters. Given the heterogeneity within pedNST, our findings suggest personalized immunogenomic profiling is needed to guide selection of immunotherapeutic strategies.

genomics↗

Syngeneic model of carcinogen-induced tumor mimics basal/squamous, stromal-rich, and neuroendocrine molecular and immunological features of muscle-invasive bladder cancer

BackgroundBladder cancer is a heterogenous disease and the emerging knowledge on molecular classification of bladder tumors could have impact to drive treatment decisions based on molecular subtype. Pre-clinical models representing each subtype are needed to test novel therapies. Carcinogen-induced bladder cancer models represent heterogeneous, immune-competent, pre-clinical testing options with many features found in the human disease. MethodsInvasive bladder tumors were induced in C57BL/6 mice when continuously exposed to N-butyl-N-(4-hydroxbutyl nitrosamine) (BBN) in the drinking water. Tumors were excised and serially passed by subcutaneous implantation into sex-matched syngeneic C57BL/6 hosts. Eight tumor lines were developed and named BBN-induced Urothelium Roswell Park (BURP) tumor lines. The BURP lines were characterized by applying consensus molecular classification to RNA expression, histopathology, and immune profiles by CIBERSORT. Two lines were further characterized for cisplatin response. ResultsEight BURP tumor lines were established with 3 male and 3 female BURP tumor lines, having the basal/squamous (BaSq) molecular phenotype and morphology. BURP-16SR was established from a male mouse and has a stromal-rich (SR) molecular phenotype and a sarcomatoid carcinoma morphology. BURP-19NE was established from a male mouse and has a neuroendocrine (NE)-like molecular phenotype and poorly differentiated morphology. The established BURP tumor lines have unique immune profiles with fewer immune infiltrates compared to their originating BBN-induced tumors. The immune profiles of the BURP tumor lines capture some of the features observed in the molecular classifications of human bladder cancer. BURP-16SR growth was inhibited by cisplatin treatment, while BURP-24BaSq did not respond to cisplatin. ConclusionsThe BURP tumor lines represent several molecular classifications, including basal/squamous, stroma-rich, and NE-like. The stroma-rich (BURP-16SR) and NE-like (BURP-19NE) represent unique immunocompetent models that can be used to test novel treatments in these less common bladder cancer subtypes. Six basal/squamous tumor lines were established from both male and female mice. Overall, the BURP tumor lines have less heterogeneity than the carcinogen-induced tumors and can be used to evaluate treatment response without the confounding mixed response often observed in heterogeneous tumors. Additionally, basal/squamous tumor lines were established and maintained in both male and female mice, thereby allowing these tumor lines to be used to compare differential treatment responses between sexes.

cancer biology↗

Early life exposure to broccoli sprouts confers stronger protection against enterocolitis development in an immunological mouse model of inflammatory bowel disease.

Crohns Disease (CD) is a presentation of Inflammatory Bowel Disease (IBD) that manifests in childhood and adolescence, and involves chronic and severe enterocolitis, immune and gut microbiome dysregulation, and other complications. Diet and gut-microbiota-produced metabolites are sources of anti-inflammatories which could ameliorate symptoms. However, questions remain on how IBD influences biogeographic patterns of microbial location and function in the gut, how early life transitional gut communities are affected by IBD and diet interventions, and how disruption to biogeography alters disease mediation by diet components or microbial metabolites. Many studies on diet and IBD use a chemically induced ulcerative colitis model, despite the availability of an immune-modulated CD model. Interleukin-10-knockout (IL-10-KO) mice on a C57BL/6 background, beginning at age 4 or 7 weeks, were fed a control diet or one containing 10% (w/w) raw broccoli sprouts, which was high in the sprout-sourced anti-inflammatory sulforaphane. Diets began 7 days prior to, and for 2 weeks after inoculation with Helicobacter hepaticus, which triggers Crohns-like symptoms in these immune-impaired mice. The broccoli sprout diet increased sulforaphane in plasma; decreased weight stagnation, fecal blood, and diarrhea associated; and increased microbiota richness in the gut, especially in younger mice. Sprout diets resulted in some anatomically specific bacteria in younger mice, and reduced the prevalence and abundance of pathobiont bacteria which trigger inflammation in the IL-10-KO mouse, for example; Escherichia coli and Helicobacter. Overall, the IL-10-KO mouse model is responsive to a raw broccoli sprout diet and represents an opportunity for more diet-host-microbiome research. ImportanceTo our knowledge, IL-10-KO mice have not previously been used to investigate the interactions of host, microbiota, and broccoli, broccoli sprouts, or broccoli bioactives in resolving symptoms of CD. We showed that a diet containing 10% raw broccoli sprouts increased the plasma concentration of the anti-inflammatory compound sulforaphane, and protected mice to varying degrees against negative disease symptoms, including weight loss or stagnation, fecal blood, and diarrhea. Younger mice responded more strongly to the diet, further reducing symptoms, as well as increased gut bacterial community richness, increased bacterial community similarity to each other, and more location-specific communities than older mice on the diet intervention. Crohns Disease disrupts the lives of patients, and requires people to alter dietary and lifestyle habits to manage symptoms. The current medical treatment is extremely expensive, and a dietary intervention represents an affordable, accessible, and simple strategy to reduce the burden of symptoms.

microbiology↗

Immunologically mediated trade-offs shaping transmission of sylvatic dengue and Zika viruses in native and novel non-human primate hosts

Mosquito-borne dengue (DENV) and Zika (ZIKV) viruses originated in Old World sylvatic cycles involving monkey hosts, spilled over into human transmission, and were translocated to the Americas, creating potential for spillback into neotropical sylvatic cycles. Studies of the trade-offs that shape within-host dynamics and transmission of these viruses are lacking, hampering efforts to predict spillover and spillback. We exposed native (cynomolgus macaque) or novel (squirrel monkey) hosts to mosquitoes infected with either sylvatic DENV or ZIKV and monitored viremia, natural killer cells, transmission to mosquitoes, cytokines, and neutralizing antibody titers. Unexpectedly, DENV transmission from both host species occurred only when serum viremia was undetectable or near the limit of detection. ZIKV replicated in squirrel monkeys to much higher titers than DENV and was transmitted more efficiently but stimulated lower neutralizing antibody titers. Increasing ZIKV viremia led to greater instantaneous transmission and shorter duration of infection, consistent with a replication-clearance trade-off.

microbiology↗

KISS1 is a potential immunological and prognostic biomarker for cancer metastasis in pan-cancer and affects breast cancer in a different way

Metastasis to other organs accounts for the majority of death in cancer patients. Metastatic capacity enables tumor cells resist to chemotherapy. KISS1 had been found to suppress metastasis in cancers like melanoma, but improve the metastatic phenotype of breast cancers, which means its role in tumor metastasis is tissue context-dependent. This character suggests the KISS1 might have promising potential to interpret tumor metastasis in a pan-cancer perspective. Here, we analyzed the potential functions of KISS1 in pan-cancer, especially in breast cancer, by the datasets of TCGA and GTEx. KISS1 exhibited a different expression status between mRNA level and protein level in pan-cancers, with a significant association between KISS1 expression and prognosis of cancer patients. Besides, the correlation between KISS1 expression and immune cell infiltration, immunosuppressive cells, immune checkpoint genes, TMB, MSI, tumor purity and HRD indicates the potential role in regulating immunotherapy. Thereafter, we further clarified the role of KISS1 in promoting metastasis in breast cancer. Furthermore, we found that the post-translational modification may explains the KISS1 protein stability in breast cancers. In summary, our first pan-cancer study offers new insights and relatively comprehensive understandings of the oncogenic roles of KISS1 across various cancers.

genetics↗

Single-cell and spatial transcriptomics reveals the human liver immunological landscape and myeloid dysfunction in PSC.

BackgroundPrimary sclerosing cholangitis (PSC) is an immune-mediated cholestatic liver disease characterized by bile retention, biliary tree destruction, and progressive fibrosis leading to end stage liver disease and transplantation. There is an unmet need to understand the cellular composition of the PSC liver and how it underlies disease pathogenesis. As such, we generated a comprehensive atlas of the PSC liver and a reference healthy liver dataset using multiple multi-omic modalities and functional validation. MethodsIn this work, we employed single-cell (12,000 cells), single-nuclei (23,000 nuclei), and spatial transcriptomics (1 sample by 10x Visium and 3 samples with multi-region profiling by Nanostring GeoMx DSP) to profile the cellular ecosystem in 5 patients with PSC. Transcriptomic profiles were compared to 100k single cell transcriptomes and spatial transcriptomics controls from 24 healthy neurologically deceased donor (NDD) livers. Flow cytometry and intracellular cytokine staining was performed to validate PSC-specific differences in immune phenotype and function. ResultsPSC explants with cirrhosis of the liver parenchyma and prominent periductal fibrosis were associated with a unique population of hepatocytes which transformed to a cholangiocyte-like phenotype. These hepatocytes were surrounded by diverse immune cell populations, including monocyte-like macrophages, liver-resident and circulating natural killer (NK) cells. Inflamed cholangiocytes, fibrosis-resident hepatic stellate cells, and endothelial cells released cytokines that recruited CD4+T-cells, dendritic cells, and neutrophils to the PSC liver. Tissue-resident macrophages, by contrast, were reduced in number and exhibited a dysfunctional inflammatory response to LPS and IFN-{gamma} stimulation. ConclusionsWe present the first comprehensive atlas of the PSC liver and demonstrate hyper-activation and exhaustion-like phenotypes of myeloid cells and markers of chronic cytokine expression in late-stage PSC lesions. Lay SummaryPrimary sclerosing cholangitis (PSC) is a rare liver disease characterized by chronic inflammation and irreparable damage to the bile ducts. Due to a limited understanding of the underlying pathogenesis of disease, there remains a paucity of treatment options. As such, we sequenced healthy and diseased livers to compare the activity, interactions, and localization of immune and non-immune cells. This revealed that outside PSC scar regions, hepatocytes are transitioning to bile duct cells, whereas within the scars, there is an accumulation of immune cells. Of these cells, macrophages that typically contribute to tissue repair were enriched in immunoregulatory genes and were less responsive to stimulation. These cells are likely involved in maintaining hepatic inflammation and could be targeted in novel therapeutic development.

cell biology↗

VirEvol platform:accurate prediction and visualization of SARS-CoV-2 evolutionary trajectory based on protein language model, structural information and immunological recognition mechanism

Predicting the mutation direction of SARS-CoV-2 using exploratory computational methods presents a challenging, yet prospective, research avenue. However, existing research methods often ignore the effects of protein structure and multi-source viral information on mutation prediction, making it difficult to accurately predict the evolutionary trend of the SARS-CoV-2 S protein receptor-binding domain (RBD). To overcome this limitation, we proposed an interpretable language model combining structural, sequence and immune information. The dual utility of this model lies in its ability to predict SARS-CoV-2s affinity for the ACE2 receptor, and to assess its potential for immune evasion. Additionally, it explores the mutation trend of SARS-CoV-2 via a genetic algorithm-directed evolution. The model exhibits high accuracy in both regards and has displayed promising early warning capabilities, effectively identifying 13 out of 14 high-risk strains, marking a success rate of 93%.". This study provides a novel method for discerning the molecular evolutionary pattern, as well as predicting the evolutionary trend of SARS-CoV-2 which is of great significance for vaccine design and drug development of new coronaviruses. We further developed VirEvol, a unique platform designed to visualize the evolutionary trajectories of novel SARS-CoV-2 strains, thereby facilitating real-time predictive analysis for researchers. The methodologies adopted in this work may inspire new strategies and offer technical support for addressing challenges posed by other highly mutable viruses.

bioinformatics↗

Do Domain-Specific Protein Language Models Outperform General Models on Immunology-Related Tasks?

Deciphering the antigen recognition capabilities by T cell and B cell receptors (antibodies) is essential for advancing our understanding of adaptive immune system responses. In recent years, the development of protein language models (PLMs) has facilitated the development of bioinformatic pipelines where complex amino acid sequences are transformed into vectorized embeddings, which are then applied to a range of downstream analytical tasks. With their success, we have witnessed the emergence of domain-specific PLMs tailored to specific proteins, such as immune receptors. Domain-specific models are often assumed to possess enhanced representation capabilities for targeted applications, however, this assumption has not been thoroughly evaluated. In this manuscript, we assess the efficacy of both generalist and domain-specific transformer-based embeddings in characterizing B and T cell receptors. Specifically, we assess the accuracy of models that leverage these embeddings to predict antigen specificity and elucidate the evolutionary changes that B cells undergo during an immune response. We demonstrate that the prevailing notion of domain-specific models outperforming general models requires a more nuanced examination. We also observe remarkable differences between generalist and domain-specific PLMs, not only in terms of performance but also in the manner they encode information. Finally, we observe that the choice of the size and the embedding layer in PLMs are essential model hyperparameters in different tasks. Overall, our analyzes reveal the promising potential of PLMs in modeling protein function while providing insights into their information-handling capabilities. We also discuss the crucial factors that should be taken into account when selecting a PLM tailored to a particular task.

bioinformatics↗

The immunological profile of RC17 hESC-derived dopaminergic neural progenitor cells in vitro: implications for the STEM-PD clinical trial.

Parkinsons Disease involves the progressive loss of dopaminergic neurons (DAn), prompting clinical trials replacing cell loss with neural grafts. This includes the transplantation of pluripotent stem cell-derived DAn progenitor cells (NPC) currently under investigation in the STEM-PD trial. To determine the likelihood of immune rejection post-grafting, we characterised the immunogenicity of the STEM-PD product (RC17-hESC-derived NPCs), comparing them to human foetal ventral mesencephalic tissue (hfVM) previously tested in trials, including our own TRANSEURO trial. Despite MHC-Class I expression, upregulated by proinflammatory cytokines, no immune response to NPCs was detected in vitro. Instead, they were immunosuppressive. Transcriptomic analysis revealed similarities between RC17-NPCs and hfVM, both strongly upregulating antigen processing and presentation pathways in response to IFN{gamma}. Furthermore, immunosuppressant mycophenolate mofetil detrimentally affected NPC survival and differentiation in vitro. Overall, our data suggest that aggressive immunosuppression is not required following hESC-NPC transplantation and that caution should be exercised when selecting the immunosuppressive regimen.

neuroscience↗

Distinct genomic and immunologic tumor evolution in germline TP53-driven breast cancers

Pathogenic germline TP53 alterations cause Li-Fraumeni Syndrome (LFS), and breast cancer is the most common cancer in LFS females. We performed first of its kind multimodal analysis of LFS breast cancer (LFS-BC) compared to sporadic premenopausal BC. Nearly all LFS-BC underwent biallelic loss of TP53 with no recurrent oncogenic variants except ERBB2 (HER2) amplification. Compared to sporadic BC, in situ and invasive LFS-BC exhibited a high burden of short amplified aneuploid segments (SAAS). Pro-apoptotic p53 target genes BAX and TP53I3 failed to be up-regulated in LFS-BC as was seen in sporadic BC compared to normal breast tissue. LFS-BC had lower CD8+ T-cell infiltration compared to sporadic BC yet higher levels of proliferating cytotoxic T-cells. Within LFS-BC, progression from in situ to invasive BC was marked by an increase in chromosomal instability with a decrease in proliferating cytotoxic T-cells. Our study uncovers critical events in mutant p53-driven tumorigenesis in breast tissue.

genetics↗

A Novel Blood-Based Epigenetic Clock for Intrinsic Capacity Predicts Mortality and is Associated with Clinical, Immunological and Lifestyle Factors

Age-related decline in intrinsic capacity (IC), defined as the sum of an individuals physical and mental capacities, is a cornerstone for promoting healthy aging and longevity, as it emphasizes maximizing function throughout the aging process instead of merely treating diseases. However, accurate assessments of IC are resource-intensive, and the molecular and cellular basis of its decline are poorly understood. Herein, we used the INSPIRE-T cohort, consisting of 1,014 individuals aged 20 to 102, to construct the IC clock, a DNA methylation (DNAm)-based predictor of IC trained on the clinical evaluation of cognition, locomotion, psychological well-being, sensory abilities, and vitality. In the Framingham Heart Study, age-adjusted DNAm IC correlates with first- and second-generation epigenetic clocks, predicts all-cause mortality, and is strongly associated with changes in molecular and cellular immune and inflammatory biomarkers, functional and clinical endpoints, health risk factors, and diet.

genomics↗

A multidimensional Pan-cancer analysis of CDKN1A identifies CDKN1A as an Immunological and Prognostic Biomarker

CDKN1A/p21 is well recognized for its role in cell cycle regulation and genomic stability. However, its functions in the Tumor microenvironment (TME) and tumor immunity are not yet fully understood. Hereby, we explored CDKN1A expression and immunological/prognostic values via various databases and analytical methods including cBioPortal, Kaplan-Meier, UCSCXenaShiny, TIMER, Single-cell RNA sequencing (scRNA-seq) analysis, etc. In addition, we explored different approaches including CCK8, EdU, Colony formation, Drug sensitivity and Annixin-V assay to explore the influence of p21 in proliferative capacity in cancer cells. We found that CDKN1A is lowly expressed in BLCA, BRCA, COAD, KICH, LUAD, LUSC, PRAD, READ and STAD compared to normal samples, whereas it is highly expressed in CHOL, HNSC, KIRC, KIRP and THCA compared to normal cohorts. CDKN1A expression is significantly correlated with overall survival, disease-specific survival, disease-free survival and progression-free interval different cancer types. Additionally, CDKN1A is associated with CD4+ T cell, CD8+ T cell, Neutrophil, Macrophage and Myeloid dendritic cell infiltration in diverse cancer types. Functional experiments reveal that p21 overexpression leads to a significant reduction in proliferative capacity, facilitates cell apoptosis and senescence in multiple cancer cell lines. In contrast, silenced p21 facilitates cell growth and wound closure, prevent cell senescence in different cancer cell lines. In conclusion, our findings suggest that CDKN1A may serve as a valuable prognostic and immunotherapeutic marker in diverse cancer.

cancer biology↗

Immunological findings of West Caucasian bat virus in an accidental host

The Lyssavirus genus includes seventeen neurotropic viral species which are able to cause rabies, an acute and almost invariably fatal encephalomyelitis of mammals. Rabies virus (RABV), the genus prototype, is a multi-host pathogen that undergoes multiple events of host-switching, thus occupying several geographical and ecological niches. In contrast, non-RABV lyssaviruses are mainly confined within a single natural host with rare spillover events never followed by adaptation to new accidental host species. In this scenario, unveiling the mechanisms underlying the host immune response against a virus is crucial to understand the dynamics of infection but also to predict the probability of colonization and adaptation to a new target species. Presently, the host response to lyssaviruses has only been partially explored, with the majority of data inferred from RABV infection, under the assumption that all members of the genus exhibit a similar behavior. Through our study we have investigated the immune response determined by the West Caucasian bat virus (WCBV). Indeed, WCBV has been recently associated with a spillover event to a domestic cat, raising concern about the risks for public health due to the circulation of the virus in its natural host. We selected the Syrian hamster as an animal model representative for an accidental host, and chose the intramuscular route in order to mimic the natural route of infection. In hamsters, WCBV was highly pathogenic, determining 100% lethality and mild encephalitis. In comparison with Duvenhage virus (DUVV) and RABV, we found that WCBV displayed an intermediate ability to promote cellular antiviral response, produce pro-inflammatory cytokines, recruit and activate lymphocytes in the hamsters central nervous system. Author SummaryViruses belonging to the genus Lyssavirus cause rabies, a zoonotic and almost invariably fatal encephalomyelitis. However, not all lyssaviruses behave in the same way, with Rabies virus (RABV) being a multi-host pathogen and non-RABV ones remaining mostly confined to their natural hosts. Host-pathogen interaction might help to elucidate the mechanisms behind the differences observed among lyssaviruses in terms of disease dynamics and ability to cross the species barrier, adapting to novel hosts. In our study, we have investigated the host immune response triggered by the WCBV strain spilled-over from its host (the bent-winged bat) to a domestic cat in 2020. Our study offers a key to understand and generalize the mechanisms underlying lyssavirus spillover and pathogenicity in accidental hosts. More generally, our work confirms and marshals previous, fragmentary evidence indicating a strong and inverse relationship between lyssavirus pathogenicity and immune response induction.

microbiology↗

nSMase2-mediated exosome secretion shapes the tumor microenvironment to immunologically support pancreatic cancer

The pleiotropic roles of nSMase2-generated ceramide include regulation of intracellular ceramide signaling and exosome biogenesis. We investigated the effects of eliminating nSMase2 on early and advanced PDA, including its influence on the microenvironment. Employing the KPC mouse model of pancreatic cancer, we demonstrate that pancreatic epithelial nSMase2 ablation reduces neoplasia and promotes a PDA subtype switch from aggressive basal-like to classical. nSMase2 elimination prolongs survival of KPC mice, hinders vasculature development, and fosters a robust immune response. nSMase2 loss leads to recruitment of cytotoxic T cells, N1-like neutrophils, and abundant infiltration of anti-tumorigenic macrophages in the pancreatic preneoplastic microenvironment. Mechanistically, we demonstrate that nSMase2-expressing PDA cell small extracellular vesicles (sEVs) reduce survival of KPC mice; PDA cell sEVs generated independently of nSMase2 prolong survival of KPC mice and reprogram macrophages to a proinflammatory phenotype. Collectively, our study highlights previously unappreciated opposing roles for exosomes, based on biogenesis pathway, during PDA progression. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=189 SRC="FIGDIR/small/614610v1_ufig1.gif" ALT="Figure 1"> View larger version (43K): org.highwire.dtl.DTLVardef@b6e6d1org.highwire.dtl.DTLVardef@1ebb41eorg.highwire.dtl.DTLVardef@17e4275org.highwire.dtl.DTLVardef@3d31f1_HPS_FORMAT_FIGEXP M_FIG C_FIG

cancer biology↗

Immunogenic shift of arginine metabolism triggers systemic metabolic and immunological reprogramming to prevent HER2+ breast cancer

Arginine metabolism in tumors is often shunted into the pathway producing pro-tumor and immune suppressive polyamines (PAs), while downmodulating the alternative nitric oxide (NO) synthesis pathway. Aiming to correct arginine metabolism in tumors, arginine deprivation therapy and inhibitors of PA synthesis have been developed. Despite some therapeutic advantages, these approaches have often yielded severe side effects, making it necessary to explore an alternative strategy. We previously reported that supplementing SEP, the endogenous precursor of BH4 (the essential NO synthase cofactor), could correct arginine metabolism in tumor cells and tumor-associated macrophages (TAMs) and induce their metabolic and phenotypic reprogramming. We saw that oral SEP treatment effectively suppressed the growth of HER2-positive mammary tumors in animals. SEP also has no reported dose-dependent toxicity in clinical trials for metabolic disorders. In the present study, we report that a long-term use of SEP in animals susceptible to HER2-positive mammary tumors effectively prevented tumor occurrence. These SEP-treated animals had undergone reprogramming of the systemic metabolism and immunity, elevating total T cell counts in the circulation and bone marrow. Given that bone marrow-resident T cells are mostly memory T cells, it is plausible that chronic SEP treatment promoted memory T cell formation, leading to a potent tumor prevention. These findings suggest the possible roles of the SEP/BH4/NO axis in promoting memory T cell formation and its potential therapeutic utility for preventing HER2-positive breast cancer.

cancer biology↗

Immunologic comparisons of strain and induction method in an improved mouse model of intrauterine fibrosis

Intrauterine adhesions are growths of fibrotic tissue within the uterine cavity and can arise from a variety of tissue-damaging stimuli. Immune cells are known to mediate fibrotic responses, but specific mechanisms require further elucidation. Here, we compared intrauterine fibrosis development and immune responses across different mouse strains and induction methods. We aimed to identify a consistent and more clinically relevant mouse model of intrauterine fibrosis, whether immune responses differ in response to different stimuli, and which potential key immune cell populations are responsible for intrauterine fibrosis susceptibility. Intrauterine fibrosis induction methods were compared using surgical curettage or transcervically administered chemical (quinacrine) models. Measurements of tissue morphology and collagen gene expression indicate BALB/c mice are more susceptible than C57BL/6 mice to intrauterine fibrosis. In chemically induced BALB/c uterine tissues, gene expression and flow cytometry data show greater pro-inflammatory macrophage responses, implicating a possible role in fibrogenesis consistent with human intrauterine adhesion data. Findings from this study demonstrate the importance of mouse strain selection in studies of intrauterine adhesions. Furthermore, we show that a new hormone-synchronized, chemically induced mouse model can more uniformly and reliably provoke fibrotic tissue response. This model may allow for greater elucidation of mechanisms involved in intrauterine adhesion development, and exploratory therapeutic studies for treatment intervention.

bioengineering↗

Bridging immunotypes and enterotypes using a systems immunology approach

Unveiling the systemic effects of disease and health requires an holistic approach that has mainly revolved around well established, directly determinable molecular relationships such as the protein synthesis cascade and epigenetic mechanisms. In this study, involving 394 individuals, we found direct linkage of branches spanning human biological functions often not studied in conjunction, using clinical data, gut microbial abundances, blood immune cell repertoires, blood transcriptomic and blood T cell receptor data. Contrary to current paradigms, we demonstrate that immunotypes and enterotypes are orthogonal, likely fulfilling distinct roles in maintaining homeostasis, only bridged via the blood transcriptome. We also identified two distinct inflammatory profiles: the first driven by interferon signalling and the other characterised by non-viral, NF-kB and IL-6 markers. Lastly, we present compelling data showing strong associations of the Ruminococcaceae and Christensenellaceae bacteria with a healthy immunotype and transcriptomic pattern, highlighting their potential role in immune health. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=194 HEIGHT=200 SRC="FIGDIR/small/625344v1_ufig1.gif" ALT="Figure 1"> View larger version (52K): org.highwire.dtl.DTLVardef@c6b5eorg.highwire.dtl.DTLVardef@15d0c3forg.highwire.dtl.DTLVardef@1cf29eeorg.highwire.dtl.DTLVardef@1c9ff8d_HPS_FORMAT_FIGEXP M_FIG C_FIG

systems biology↗