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Lanza, M.

Publications and source records attributed to Lanza, M..

6 recordsLinked to original sources

TNF signaling maintains local restriction of bacterial founder populations in intestinal and systemic sites during oral Yersinia infection

Enteroinvasive bacterial pathogens are responsible for an enormous worldwide disease burden that critically affects the young and immunocompromised. Yersinia pseudotuberculosis is a Gram-negative enteric pathogen, closely related to the plague agent Y. pestis, that colonizes intestinal tissues, induces the formation of pyogranulomas along the intestinal tract, and disseminates to systemic organs following oral infection of experimental rodents. Prior studies proposed that systemic tissues were colonized by a pool of intestinal replicating bacteria distinct from populations within Peyers patches and mesenteric lymph nodes. Whether bacteria within intestinal pyogranulomas serve as the source for systemic dissemination, and the relationship between bacterial populations within different tissue sites is poorly defined. Moreover, the factors that regulate Yersinia colonization and dissemination are not well understood. Here, we demonstrate, using Sequence Tag-based Analysis of Microbial Populations in R (STAMPR), that remarkably small founder populations independently colonize intestinal and systemic tissues. Notably, intestinal pyogranulomas contain clonal populations of bacteria that are restricted and do not spread to other tissues. However, populations of Yersinia are shared among systemic organs and the blood, suggesting that systemic dissemination occurs via hematogenous spread. Finally, we demonstrate that TNF signaling is a key contributor to the bottlenecks limiting both tissue colonization and lymphatic dissemination of intestinal bacterial populations. Altogether, this study reveals previously undescribed aspects of infection dynamics of enteric bacterial pathogens. ImportanceBacterial escape from the intestine can lead to severe disease, including sepsis, organ damage, and death. However, the intestinal bacterial population dynamics governing the colonization of mucosal and systemic tissues and the intestinal sites that seed systemic spread are not clear. Yersinia pseudotuberculosis is a rodent and human intestinal pathogen closely related to the plague agent and provides a natural rodent-adapted model to study systemic bacterial dissemination. Our findings define the infection dynamics of enteric Yersinia and the impact of the innate immune system on Yersinia colonization of the intestine and systemic organs.

microbiology↗

ZFAND6 is a subunit of a TRAF2-cIAP E3 ubiquitin ligase complex essential for mitophagy

The A20 ubiquitin-editing enzyme is a critical negative regulator of NF-{kappa}B signaling and inflammation. While the mechanisms by which A20 restricts inflammation have been extensively studied, the physiological functions of other A20-like proteins are largely unknown. Here, we report a previously unknown function of the A20 family member ZFAND6 as a novel regulator of mitophagy. Deletion of ZFAND6 in bone marrow-derived macrophages (BMDMs) promotes the upregulation of reactive oxygen species (ROS) and the accumulation of damaged mitochondria due to impaired mitophagy. Consequently, mitochondrial DNA (mtDNA) is released into the cytoplasm, triggering the spontaneous expression of interferon-stimulated genes (ISGs) in a cGAS-STING dependent manner, which leads to enhanced viral resistance in vitro. However, mice lacking ZFAND6 exhibit increased morbidity and mortality upon challenge with a sublethal dose of influenza A virus (IAV) due to impaired myeloid cell activation and diminished type I IFN signaling. Mechanistically, ZFAND6 bridges a TRAF2-cIAP1 interaction, which is required for the initiation of ubiquitin-dependent mitophagy. Our results suggest that ZFAND6 is a subunit of a TRAF2-cIAP E3 ligase complex that promotes the clearance of damaged mitochondria by mitophagy to maintain mitochondrial homeostasis.

immunology↗

A TNF-IL-1 circuit controls Yersinia within intestinal granulomas

SummaryMonocytes restrict Yersinia infection within intestinal granulomas. Here, we report that monocyte-intrinsic TNF signaling drives production of IL-1 that signals to non-hematopoietic cells to control intestinal Yersinia infection within granulomas. Tumor necrosis factor (TNF) is a pleiotropic inflammatory cytokine that mediates antimicrobial defense and granuloma formation in response to infection by numerous pathogens. Yersinia pseudotuberculosis colonizes the intestinal mucosa and induces recruitment of neutrophils and inflammatory monocytes into organized immune structures termed pyogranulomas that control the bacterial infection. Inflammatory monocytes are essential for control and clearance of Yersinia within intestinal pyogranulomas, but how monocytes mediate Yersinia restriction is poorly understood. Here, we demonstrate that TNF signaling in monocytes is required for bacterial containment following enteric Yersinia infection. We further show that monocyte-intrinsic TNFR1 signaling drives production of monocyte-derived interleukin-1 (IL-1), which signals through IL-1 receptor on non-hematopoietic cells to enable pyogranuloma-mediated control of Yersinia infection. Altogether, our work reveals a monocyte-intrinsic TNF-IL-1 collaborative circuit as a crucial driver of intestinal granuloma function, and defines the cellular target of TNF signaling that restricts intestinal Yersinia infection.

immunology↗

Inflammatory monocytes promote pyogranuloma formation to counteract Yersinia blockade of host defense

Granulomas are organized immune cell aggregates that form in response to chronic infection or antigen persistence. Yersinia pseudotuberculosis (Yp) blocks innate inflammatory signaling and phagocytosis, inducing formation of neutrophil-rich pyogranulomas within lymphoid tissues. Here, we uncover that Yp triggers pyogranuloma formation within the murine intestinal mucosa, a site not known to contain such structures. Mice lacking circulating monocytes fail to form defined pyogranulomas, have defects in neutrophil activation, and succumb to Yp infection. Yersinia lacking the virulence factors that block phagocytosis did not induce pyogranulomas, indicating that intestinal pyogranulomas form in response to Yp disruption of phagocytosis. Notably, mutation of a single anti-phagocytic virulence factor, YopH, restored pyogranuloma formation and control of Yp infection in monocyte-deficient mice, demonstrating that monocytes override YopH-dependent blockade of innate immune defense. This work reveals an unappreciated site of Yersinia intestinal invasion, and defines host and pathogen drivers of intestinal granuloma formation.

microbiology↗

Arresting microbiome development limits immune system maturation and resistance to infection.

Disruptions to the intestinal microbiome during weaning lead to long-term negative effects on host immune function. However, the critical host-microbe interactions occurring during weaning required for healthy immune system development remain poorly understood. We find that restricting microbiome maturation during weaning leads to stunted immune system development and increased susceptibility to enteric infection. We developed a gnotobiotic mouse model of the early-life microbiome designated as Pediatric Community (PedsCom). This nine-member consortium of microbes derived from intestinal microbiomes of preweaning mice stably colonized germfree adult mice and was efficiently transmitted to offspring for multiple generations. Unexpectedly, the relative abundance of PedsCom microbes were largely unaffected by the transition from a milk-based to a fiber rich solid food diet. PedsCom mice developed less peripheral regulatory T cells and Immunoglobulin A, hallmarks of microbiota-driven immune system development. Consistent with defects in maturation, adult PedsCom mice retain high susceptibility to salmonella infection characteristic of young mice and humans. Altogether, our work illustrates how the post-weaning transition in intestinal microbiome composition contributes to normal immune maturation and protection from enteric infection. Accurate modelling of the pre-weaning microbiome provides a window into the microbial requirements of healthy immune development and suggests an opportunity to design microbial interventions at weaning to improve immune system development in human infants. One Sentence SummaryArresting microbiome development stunts immune ontogeny

immunology↗

"Running with cancer": a qualitative study to evaluate barriers and motivations in running for female oncological patients.

Nowadays, it is widely acknowledged that low physical activity levels are associated with an increase in terms of both disease recurrence and mortality in cancer survivors. In this light, deciphering those factors able to hamper or facilitate an active lifestyle is crucial in order to increase patients adherence to physical activity. The purpose of this study was to explore barriers and motivations in a sample of female oncological patients, practising running using the ecological model and compare them with healthy controls. Focus group interviews were conducted at Verona University. Participants were 12 female cancer survivors and 7 matched healthy controls who had participated at "Run for Science" project. The interviews were transcribed verbatim and analyzed using content analysis. Two main themes, motivations and barriers were found. About motivations, three sub-themes were identified: personal, interpersonal and environmental/organizational factors. Regarding barriers, another sub-theme was recognized: community/policy factors. Compare to healthy controls, survivors expressed motivations and barriers specifically related to their oncological disease. Running was a challenge with their cancer and a hope to give to other patients. Main barriers were represented by treatment-related side effects, inexperienced trainers and external factors, e.g. delivery of incorrect information. Running program dedicated to oncological patients should consider intrinsic obstacles, related to cancer and its treatment, offering a personalized intervention performed by qualified trainers, together with a motivational approach able to improve participants adherence to an active lifestyle.

scientific communication and education↗