The gene expression of MZ B cells and neutrophils after Staphylococcus aureus infection in B6 mice
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ABSTRACT:
PROVIDER: PRJNA660401 | ENA |
REPOSITORIES: ENA
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Project description:Marginal zone B cells can quickly respond to the bacterial invasion by providing the first-line of antibodies. Neutrophil can help marginal zone B cells activation and differentiation. We investigated the specific gene expression that interacts between the MZ B cells and neutrophils at the initial stage after Staphylococcus aureus infection.
2021-06-02 | GSE157176 | GEO
Project description:Nosocomial infections resulting from growing biofilms on the surface of indwelling medical devices represent a major therapeutic challenge in an aging population. In this context, current models have so far not addressed the synergy between a developing biofilm and the host’s immune response. Here we employed a mouse model for implant-associated infection from Staphylococcus aureus biofilms and, through functional assays, next generation single cell sequencing and spectral flow cytometry, observed a direct influence of the developing biofilms in the phenotype of tissue infiltrating neutrophils over the course of infection. Our results allowed us to differentiate neutrophil subpopulations, identifying some which may be protective of the biofilm and which could be the target for future therapies.
2024-07-03 | GSE264548 | GEO
Project description:Neutrophil lysis after phagocytosis is a process potentially important in the pathogenesis of community-associated methicillin-resistant S. aureus (CA-MRSA) infection. The mechanism for this process is not currently known. Therefore, to better understand CA-MRSA virulence we used human oligonucleotide microarrays to investigate the mechanism underlying enhanced PMN lysis that occurs after phagocytosis of CA-MRSA. In order to examine the effect of S. aureus on the neutrophil transcriptome and to elucidate any possible differences in this effect between hospital- and community-associated S. aureus, we performed microarray expression analysis on human neutrophils treated with hospital- and community-associated S. aureus. Polymorphonuclear leukocytes (PMNs) were isolated from the blood of healthy donors. Control and S. aureus-exposed PMNs were incubated at 37C for 1, 2, 3 or 6 hours.
2010-06-09 | E-GEOD-16837 | biostudies-arrayexpress
Project description:Neutrophil abscess formation is critical in innate immunity against many pathogens. Here, the mechanism of neutrophil abscess formation was investigated using a mouse model of Staphylococcus aureus cutaneous infection. Gene expression analysis of S. aureus-infected skin revealed that induction of neutrophil recruitment genes was largely dependent upon IL-1beta/IL-1R activation. Unexpectedly, using IL 1beta reporter mice, neutrophils were identified as the primary source of IL-1beta at the site of infection. Furthermore, IL-1beta-producing neutrophils were necessary and sufficient for abscess formation and bacterial clearance. S. aureus-induced IL 1beta production by neutrophils required TLR2, NOD2, FPRs and the ASC/NLRP3 inflammasome. Taken together, IL-1beta and neutrophil abscess formation during an infection are functionally, spatially and temporally linked as a consequence of direct IL-1beta production by neutrophils. Lesional skin biopsies obtained from C57BL/6J WT mice or IL-1R-deficient mice at 4 hours post-infection with Staphylococcus aureus. Uninfected skin biopsies were also collected from WT and IL-1R-deficient mice.
2012-12-05 | E-GEOD-36826 | biostudies-arrayexpress
Project description:Panton-Valentine Leukocidin (PVL) is a Staphylococcus aureus toxin that binds to and kills human neutrophils resulting in the formation of neutrophil extracellular traps. A subset of individuals colonized with PVL expressing S. aureus suffer from recurring infections. We found that neutrophils from affected individuals display increased spontaneous NET formation after isolation, and increased sensitivity to killing by PVL. Compared to healthy controls, the expression of the target receptors for PVL, CD45 and C5L2, but not CD88, was increased in these patients, and the expression correlated to the amount of PVL-induced NETs produced. NADPH-oxidase activity was not important for PVL induced NETosis as neutrophils from CGD patients produced NETs in response to PVL. Through NET proteome analysis we identified that the protein content of PVL induced NETs is different from mitogen induced NETs. The abundance of the antimicrobial proteins LL37, myeloperoxidase, azurocidin, and proteinase 3 was lower on PVL NETs and PVL-induced NETs were deficient in killing Staphylococcus aureus. Neutrophils from patients that suffer from recurring PVL-positive infections may be more sensitive to PVL-induced NETosis, impairing their ability to combat the infection.
2023-11-23 | PXD025702 | Pride
Project description:Severe infections and sepsis is an increasing clinical problem that cause prolonged morbidity and substantial mortality. At present, antibiotics are essentially the only pharmacological treatment for sepsis. The incidence of antibiotic resistance is increasing and it is therefore critical to find new therapies for sepsis. Staphylococcus aureus (S. aureus) is a major cause of septic mortality. Neutrophils play a major role in defense against bacterial infections. We have recently shown that a saturated high fat diet decreases survival in septic mice, but the mechanisms behind remain elusive. The aim of the present study was to investigate how the dietary fat composition affects survival and neutrophils function after experimental septic infection in mice. We found that, after S. aureus infection, mice fed polyunsaturated high fat diet (HFD/P) for 8 weeks had increased septic survival and decreased bacterial load compared with mice fed saturated HFD (HFD/S), and similar to that of mice given low fat diet (LFD). Furthermore, uninfected mice fed HFD/P had increased number of Ly6G+ neutrophils in bone marrow. In addition, mice fed HFD/P had a higher number Ly6G+ neutrophils recruited to the site of inflammation after peritoneal injection of thioglycollate. In conclusion, polyunsaturated dietary fat increased both survival and the efficiency of the bacterial clearance during septic S. aureus infection. Moreover, this diet enhanced the number and chemotaxis of neutrophils, a key component of the immune response to S. aureus infections. Mice (non-infected) fed saturated high fat diet, low fat diet, or polyunsaturated high fat diet
2014-11-24 | E-GEOD-58358 | biostudies-arrayexpress
Project description:Methicillin resistant Staphylococcus aureus (MRSA) is an opportunistic pathogen chief amongst bloodstream infecting pathogens. MRSA produces an array of human specific virulence factors that may contribute to immune suppression. Here, we defined the response of primary human phagocytes to infection with MRSA using RNA-Seq. We found that the overall transcriptional response to MRSA was weak both in the number of genes and the magnitude of response. Using an ex vivo bacteremia model with fresh human blood, we found that infection with live MRSA resulted in the down-regulation of genes related to innate immune response, and cytokine and chemokine signaling. This muted transcriptional response was conserved across diverse S. aureus clones but absent in heat-killed MRSA or blood infected with live Staphylococcus epidermidis. Importantly, the muted signature was also present in patients with S. aureus bacteremia. We next identified the master regulator SaeRS and the SaeRS-regulated pore-forming toxins as key mediators of transcriptional suppression. The impaired chemokine and cytokine responses were reflected by circulating protein levels in the plasma. MRSA elicits a soluble milieu that is restrictive in the recruitment of human neutrophils compared to strains lacking saeRS. Thus, MRSA blunts the inflammatory response resulting in impaired neutrophil recruitment, which could promote the survival of S. aureus during invasive infection.
2022-07-20 | GSE193219 | GEO
Project description:Severe infections and sepsis is an increasing clinical problem that cause prolonged morbidity and substantial mortality. At present, antibiotics are essentially the only pharmacological treatment for sepsis. The incidence of antibiotic resistance is increasing and it is therefore critical to find new therapies for sepsis. Staphylococcus aureus (S. aureus) is a major cause of septic mortality. Neutrophils play a major role in defense against bacterial infections. We have recently shown that a saturated high fat diet decreases survival in septic mice, but the mechanisms behind remain elusive. The aim of the present study was to investigate how the dietary fat composition affects survival and neutrophils function after experimental septic infection in mice. We found that, after S. aureus infection, mice fed polyunsaturated high fat diet (HFD/P) for 8 weeks had increased septic survival and decreased bacterial load compared with mice fed saturated HFD (HFD/S), and similar to that of mice given low fat diet (LFD). Furthermore, uninfected mice fed HFD/P had increased number of Ly6G+ neutrophils in bone marrow. In addition, mice fed HFD/P had a higher number Ly6G+ neutrophils recruited to the site of inflammation after peritoneal injection of thioglycollate. In conclusion, polyunsaturated dietary fat increased both survival and the efficiency of the bacterial clearance during septic S. aureus infection. Moreover, this diet enhanced the number and chemotaxis of neutrophils, a key component of the immune response to S. aureus infections.
2014-11-24 | GSE58358 | GEO
Project description:Influence of Staphylococcus aureus biofilm infection phase on functional composition of host neutrophils
| PRJNA1103133 | ENA
Project description:Neutrophil abscess formation is critical in innate immunity against many pathogens. Here, the mechanism of neutrophil abscess formation was investigated using a mouse model of Staphylococcus aureus cutaneous infection. Gene expression analysis of S. aureus-infected skin revealed that induction of neutrophil recruitment genes was largely dependent upon IL-1beta/IL-1R activation. Unexpectedly, using IL 1beta reporter mice, neutrophils were identified as the primary source of IL-1beta at the site of infection. Furthermore, IL-1beta-producing neutrophils were necessary and sufficient for abscess formation and bacterial clearance. S. aureus-induced IL 1beta production by neutrophils required TLR2, NOD2, FPRs and the ASC/NLRP3 inflammasome. Taken together, IL-1beta and neutrophil abscess formation during an infection are functionally, spatially and temporally linked as a consequence of direct IL-1beta production by neutrophils.
2012-12-05 | GSE36826 | GEO