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The first proposed invisibility cloaks required materials that are highly anisotropic, spatially inhomogeneous, and that possess a magnetic response. These properties are still difficult or impractical to achieve in practice, leading many researchers to explore simplified invisibility schemes that trade perfection for simplicity in design. In this paper, we investigate a traditional method by Devaney for constructing multi-angle invisibility devices, i.e., devices that are invisible for a finite number of directions of illumination in the weak scattering limit. We demonstrate that the scattering cross-section of these objects decreases dramatically as the number of invisibility directions is increased.

Tumor resistance to radiotherapy continues to be a significant problem in improving cancer patient outcomes. To overcome radioresistance, drugs that sensitize cancer cells to ionizing radiation have been tested. In theory, radiosensitizers should increase irradiated tumor kill and improve patient outcomes. In practice, the clinical utility of such drugs is curtailed by radiosensitization of peri-tumoral normal tissues causing toxicities. To address these issues, we developed an activatable cell penetrating peptide-drug conjugate to deliver a small molecule radiosensitizer with spatial precision to tumors. The activatable cell penetrating peptide (ACPP) scaffold cloaks a cell penetrating peptide-drug conjugate until it is unmasked within tumors through matrix metalloproteinase cleavage. Using antibody-drug conjugate linker chemistry, we attached the potent ataxia-telangiectasia mutated (ATM) kinase inhibitor AZD0156 to ACPP and created ACPP-AZD0156. In immune-competent murine cancer models, tumor-targeted ACPP-AZD0156 in combination with ionizing radiation stimulated tumor immune infiltration by CD8+ T cells and increased tumor control when compared to non-targeted ATM inhibitor. Mechanistically, ACPP-AZD0156 radiosensitized tumor control was dependent on the adaptive arm of the immune system. Finally, the combination of radiotherapy and ACPP-AZD0156 potentiated immune checkpoint inhibitors that resulted in durable tumor control. The therapeutic synergies of ACPP targeted ATM inhibitor to radiosensitize and stimulate anti-tumor immune responses provides a rationale for developing tumor-targeted radiosensitizer drug conjugates that restrict radiosensitization to cancer cells that then engages anti-tumor immune responses to improve cancer patient outcomes.

To disrupt the glycolytic metabolism vital for pancreatic cancer (PC), we developed a cascade-amplified and PC-targeted nanosystem, HMAD@EP-XQ2d. It integrates a DNAzyme for GLUT1 gene silencing, AuNPs-based nanozymes for catalytic activity, and a HMnO2 carrier, cloaked in an aptamer-modified erythrocyte membrane. The system actively targets CD71-overexpressing PC cells. Upon accumulation in the tumor microenvironment (TME), the HMnO2 degrades, initiating a therapeutic cascade: the released Mn2+ serves a dual function-they activate the DNAzyme for upstream blockade of glucose uptake, and act as a contrast agent for magnetic resonance imaging (MRI), enabling real-time monitoring of drug delivery and accumulation; concurrently, the exposed gold nanozymes exert glucose oxidase-like (GOx-like) activity to deplete glucose (downstream depletion) and peroxidase-like (POD-like) activity to convert the resultant H2O2 into cytotoxic hydroxyl radicals (oxidative stress). This three-pronged, synergistic attack on glycolysis induces a severe energy crisis in PC cells. Both in vitro and in vivo studies demonstrate potent antitumor efficacy, favorable biocompatibility, and MRI contrast capability. By integrating gene silencing, enzymatic catalysis, and imaging into a single responsive system triggered by the TME, this all-in-one theranostic platform offers a novel precise metabolic intervention strategy for pancreatic cancer.

Acute myeloid leukemia (AML) remains a challenging hematologic malignancy with limited treatment options and poor prognosis. Here, we report the development of a multifunctional, pH-responsive, and biodegradable nanoparticle system, Membrane/Cu-HMPB@DSF/RSL3, for synergistic AML therapy. Constructed upon the Prussian blue-based frameworks and cloaked with leukemia cell membranes, these nanoparticles preferentially accumulate in AML cells and release copper, iron, and manganese ions, along with disulfiram (DSF) and RSL3, under mildly acidic intracellular conditions. The released metal ions catalyze Fenton-like reactions, deplete intracellular glutathione (GSH), and induce ferroptosis and cuproptosis in cooperation with the loaded small-molecule drugs. Meanwhile, manganese ions activate the cGAS-STING pathway, triggering innate immune responses and promoting immune cell recruitment. Both in vitro and in vivo studies demonstrated robust anti-AML efficacy with minimal systemic toxicity. This work presents a modular and immunogenic nanoplatform that holds broad potential for AML treatment and beyond.

Photodynamic therapy (PDT) is an effective adjunct treatment for oral squamous cell carcinoma (OSCC). Enhancing photosensitizer targeting and inducing effective cytotoxic T-cell responses through photoimmunotherapy have become key strategies to improve PDT efficacy. Migrasomes, as vesicular structures assembled by TSPAN4 and cholesterol microdomains, are implicated in immune escape and are emerging as sensitization targets for PDT. Here, we report a biomimetic nanoplatform, MOF-919@CCM, that combines enhanced tumor-cell membrane adhesion with light-controlled cholesterol degradation. Cloaking with a homologous cancer-cell membrane (CCM) imparts specific adhesion to tumor cells and improves targeted delivery of the photosensitizer. Moreover, the transition-metal nodes of MOF-919 exhibit peroxidase- and catalase-like activities that alleviate tumor hypoxia and, under laser irradiation, effectively reduce cellular cholesterol levels. Experiments further revealed that PDT based on MOF-919@CCM markedly suppresses migrasome formation via effective degradation of cholesterol and promotes CD8⁺ T-cell infiltration and cytotoxic activity against tumor cells. This work develops a targeted PDT approach using MOF-919@CCM and provides a new strategy for the immunotherapy of OSCC.

Pyroptosis triggered by pore-forming Gasdermin proteins in cancer cells facilitates anti-tumor immune activation by releasing pro-inflammatory cytokines and immunogenic contents following cellular rupture. However, selectively triggering pyroptosis in tumors still remain limited in clinical applications. Here, it is reported a microfluidic-assisted bacterial delivery system using attenuated Salmonella typhimurium VNP20009 encapsulated with metal-phenolic networks composed of ferric ions (Fe3 +) and tannic acid (TA) to enhance intracellular gasdermin D (GSDMD) expression through targeted CRISPR/dCas9 delivery, thereby inducing robust tumor pyroptosis. Mechanistically, this system achieves cascade amplification of pyroptotic cell death through coordinated multi-modal mechanisms. Following systemic administration, VNP20009 specifically accumulates in hypoxic tumor regions while the coated Fe3 +-TA nanofilm undergoes pH-responsive dissolution in the acidic tumor microenvironment (TME), simultaneously generating ROS through Fenton reaction and releasing CRISPR/dCas9 system to upregulate GSDMD expression. Concurrently, the abundant flagella of VNP activate caspase-1, which in turn cleaves the overexpressed GSDMD proteins into its active form, thereby triggering robust pyroptosis in tumor cells. Taken together, by coupling bacterial adjuvanticity with ROS-mediated stress and CRISPR-driven GSDMD upregulation, this strategy achieves efficient amplification of pyroptosis and promotes antitumor immune activation.

Wetting of micropatterned surfaces is ubiquitous in nature and key to many technological applications like spray cooling, inkjet printing, and semiconductor processing. Overcoming the intrinsic, chemistry- and topography-governed wetting behaviors often requires specific materials which limits applicability. Here, we demonstrate that droplet spreading and wicking on hydrophilic patterns can be controlled by the vapor of a lower-surface-tension liquid. Condensation of the vapor induces Marangoni forces that delay capillary wicking and contract liquid into a droplet on top of the imbibed film. Thereby, macroscopic droplets can be maintained in an apparent partial wetting state, effectively cloaking the pattern. We quantify how pattern characteristics and vapor condensation compete, balancing in different wetting states from pinning to complete imbibition. Since this balance is the result of nonequilibrium processes rather than static wetting phenomena, it can be reversibly tuned by modifying the vapor concentration. This way, we guide droplets across patterns and even extract previously imbibed liquids, devising strategies for coating, cleaning, and drying functional surfaces.

Thermal invisibility has captivated the research interest for decades. Recent theories envisioned the promising schemes for this purpose using the near-wavelength antennas; because it enabled precise control over the radiation for invisibly cooling while preserving the cloaking within detectable band. However, pushing this delicate device to real-world applications raises two essential challenges: large-scale fabrication of the structures featuring nanoscale accuracy and durably safeguarding the function from both erosion and various contaminant intakes. Here, we report a self-cleaning hierarchical thermal cloak using femtosecond laser direct writing. The cloak is engineered with finely configured dynamic superhydrophobic micropillar arrays; on top of the micropillars, the antennas are devised for direct tailoring to ensure the large-area manufacturing scalability and feasibility. We demonstrate that the co-created architecture has superior cloaking performance with boosted mechanical and thermodynamic durability; moreover, it enables self-sweeping of the contaminants through van der Waals forces of an impact bulk droplet, thus completely regaining the excellent thermal cloaking. Notably, both the self-cleaning and cloaking functionalities remain robust even after over 24 hours of harsh treatments, including UV irradiation, water-flow flushing and thermal cycling.

Time-varying or temporal metamaterials and metasurfaces, in which electromagnetic parameters are deliberately modulated in time, have emerged as a powerful route to engineer wave-matter interaction beyond what is possible in static media. By enabling the controlled exchange of energy and momentum with the fields, they underpin magnet-free nonreciprocity, low-loss frequency conversion, temporal impedance matching beyond Bode-Fano limit, and unconventional parametric gain and noise control. This survey provides a coherent framework that unifies the main theoretical and experimental developments in the area, from early analyses of velocity-modulated dielectrics to recent demonstrations of temporal photonic crystals, non-Foster temporal boundaries, and spatiotemporally driven metasurfaces relevant to nanophotonic platforms. We systematically compare time-varying permittivity, joint ε-μ modulation, time-varying conductivity, plasmas, and circuit-equivalent implementations, including stochastic and rapidly sign-switching regimes, and relate them to acoustic and quantum analogs using common figures of merit, such as conversion efficiency, isolation versus insertion loss, modulation depth and speed, dynamic range, and stability. Our work concludes by outlining key challenges, loss and pump efficiency, high-speed modulation at the nanoscale, dispersion engineering for broadband operation, and fair benchmarking, which must be addressed for robust, integrable temporal metasurfaces.

Endothelial cell (EC) activation, characterized by upregulation of adhesion molecules that drive monocyte recruitment, contributes to plaque progression while also providing an opportunity for targeted therapeutic delivery. Leveraging the cell membrane cloaking strategy, we recently developed a monocyte-mimetic nanoparticle (MoNP) platform that exploits the natural inflammatory tropism of monocytes for site-specific delivery to atherosclerotic vessels. Recognizing that integrin activation is a key determinant of monocyte adhesion to ECs, this study investigates whether pre-activating integrins on MoNP enhances their binding affinity and accumulation at atherosclerotic lesions. Mouse bone marrow-derived monocytes were pretreated with CCL2 or Mn 2 □ to activate membrane integrins. Isolated monocyte plasma membranes were cloaked onto fluorescently labeled polymeric cores to generate integrin-activated MoNPs (IA@MoNPs). The targeting capability of IA@MoNPs toward endothelial ligands, inflamed ECs, and atherosclerotic lesions was evaluated using in vitro and in vivo models. IA@MoNPs exhibited markedly enhanced binding to VCAM1, the primary endothelial ligand mediating integrin-dependent monocyte adhesion, and significantly increased uptake by ECs under atheroprone conditions compared to standard MoNPs. In vivo , IA@MoNPs demonstrated enhanced accumulation in atherosclerotic arteries without increasing nonspecific binding, and blocking β1-integrins on IA@MoNPs abolished this targeting effect. Importantly, integrin activation on IA@MoNPs did not compromise circulatory stability or induce immune or organ toxicity. Integrin activation represents a simple yet effective strategy to enhance MoNP targeting to inflamed ECs and atherosclerotic lesions. This mechanism-driven approach improves targeting performance while maintaining specificity and safety, advancing the translational potential of the biomimetic nanomedicine platform for atherosclerosis.

Esophageal cancer (EC) remains a highly aggressive malignancy with limited therapeutic options and poor prognosis. To address the shortcomings of conventional therapies, we developed a biomimetic, reactive oxygen species (ROS)-responsive nanoprodrug for synergistic photothermal-chemotherapy of EC. Tannic acid and ellagic acid were chemically linked via boronate ester bonds to form a polyphenol-based nanoparticle (TPE). The epidermal growth factor receptor (EGFR)-targeting peptide GE11 was subsequently introduced onto red blood cell membranes (RBCM) to obtain GE11-RBCM, which was then used to cloak the TPE nanoparticles, yielding GE11-RBCM@TPE. The resulting nanoplatform exhibited excellent photothermal conversion capability under near-infrared irradiation and selectively released the therapeutic payload in response to elevated ROS levels within the tumor microenvironment. In vitro studies showed enhanced cellular uptake in EGFR-overexpressing EC cells and markedly increased cell death following combined photothermal and chemotherapeutic treatment. In vivo, GE11-RBCM@TPE significantly inhibited tumor growth with negligible systemic toxicity and prolonged blood circulation. Transcriptomic analysis further revealed up-regulation of pro-apoptotic (PER1, HK2, BMF, DAPK2) and autophagy-related genes (ATP6V0D2, HDAC10, BNIP3, DEPP1, ATG9B, NAT16), while SQSTM1 and IL6 were down-regulated, indicating simultaneous activation of apoptosis and autophagy. These findings suggest that GE11-RBCM@TPE represents a promising strategy for precise and effective treatment of esophageal cancer.

Oncolytic adenoviruses (OVs) can directly eliminate cancer cells and subsequently activate immune responses, exhibiting potent antitumor therapeutics. However, it was observed that the immune cells can also be lysed during viral treatment, evidently dampening the OVs-mediated antitumor immune response. In this study, we develop a microneedle (MN)-based in situ tumor cell-derived extracellular nanovesicle (TDEV)-cloaked OVs platform to enhance cancer immunotherapy and reduce immune cell exhaustion. In this platform, tumor cells pre-infected with OVs are loaded into the upper reservoir of the MN device. Following the transdermal administration, the hollow MN would constantly facilitate the transport of in situ the generated TDEV-encapsulating OVs into the tumor site for sustained delivery of OVs, which could subsequently infect cancer cells selectively rather than immune cells. Enhanced antigens triggered by improved intratumoral OVs killing can be presented by non-exhausted dendritic cells, further evoking significant immunotherapeutic effects in both TC-1-hCD46 xenograft tumor-bearing mice and postoperative tumor recurrence mice models.

Adoptive natural killer (NK) cell therapy (ANKCT) is a promising strategy for hepatocellular carcinoma (HCC); however, its efficacy is hampered by insufficient NK cell homing and the immunosuppressive activity of M2-polarized tumor-associated macrophages (TAMs). Activation of the cyclic guanosine monophosphate (GMP)-adenosine monophosphate synthase (AMP) synthase-stimulator of interferon genes (cGAS-STING) pathway enhances NK-cell recruitment and reprograms TAMs toward a proinflammatory M1 phenotype. Radiation therapy (RT) activates the cGAS-STING pathway by inducing reactive oxygen species (ROS)-mediated DNA damage. Compared with high-dose irradiation, low-dose radiotherapy (LDRT) offers advantages, including reduced toxicity and enhanced antitumor immunity. However, the robust thioredoxin (Trx) and glutathione (GSH) antioxidant systems in HCC inhibit LDRT-induced ROS accumulation, thereby limiting immune activation. These limitations highlight the need for auxiliary strategies to complement LDRT-induced immunogenicity. Here, we developed a biomimetic nanoparticle in which auranofin-loaded MOF-199 is cloaked with tumor cell membranes (A@MMOF). A@MMOF disrupts tumor redox homeostasis by irreversibly inhibiting the GSH and Trx antioxidant systems while inducing GSH-dependent Cu²⁺ release from the MOF framework. The subsequent reduction of Cu²⁺ to Cu⁺ catalyzes Fenton-like reactions, markedly amplifying the intracellular ROS levels. By providing a sustained redox-driven stimulus, A@MMOF compensates for the insufficient oxidative stress induced by LDRT, leading to robust activation of the cGAS-STING pathway. Thus, A@MMOF synergizes with LDRT to remodel the tumor microenvironment, enhance NK cell infiltration and activation, and ultimately improve the efficacy of ANKCT in HCC.

Doxorubicin (DOX)-induced cardiomyopathy remains therapeutically challenging due to the absence of pathway-specific interventions. Ferroptosis of cardiac microvascular endothelial cells (CMECs) is a major driver of disease progression, yet precise therapeutic strategies remain limited. Here, mechanistic analyses identified lncRNA TUG1 as an upstream promoter of CMEC ferroptosis through the miR-153-5p/MMP2-TIMP2/TFR-1 axis. Guided by this mechanism, a translational construct was developed by cloaking mesoporous silica nanoparticles carrying TUG1-targeting siRNA with neutrophil membranes (NM@si-TUG1/MSN). The neutrophil membrane coating enabled robust cardiac tropism and preferential CMEC uptake. In a murine model of DOX-induced cardiomyopathy, NM@si-TUG1/MSN accumulated in the heart, achieved effective TUG1 knockdown, and markedly reduced ferroptosis. Relative to free siRNA and uncoated nanoparticles, the nanocomplex produced superior outcomes, including restoration of microvascular integrity, reduced fibrosis, and significant improvement in cardiac function. This study characterizes a regulatory axis in DOX-induced cardiomyopathy and demonstrates a targeted biomimetic nanotherapy that interrupts microvascular ferroptosis and limits disease progression. The data support the feasibility of this approach for clinical translation.

Glycosyltransferases (GTs) catalyze the formation of new glycosidic bonds and thus are vital for synthesizing nature's vast repertoire of glycans and glycoconjugates and for engineering glycan-related medicines and materials. However, obtaining detailed structural and functional insights for the >750,000 known GTs is limited by difficulties associated with their efficient recombinant expression. Members of the GT-C fold, in particular, pose the most significant expression challenges due to the integration and folding requirements of their multiple membrane-spanning regions. Here, we address this challenge by engineering water-soluble variants of an archetypal GT-C fold enzyme, namely the oligosaccharyltransferase PglB from Campylobacter jejuni (CjPglB), which possesses 13 hydrophobic transmembrane helices. To render CjPglB water-soluble, we leveraged two advanced protein engineering methods: one that is universal called SIMPLEx (solubilization of IMPs with high levels of expression) and the other that is custom tailored called WRAPs (water-soluble RFdiffused amphipathic proteins). Each approach was able to transform CjPglB into a water-soluble enzyme that could be readily expressed in the cytoplasm of Escherichia coli cells at yields in the 3-6 mg/L range. Importantly, solubilization was achieved without the need for detergents and with retention of catalytic function. Collectively, our findings demonstrate that both SIMPLEx and WRAPs are promising platforms for advancing the molecular characterization of even the most structurally complex GTs, while also enabling broader GT-mediated glycosylation capabilities within synthetic glycobiology applications.

Soccer requires repeated changes of direction (COD)&#xa0;and single-leg decelerations (SLD), which accrue considerable mechanical stress on the lower limbs. These actions place significant demands on the players' musculoskeletal system. An uneven utilization of these actions between limbs, arising from disparities in neuromuscular control&#xa0;and skill acquisition, may lead to asymmetries and increased injury risk. This study aimed to examine the effects of player position and footedness on the frequency of intense CODs, SLDs, and the total sum of the 2 actions (TOT) performed by the dominant and nondominant foot in elite male youth soccer players. Twenty-five elite English youth soccer players were grouped by their playing positions (lateral: full-backs and wide midfielders; central: center defenders, center midfielders, and strikers)&#xa0;and footedness (left or right footed). High-intensity CODs and SLDs were identified using video analysis and GPS data across 6 matches. The frequency and distribution of these actions were analyzed to assess the impact of player position and limb dominance. No significant differences were found in the percentage distribution of SLDs or TOT between the central and lateral groups. However, central players exhibited a significantly greater imbalance in COD frequency compared with lateral players (51.8% [31.5%] vs 29.9% [31.1%]; P < .05; d = 0.70). Players performed more CODs in the direction opposite to their dominant limb, indicating a preference for using the dominant limb as the plant limb (4.6 [3.2] vs 3.7 [2.6]; P < .05; d = 0.31). The study highlights the mechanical and positional demands placed on soccer players, with central players showing greater COD frequency asymmetry.

Conventional targeted therapies for inflammatory bowel disease (IBD) often rely on unstable biological recognition elements. While molecularly imprinted polymers (MIP) offer robust synthetic alternatives, their utility is limited by an "always-on" binding state: even weak non-specific adsorption can significantly compromise their target-binding capacity. We convert static MIP into reactive oxygen species (ROS)-activated therapeutic actuators by conjugating mannose to transferrin-imprinted MIP via a ROS-cleavable linker. The saccharide acts dually as a therapeutic agent and a protective cloak. It sterically blocks non-specific binding during intestinal transit. At inflammatory sites, elevated ROS levels (higher than in healthy tissue) trigger simultaneous mannose release and activation of high-affinity targeting. This enables precise MIP anchoring to the inflamed epithelium for physical barrier formation and localized microbiome modulation. In murine colitis models, this achieved mucosal healing, mitigated inflammation, and microbiota rebalancing using a mannose equivalent dose of 27.2&#xa0;mg/kg/d, benchmarking against free mannose and non-responsive MIP controls. This work establishes a generalizable paradigm for targeted recognition and drug delivery in complex physiological environments, paving the way for intelligent, disease-responsive nanomedicines.

Lipid nanoparticles (LNPs) have emerged as a clinically validated nonviral RNA delivery system. However, their limited tumor targeting remains challenging in oncology. In this work, LNPs were functionally integrated with cancer cell membrane components to enhance their targeting capabilities. The natural composition of tumor membranes was leveraged to promote both homotypic and heterotypic adhesion, exploiting cancer cell self-recognition and interactions with stromal cells in the tumor microenvironment. A biomimetic nanocarrier was developed by cloaking RNA-loaded LNPs with nanoghosts obtained from the membrane of triple negative breast cancer cells. Nanoghosts were dye-labeled and comprehensively characterized in terms of size, surface charge, protein composition, and membrane sidedness. The functional orientation of nanoghost membrane-associated proteins mediated homotypic binding with 4&#xa0;T1 cells and heterotypic recognition of functionally validated cancer-associated fibroblasts and exhibited higher affinity for the latter, as confirmed through flow cytometry and confocal microscopy. RNA-LNPs were incorporated into nanoghosts using ultrasound-assisted fusion, yielding stable biomimetic LNPs with a multilamellar mRNA-LNP core enveloped by a nanoghost shell, as confirmed by Small-Angle X-ray Scattering. While uncoated LNPs showed negligible interaction with heterotypic cells, biomimetic LNPs displayed strong affinity for cancer-associated fibroblasts, enabling efficient internalization and RNA transfection. Additionally, the biomimetic coating enhanced LNP uptake in homotypic 4&#xa0;T1 cells, resulting in significantly improved biological activity compared to uncoated LNPs. This work provides proof of concept that RNA-LNPs can be effectively integrated into biomimetic carriers to enable dual targeting of tumor and stromal cells. The enhanced selectivity and delivery performance of biomimetic LNPs highlight their therapeutic potential for overcoming stromal barriers in desmoplastic tumors such as triple negative breast cancer.

People with cystic fibrosis (pwCF) are susceptible to chronic lung infections, particularly with Pseudomonas aeruginosa. During infection, a subset of patients develops cloaking antibodies specific to O-antigen lipopolysaccharide that impair complement-mediated bactericidal killing. These antibodies associate with worse disease, and their removal via plasmapheresis has been used as a successful treatment for multidrug-resistant P aeruginosa. Whether a similar mechanism of antibody-mediated serum resistance exists toward common polysaccharide antigen (CPA) lipopolysaccharide is unknown. Forty-two serum samples and 63 matched P aeruginosa isolates were collected from pwCF. The titers of antibodies specific to CPA in patient sera were determined, and the ability of these antibodies to inhibit serum-mediated killing of P aeruginosa was assessed. Despite widespread anti-CPA antibodies, only 1 serum-strain pair showed evidence of complement inhibition. Patient serum IgG and IgA responses to CPA were elevated in 86% and 69% of sera, respectively. Furthermore, 69% of pwCF were colonized with CPA-expressing isolates. Despite the high prevalence of elevated anti-CPA antibodies, only 1 patient had antibodies capable of inhibiting complement killing of the cognate P aeruginosa. This isolate, CFP3A, had significantly higher expression of CPA than all other strains. Complement-mediated killing toward it was inhibited by anti-CPA antibodies in a titer-dependent manner. This investigation reveals that although antibody specific for CPA is prevalent in pwCF, it cannot inhibit complement killing of the majority of CPA-expressing strains. Thus, when Pseudomonas is treated by removal of cloaking antibodies, it is unlikely that CPA-specific antibodies will also need to be eliminated.