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Meunier, E.

Publications and source records attributed to Meunier, E..

18 recordsLinked to original sources

Free-Living Amoeba act as transient permissive hosts for Leptospira spp.

BackgroundLeptospirosis is a zoonotic disease caused by pathogenic Leptospira spp., which persist in soil and water environments for extended periods of time. The mechanisms enabling this environmental survival remain elusive. Free-living amoebae (FLA) are widespread protozoa that act as reservoirs or "Trojan horses" for numerous bacterial pathogens, protecting them from stress and contributing to their persistence. Whether pathogenic Leptospira exploit similar interactions with FLA has not been resolved. Methodology/Principal FindingsUsing live confocal microscopy, flow cytometry, and gentamicin protection assays, we investigated the interactions between pathogenic (Leptospira interrogans) and saprophytic (Leptospira biflexa) leptospires with three FLA species: Acanthamoeba castellanii, Dictyostelium discoideum, and Hartmannella vermiformis. While rapid internalization was observed, entry was only partially dependent on actin-driven processes and was enhanced by the presence of live bacteria. Following internalization, bacteria persisted for at least 48h as indicated by colony-forming assays. However, no evidence of intracellular replication was detected. The number of fluorescently labeled leptospires progressively declined over time, providing further evidence of leptospires survival without multiplication. Finally, analysis of environmental soils in New Caledonia showed co-occurrence of FLA and Leptospira. Soil-derived FLA also internalized pathogenic Leptospira in vitro, showing that these interactions extend to natural isolates. Conclusions/SignificanceOur results demonstrate that free-living amoebae internalize both pathogenic and saprophytic leptospires and allow their transient persistence without replication. By providing protection and prolonging viability in soil environments, FLA may contribute to the ecological maintenance of Leptospira. These findings pinpoint FLA as potential environmental reservoirs that could play a role in shaping leptospires survival strategies relevant for transmission and host infection. Author SummaryFor bacteria living in soils and freshwater environments, survival depends on their ability to adapt to complex ecological landscapes populated by numerous predators and competitors. In such habitats, interactions with other microorganisms are unavoidable and may shape long-term survival strategies. Pathogenic Leptospira, the bacteria responsible for leptospirosis, can persist for long periods outside their hosts, yet the ecological mechanisms supporting this environmental survival remain poorly understood. In soil and freshwater ecosystems, microscopic predators known as free-living amoebae commonly feed on bacteria. However, several bacterial pathogens can survive inside these amoebae and use them as temporary shelters. Because ancestral Leptospira were soil-dwelling saprophytes, interactions with amoebae likely represent an ancient ecological relationship in which successful survival strategies may have evolved and remain conserved in present-day pathogenic species. With this perspective in mind, we used microscopy approaches and bacterial viability assays to investigate whether Leptospira interacts with amoebae. We found that several amoeba species rapidly engulf both pathogenic and non-pathogenic Leptospira. Once internalized, the bacteria remained viable for up to two days but did not multiply. We also detected both amoebae and Leptospira in the same soil samples and showed that environmental amoebae could internalize the bacteria. These findings suggest that amoebae may act as temporary shelters for Leptospira, helping them persist in soils and water and potentially contributing to the environmental stage of leptospirosis transmission.

microbiology↗

The capsule of hypervirulent Klebsiella pneumoniae maintains neutrophils in neutral activation state

Hypervirulent Klebsiella pneumoniae (hvKp) cause invasive infections despite robust neutrophil recruitment, yet the mechanisms enabling persistence in neutrophil-rich environments remain poorly defined. Here, we show that hvKp do not simply resist neutrophil antimicrobial mechanisms but instead constrain neutrophils into a neutral functional state characterised by limited bactericidal activity. Using genetic dissection of the rmpADC locus, pharmacological inhibition of neutrophil effector pathways, and analysis of a diverse panel of clinical isolates, we demonstrate that rmpADC-driven capsule properties uncouple neutrophil recognition and activation from bacterial killing. Deletion of rmpADC restores phagocytosis, degranulation, and intraphagosomal killing, whereas loss of individual rmpD or rmpC permits neutrophil activation without bacterial killing. Moreover, hypermucoviscosity alone is sufficient to protect bacteria from neutrophil-mediated killing across multiple genetic backgrounds. Together, these findings identify capsule-driven immune state control as a central mechanism of hvKp neutrophil evasion and reveal distinct thresholds governing neutrophil activation and bactericidal outcome.

immunology↗

Two orthogonal MAP3K-driven pathways of NLRP1 inflammasome activation revealed by poisonous beetles.

Environmental toxins that cause irritant dermatitis remain poorly understood as activators of innate immune pathways. Here, we identify rove beetle (Paederus) and blister beetle (Meloidae) toxins as previously unrecognized triggers of the human NLRP1 inflammasome in keratinocytes. Rove beetles, likely through the ribosome inhibitor pederin, activate NLRP1 via translational stalling and the ZAK-dependent ribotoxic stress response. In contrast, the phosphatase inhibitor cantharidin from blister beetles induces NLRP1 through TAK1-driven hyperphosphorylation of its linker region, independent of ZAK. In their hyperactivated states, ZAK and TAK1 share overlapping phosphosites on the NLRP1 disordered linker, including a common essential TZ motif. In addition, we show that TAK1 and ZAK are jointly responsible for NLRP1 linker phosphorylation and activation caused by dsRNA and CHIKV infection. These findings reveal medically relevant insect toxins as activators of NLRP1, and uncover parallel MAP3 kinase pathways as converging upstream activating signals for the human NLRP1 inflammasome. GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=172 HEIGHT=200 SRC="FIGDIR/small/701189v1_ufig1.gif" ALT="Figure 1000"> View larger version (50K): org.highwire.dtl.DTLVardef@ee34b9org.highwire.dtl.DTLVardef@c79ec9org.highwire.dtl.DTLVardef@189c373org.highwire.dtl.DTLVardef@17ec853_HPS_FORMAT_FIGEXP M_FIG C_FIG KEY POINTSTwo dermatitis-causing beetle species induce NLRP1-driven pyroptosis of human keratinocytes Rove beetles, likely via pederin, activate NLRP1 via ribosome inhibition and ZAK[a]-driven RSR Cantharidin from blister beetles activates human via TAK1-, instead of ZAK[a]-driven hyperphosphorylation of the NLRP1 linker region Shared phosphosites by TAK1 and ZAK[a] on NLRP1 contribute to dsRNA-driven NLRP1 activation

immunology↗

A TAK1-Driven NLRP1 Inflammasome Pathway Revealed by Phosphatase-Targeting Environmental Toxins

Human NLRP1 is highly sensitive to phosphorylation-dependent activation, indicating a need for tight phosphatase control to prevent excessive inflammasome activity. In this study, we identified the phosphatases PP1 and PP2A as negative regulators of the NLRP1 inflammasome in human keratinocytes. Accordingly, exposure to the environmental toxins Dinophysistoxin, Okadaic acid, and Cantharidin, which inhibit PP1 and PP2A, triggered NLRP1 inflammasome activation. Notably, this toxin-induced activation process relied on hyperactivation of the MAP3 kinase TAK1. Mechanistically, both TAK1 and its downstream effectors p38 kinases phosphorylated and activated the NLRP1 inflammasome. Further studies underscored that TAK1 also contributed to the NLRP1 inflammasome activation during double-stranded RNA stimulation and viral infection. Finally, human native skins exposed to environmental toxins underlined the role of the PP1/PP2A-regulated TAK1/p38 axis in the development of skin dermatitis. Thus, these findings reveal a novel pathway of phosphorylation-driven NLRP1 activation and expand our understanding of its regulation in epithelial immunity. One Sentence SummaryPP1/PP2A phosphatases restrict TAK1-driven NLRP1 inflammasome response. O_FIG O_LINKSMALLFIG WIDTH=146 HEIGHT=200 SRC="FIGDIR/small/701233v1_ufig1.gif" ALT="Figure 1"> View larger version (24K): org.highwire.dtl.DTLVardef@128de37org.highwire.dtl.DTLVardef@151fbdorg.highwire.dtl.DTLVardef@d6b98aorg.highwire.dtl.DTLVardef@12f419d_HPS_FORMAT_FIGEXP M_FIG O_FLOATNOGraphical abstractC_FLOATNO Schematic representation of the phosphorylation-driven hNLRP1 inflammasome response upon exposure to environmental toxins and to dsRNA/viral infection. C_FIG

immunology↗

Dual human lung models reveal compartment-specific activity of anti-tuberculosis drugs and host-directed therapies

Tuberculosis (TB) remains a major global health challenge that requires new therapeutic strategies to improve drug efficacy, shorten treatment duration, prevent drug resistance, and limit Mycobacterium tuberculosis (Mtb) persistence. Here, we established complementary in vitro human lung models integrating alveolar macrophage-like (AML) cells and airway air-liquid interface (ALI) cultures to evaluate standard-of-care antibiotics, host-directed therapies, and virulence-targeting agents. AMLs recapitulated key morphological, transcriptional, and functional features of primary alveolar macrophages, including a CD16+ immunoregulatory phenotype highly permissive to Mtb infection. In parallel, ALI cultures maintained epithelial barrier integrity and secretory functions, allowing apical Mtb infection, drug penetration analysis, and inflammatory profiling. Benchmarking of standard-of-care antibiotics revealed compartment-specific activity: isoniazid, rifampicin, and moxifloxacin were effective in both systems, while pyrazinamide was active only in AMLs. Anti-inflammatory host-directed therapies such as ibuprofen and doramapimod selectively reduced cytokine production without affecting bacterial load. Together, this dual-platform system offers a physiologically relevant and scalable model to assess antimicrobial efficacy and host modulation across distinct pulmonary niches, bridging the gap between conventional macrophage assays and the complex human lung.

immunology↗

Capsule-mediated O-antigen masking protects hypervirulent Klebsiella pneumoniae from neutrophil killing

Klebsiella pneumoniae is listed as a critical priority pathogen by the WHO due to prevalent extended-spectrum {beta}-lactamase and carbapenem resistance and high mortality rates Hypervirulent K. pneumoniae (hvKp) causes life-threatening infections in immunocompetent individuals, while classical K. pneumoniae (cKp) causes nosocomial infections in immunosuppressed patients. The convergence of hypervirulence with antibiotic resistance is now a major global health threat. Using a murine pulmonary infection model, we show that hvKp resisted clearance despite significant neutrophil recruitment. Using clinical hvKp and cKp isolates, bone marrow derived neutrophils, cell biology, pharmacology and imaging (both light and electron microscopy) in ex vivo assays revealed that the hvKp hypermucoviscous capsule prevents bacterial recognition and neutrophil activation, blocking ROS production, degranulation, and neutrophil extracellular traps (NETs) formation. In the absence of capsule ({Delta}wcaJ) or hypermucoid capsule determinants ({Delta}rmpADC), hvKp activates neutrophils, leading to degranulation, NET formation and bacterial killing. While superimposing the absence of O-antigen ({Delta}rfb) on the {Delta}wcaJ abrogates degranulation, neutrophils still elaborate NETs that eliminate the {Delta}wcaJ/{Delta}rfb mutant at high efficiency. This suggests that O-antigen is a double-edged sword, functioning as a PAMP triggering neutrophil degranulation yet assisting the pathogen to evade NET-mediated destruction. These findings shed light on the mechanism underpinning immune evasion by the hypervirulent capsule in hvKp.

microbiology↗

Gasdermin D mediates a fast transient release of ATP after NLRP3 inflammasome activation before ninjurin 1-induced lytic cell death

Pyroptosis is a lytic cell death triggered by the cleavage of gasdermin (GSDM) proteins and subsequent pore formation by the N-terminal domain oligomerization in the plasma membrane. GSDMD is cleaved by caspase-1/-4/-5/-11 upon inflammasome activation and mediates IL-1{beta} and IL-18 release. GSDMD pores favors ninjurin-1 (NINJ1) induced plasma membrane rupture and cell death. Here, we demonstrate that GSDMD mediates early ATP release upon NLRP3 inflammasome activation independently of NINJ1, occurring before IL-1{beta} release and cell death and constituting an early danger signal. The release of ATP is a transient signal terminated before the cells continue to permeabilize and die. The different N-terminal of GSDMA to E are also able to release ATP and induce monocyte migration towards pyroptotic cells. This study reveals ATP release as an early, and transient danger signal depending on GSDMD plasma membrane permeabilization, independently of the late stages of lytic cell death.

immunology↗

State-dependent alteration of respiration in a rat model of Parkinson disease

Parkinson disease (PD) is the second most frequent neurodegenerative disorder. Besides major deficits in motor coordination, patients may also display sensory and cognitive impairments, which are often overlooked despite being inherently part of the PD symptomatology. Amongst those symptoms, respiration, a key mechanism involved in the regulation of multiple physiological and neuronal processes, appears to be altered. Importantly, breathing patterns are highly correlated with the animals behavioral states, and although respiration has been investigated in different models of PD, no study has yet taken into consideration the potential impact of behavioral state on respiration deficits in these models. To explore this variable, we first characterized the respiratory parameters in a neurotoxin-induced rat model of PD (6-OHDA) across different vigilance states: sleep, quiet waking and exploration. We noted a significantly higher respiratory frequency in 6-OHDA rats during quiet waking compared to Sham rats. A higher respiratory amplitude was also observed in 6-OHDA rats during both quiet waking and exploration. No effect of the treatment was noted during sleep. Given the relation between respiration and olfaction and the presence of olfactory deficits in PD patients, we then investigated the odor-evoked sniffing response in PD rats, using an odor habituation/cross-habituation paradigm. No substantial differences were observed in olfactory abilities between the two groups, as assessed through sniffing frequency. These results corroborate the hypothesis that respiratory impairments in 6-OHDA rats are vigilance-dependent. Our results also shed light on the importance of considering the behavioral state as an impacting factor when analyzing respiration. HighlightsO_LISpecific respiratory patterns associated to different vigilance states C_LIO_LISpecific alteration of respiration during quiet waking in a rodent model of PD C_LIO_LIPreserved olfactory abilities as assessed through sniffing in a rodent model of PD C_LI

neuroscience↗

Leishmania infantum-exploited Nrf2 transcription factor as a virulence process to escape macrophage-driven ferroptosis-like leishmanicidal process

Macrophages are the main effector cells during Leishmania infection. They contribute to the detection and elimination of Leishmania spp. and may also promote parasite resilience. Here, we report that the activation of the transcription factor Nrf2 in macrophages plays a pivotal role in the progression of Leishmania infantum infection by controlling inflammation and redox balance of macrophages. We also highlight the involvement of NOX2/ROS axis in the early Nrf2 activation and subsequently of PGE2/EP2r signalling in the sustainment of Nrf2 activation upon L. infantum infection. Moreover, we establish macrophage-driven ferroptosis-like process as a cell death program of L. infantum and the protective effect of Nrf2 in macrophages against L. infantum death. Altogether, these results identify Nrf2 as a critical factor for the susceptibility of Leishmania infantum infection, highlighting Nrf2 as a promising pharmacological target for the development of new therapeutic approaches for the treatment of visceral leishmaniasis.

microbiology↗

Mechanistic basis for nigericin-induced NLRP1 inflammasome activation in human epithelial cells

Nigericin, an ionophore derived from Streptomyces hygroscopicus, is arguably the most commonly used tool compound to study the NLRP3 inflammasome. Recent findings, however, showed that nigericin also activates the NLRP1 inflammasome in human keratinocytes. In this study, we resolve the mechanistic basis of nigericin-driven NLRP1 inflammasome activation. In multiple non-hematopoietic cell types, nigericin rapidly and specifically inhibits the elongation stage of the ribosome cycle by depleting cytosolic potassium ions. This activates the ribotoxic stress response (RSR) sensor kinase ZAK[a], p38 and JNK, as well as the hyperphosphorylation of the NLRP1 linker domain. As a result, nigericin-induced pyroptosis in human keratinocytes is blocked by extracellular potassium supplementation, ZAK[a] knockout or pharmacologic inhibitors of ZAK[a] and p38 kinase activities. By surveying a diverse panel of ionophores, we show that the electroneutrality of potassium efflux is essential to activate ZAK[a]-driven RSR, likely because a greater extent of K+ depletion is necessary to activate ZAK[a]-NLRP1 than NLRP3. These findings resolve the mechanism by which nigericin activates NLRP1 in nonhematopoietic cell types and demonstrate an unexpected connection between RSR, perturbations of potassium ion flux and innate immunity. GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=148 SRC="FIGDIR/small/546021v1_ufig1.gif" ALT="Figure 1"> View larger version (40K): org.highwire.dtl.DTLVardef@1afe96aorg.highwire.dtl.DTLVardef@53c59org.highwire.dtl.DTLVardef@1bd14d1org.highwire.dtl.DTLVardef@a1bccc_HPS_FORMAT_FIGEXP M_FIG C_FIG SIGNIFICANCENigericin is familiar to the inflammasome field as the most robust and commonly used NLRP3 inducer. It has enabled numerous breakthroughs in the field linking NLRP3 activation to potassium efflux. In this manuscript, we report that nigericin activates an alternate inflammasome sensor, NLRP1 in primary human skin, nasal and corneal epithelial cells. NLRP1 activation by nigericin requires K+ efflux-driven ribosome stalling and the ribotoxic stress response (RSR) sensor MAP3K, ZAK[a]. We further identify the key biophysical principles that explain why only a subset of K+ ionophores, exemplified by nigericin, function as super inflammasome agonists that can activate either NLRP1 or NLRP3, depending on cell type. These results reveal an unexpected connection between RSR, potassium ion flux and innate immunity.

immunology↗

EEF2-inactivating toxins engage the NLRP1 inflammasome and promote epithelial barrier disruption upon Pseudomonas infection

The intracellular inflammasome complex have been implicated in the maladaptive tissue damage and inflammation observed in chronic Pseudomonas aeruginosa infection. Human airway and corneal epithelial cells, which are critically altered during chronic infections mediated by P. aeruginosa, specifically express the inflammasome sensor NLRP1. Here, together with a companion study, we report that the NLRP1 inflammasome detects Exotoxin A (EXOA), a ribotoxin released by P. aeruginosa Type 2 Secretion System (T2SS) during chronic infection. Mechanistically, EXOA-driven Eukaryotic Elongation Factor 2 (EEF2) ribosylation and covalent inactivation promotes ribotoxic stress and subsequent NLRP1 inflammasome activation, a process shared with other EEF2-inactivating toxins, Diphtheria Toxin and Cholix Toxin. Biochemically, irreversible EEF2 inactivation triggers ribosome stress-associated kinases ZAK- and P38-dependent NLRP1 phosphorylation and subsequent proteasome-driven functional degradation. Finally, Cystic Fibrosis cells from patients exhibit exacerbated P38 activity and hypersensitivity to EXOA-induced ribotoxic stress-dependent NLRP1 inflammasome activation, a process inhibited by the use of ZAK inhibitors. Altogether, our results show the importance of P. aeruginosa virulence factor EXOA at promoting NLRP1-dependent epithelial damage and identify ZAK as a critical sensor of virulence-inactivated EEF2. KEY POINTSO_LIP. aeruginosa induces NLRP1-dependent pyroptosis in human corneal and nasal epithelial cells C_LIO_LIP. aeruginosa Exotoxin A (EXOA) and other EEF2-inactivating bacterial exotoxins activate the human NLRP1 inflammasome C_LIO_LIEEF2 inactivation promotes ribotoxic stress response and ZAK kinase-dependent NLRP1 inflammasome activation. C_LIO_LIBronchial epithelial cells from Cystic Fibrosis patients show extreme sensitivity to ribotoxic stress-dependent NLRP1 inflammasome activation in response to Exotoxin A C_LIO_LIP38 and ZAK inhibition protects Cystic Fibrosis epithelial cell from EXOA-induced pyroptosis C_LI

immunology↗

Cystic fibrosis patient-derived bronchial organoids unveil druggable pathways against Mycobacterium abscessus infection.

Mycobacterium abscessus (Mabs) drives life-shortening mortality in cystic fibrosis (CF) patients, primarily because of its resistance to chemotherapeutic agents. To date, our knowledge on the host and bacterial determinants driving Mabs pathology in CF patient lung remains rudimentary. Here, we used human airway organoids (AOs) microinjected with smooth (S) or rough (R-)Mabs to evaluate bacteria fitness, host responses to infection, and new treatment efficacy. We show that S Mabs formed biofilm, R Mabs formed cord serpentines and displayed a higher virulence. While Mabs infection triggers enhanced oxidative stress, pharmacological activation of antioxidant pathways resulted in better control of Mabs growth. Genetic and pharmacological inhibition of the CFTR is associated with better growth and higher virulence of S and R Mabs. Finally, pharmacological activation of antioxidant pathways inhibited Mabs growth and improved efficacy in combination with cefoxitin, a first line antibiotic. In conclusion, we have established AOs as a suitable human system to decipher mechanisms of CF-driven respiratory infection by Mabs and propose antioxidants as a potential host-directed strategy to improve Mabs infection control.

cell biology↗

Pseudomonas aeruginosa infection reveals a Caspase-1-dependent neutrophil pyroptosis pathway that restrains damaging Histone release

Multiple neutrophil death programs contribute to host defense against infections. Although expressing all necessary components, neutrophils specifically fail to undergo pyroptosis, a lytic form of cell death triggered by the activation of the pro-inflammatory complex inflammasome. In the light of the arm race, we hypothesized that intrinsic neutrophil pyroptosis resistance might be bypassed in response to specific microbial species. We show that Pseudomonas aeruginosa (P. aeruginosa) stimulates Caspase-1-dependent pyroptosis in human and murine neutrophils. Mechanistically, activated NLRC4 inflammasome supports Caspase-1-driven Gasdermin-D (GSDMD) activation, IL-1{beta} cytokine release and neutrophil pyroptosis. Furthermore, GSDMD activates Peptidyl Arginine Deaminase-4 which drives an "incomplete NETosis" where neutrophil DNA fills the cell cytosol but fails crossing plasma membrane. Finally, we show that neutrophil Caspase-1 account for IL-1{beta} production and contributes to various P. aeruginosa strains spread in mice. Overall, we demonstrate that neutrophils are fully competent for Caspase-1-dependent pyroptosis, which drives an unsuspected "incomplete NETosis". SummaryNeutrophils play an essential roles against infections. Although multiple neutrophil death programs contribute to host defense against infections, they fail to undergo pyroptosis, a pro-inflammatory form of cell death. Upon Infections, pyroptosis can be induced in macrophages or epithelial cells upon activation of pro-inflammatory complexes, inflammasomes that trigger Caspase-1-driven Gasdermin dependent plasma membrane lysis. In the light of host-microbe interactions, we hypothesized that yet to find microbial species might hold the capacity to overcome neutrophil resistance to inflammasome-driven pyroptosis. Among several bacterial species, we describe that the bacterium Pseudomonas aeruginosa specifically engages the NLRC4 inflammasome, which promotes Caspase-1-dependent Gasdermin-D activation and subsequent neutrophil pyroptosis. Furthermore, inflammasome-driven pyroptosis leads to DNA decondensation and expansion into the host cell cytosol but not to the so called Neutrophil Extracellular Trap (NET) release as DNA fails breaching the plasma membrane. Finally, in vivo P. aeruginosa infections highlight that Caspase-1-driven neutrophil pyroptosis is functional and is detrimental upon P. aeruginosa infection. Altogether, our results unexpectedly underline neutrophil competence for Caspase-1-dependent pyroptosis, a process that contributes to host susceptibility to P. aeruginosa infection.

immunology↗

Outer membrane vesicles produced by pathogenic strains of Escherichia coli block autophagic flux and exacerbate inflammasome activation

Escherichia coli strains are responsible for a majority of human extra-intestinal infections, resulting in huge direct medical and social costs. We had previously shown that HlyF encoded by a large virulence plasmid harbored by pathogenic E. coli is not a hemolysin but a cytoplasmic enzyme leading to the overproduction of outer membrane vesicles (OMVs). Here, we show that these specific OMVs inhibit the autophagic flux by impairing the autophagosome - lysosome fusion, thus preventing the formation of acidic autophagolysosome and autophagosome clearance. Furthermore, HlyF-associated OMVs are more prone to activate the non-canonical inflammasome pathway. Since autophagy and inflammation are crucial in the hosts response to infection especially during sepsis, our findings reveal an unsuspected role of OMVs in the crosstalk between bacteria and their host, highlighting the fact that these extracellular vesicles have exacerbated pathogenic properties.

microbiology↗

Phospholipid peroxidation fuels ExoU phospholipase-dependent cell necrosis and supports Pseudomonas aeruginosa-driven pathology

Regulated cell necrosis supports immune and anti-infectious strategies of the body; however, dysregulation of these processes drives pathological organ damage. Pseudomonas aeruginosa expresses a phospholipase, ExoU that triggers pathological host cell necrosis through a poorly characterized pathway. Here, we investigated the molecular and cellular mechanisms of ExoU-mediated necrosis. We show that cellular peroxidised phospholipids enhance ExoU phospholipase activity, which drives necrosis of immune and non-immune cells. Conversely, both the endogenous lipid peroxidation regulator GPX4 and the pharmacological inhibition of lipid peroxidation delay ExoU-dependent cell necrosis and improve bacterial elimination in vitro and in vivo. Our findings also pertain to the ExoU-related phospholipase from the bacterial pathogen Burkholderia thailandensis, suggesting that exploitation of peroxidised phospholipids might be a conserved virulence mechanism among various microbial phospholipases. Overall, our results identify an original lipid peroxidation-based virulence mechanism as a strong contributor of microbial phospholipase-driven pathology.

immunology↗

Mycobacteria-host interactions in human bronchiolar airway organoids

Tuberculosis, one of the oldest human pathogens remains a major global health threat. Recent advances in organoid technology offer a unique opportunity to grow different human "organs" in vitro, including the human airway, that faithfully recapitulate tissue architecture and function. We have explored the potential of human airway organoids (AOs) as a novel system in which to model tuberculosis infection. To this end, we adapted biosafety containment level 3-approved procedures to allow successful microinjection of Mycobacterium tuberculosis, the causative agent of tuberculosis, into AOs. We reveal that mycobacteria infected epithelial cells with low efficiency, and that the organoid microenvironment was able to control, but not eliminate the pathogen. We demonstrate that AOs responded to infection by inducing cytokine and antimicrobial peptide production, and inhibiting mucins. Given the importance of myeloid cells in tuberculosis infection, we co-cultured mycobacteria-infected organoids with human monocyte-derived macrophages, and found that these cells were recruited to the organoid epithelium. We conclude that adult stem cell-derived airway organoids can be used to model early events of tuberculosis infection and offer new avenues for fundamental and therapeutic research.

systems biology↗

Irgm2 and Gate-16 cooperatively dampen targeting of caspase-11 to Gram-negative bacterial products

Inflammatory caspase-11 (rodent) and caspases-4 and -5 (human) detect gram-negative bacterial component LPS in the host cell cytosol, which promotes activation of the non-canonical inflammasome. Although non-canonical inflammasome-induced pyroptosis and IL-1 related cytokine release is of importance to mount an efficient immune response against various bacteria, its unrestrained activation drives sepsis. This suggests that cellular components might tightly control the threshold level of the non-canonical inflammasome in order to ensure efficient but not deleterious inflammatory response. Here we show that the IFN-inducible protein Irgm2 and the ATG8 family member Gate-16 cooperatively slow down non-canonical inflammasome activation both in macrophages and in vivo. Specifically, the Irgm2/Gate-16 axis dampens caspase-11 targeting to intracellular bacteria, which lower caspase-11-mediated pyroptosis and cytokine release. Specifically, deficiency in Irgm2 or Gate16 opens an alternative road for caspase-11 targeting to intracellular bacteria, independently of the classical pathway driven by the Guanylate Binding Proteins (GBPs). Thus, our findings provide new molecular effectors involved at fine-tuning the optimal non-canonical inflammasome response and add novel insights in the understanding of the immune pathways they control.

immunology↗

Type-3 Secretion System-induced pyroptosis protects Pseudomonas against cell-autonomous immunity

Inflammasome-induced pyroptosis comprises a key cell-autonomous immune process against intracellular bacteria, namely the generation of dying cell structures. These so-called pore-induced intracellular traps (PITs) entrap and weaken intracellular microbes. However, the immune importance of pyroptosis against extracellular pathogens remains unclear. Here, we report that Type-3 secretion system (T3SS)-expressing Pseudomonas aeruginosa (P. aeruginosa) escaped PIT immunity by inducing a NLRC4 inflammasome-dependent macrophage pyroptosis response in the extracellular environment. To the contrary, phagocytosis of Salmonella Typhimurium promoted NLRC4-dependent PIT formation and the subsequent bacterial caging. Remarkably, T3SS-deficient Pseudomonas were efficiently sequestered within PIT-dependent caging, which favored exposure to neutrophils. Conversely, both NLRC4 and caspase-11 deficient mice presented increased susceptibility to T3SS-deficient P. aeruginosa challenge, but not to T3SS-expressing P. aeruginosa. Overall, our results uncovered that P. aeruginosa uses its T3SS to overcome inflammasome-triggered pyroptosis, which is primarily effective against intracellular invaders.\n\nImportanceAlthough innate immune components confer host protection against infections, the opportunistic bacterial pathogen Pseudomonas aeruginosa (P. aeruginosa) exploits the inflammatory reaction to thrive. Specifically the NLRC4 inflammasome, a crucial immune complex, triggers an Interleukin (IL)-1{beta} and -18 deleterious host response to P. aeruginosa. Here, we provide evidence that, in addition to IL-1 cytokines, P. aeruginosa also exploits the NLRC4 inflammasome-induced pro-inflammatory cell death, namely pyroptosis, to avoid efficient uptake and killing by macrophages. Therefore, our study reveals that pyroptosis-driven immune effectiveness mainly depends on P. aeruginosa localization. This paves the way toward our comprehension of the mechanistic requirements for pyroptosis effectiveness upon microbial infections and may initiate targeted approaches in order to ameliorate the innate immune functions to infections.\n\nGraphical abstractMacrophages infected with T3SS-expressing P. aeruginosa die in a NLRC4-dependent manner, which allows bacterial escape from PIT-mediated cell-autonomous immunity and neutrophil efferocytosis. However, T3SS-deficient P. aeruginosa is detected by both NLRC4 and caspase-11 inflammasomes, which promotes bacterial trapping and subsequent efferocytosis of P. aeruginosa-containing-PITs by neutrophils.\n\n\n\nO_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=64 SRC=\"FIGDIR/small/650333v1_ufig1.gif\" ALT=\"Figure 1\">\nView larger version (15K):\norg.highwire.dtl.DTLVardef@17e05c4org.highwire.dtl.DTLVardef@aca55forg.highwire.dtl.DTLVardef@9d2853org.highwire.dtl.DTLVardef@1c275f9_HPS_FORMAT_FIGEXP M_FIG C_FIG

immunology↗