Following the escalation of the Israeli–Palestinian conflict after the Hamas attack of October 7, 2023, pro-Palestinian activists occupied universities in the United States, Canada, and Europe, demanding that academic authorities cut ties with Israeli institutions. This article examines the response of Belgian universities to these mobilizations. At first, several institutions rejected calls for an academic boycott and reaffirmed their commitment to institutional neutrality, emphasizing the importance of protecting academic freedom. Their actions were limited to reviewing whether collaborations with Israeli universities posed risks of harmful applications, particularly in the context of dual-use research. In contrast, the Ghent University and the Université Libre de Bruxelles quickly declared that a boycott was a necessity in light of Israel’s violations of international law and human rights. Both established Committees on Respect for International Law to reassess partnerships with foreign institutions. This stance soon became dominant within Belgian higher education. Through joint declarations, all Belgian universities endorsed an academic boycott and urged the European Union to suspend agreements with Israel. Such a position marks a clear departure from traditional academic norms. By abandoning institutional neutrality, universities positioned themselves as political actors, a shift that may reshape how both the public and policymakers perceive academic expertise, while also exposing institutions to political targeting. Moreover, by presenting the academic boycott as a moral and legal obligation, universities risk legitimizing the idea that scholarly communities can be held collectively responsible for state actions. If generalized across Europe, these practices could endanger academic freedom and normalize academic boycotts as a form of collective punishment.

BackgroundAcinetobacter baumannii is an opportunistic bacterium that causes serious nosocomial infections, including pneumonia and bacteremia, especially in immunocompromised individuals.MethodsHere, we first evaluated the protective efficacy of a vaccination protocol with the heat-killed (HK) A. baumannii strain LAC-4 in various models of immunodeficient C57BL/6 mice challenged with pulmonary infection by LAC-4. We then examined the ability of HK LAC-4 to stimulate peripheral blood mononuclear cells (PBMCs) from healthy donors in vitro.ResultsWe observed that mice deficient in Th1 (IL-12p35-/-, IFN-γ-/-), Th17 (IL-17RA-/-) and T cells (δTCR-/-, TAP1-/-, CD3-/-) display higher susceptibility to LAC-4 infection, but that our protocol improves their resistance. In contrast, vaccinated B cell-deficient (MuMT-/-) mice appear unable to control the infection, demonstrating that humoral immunity is essential to vaccine protection. Vaccination of wild-type mice with an HK ΔitrA strain deficient for capsule production failed to induce protection, showing that protective antibodies are mainly directed against the capsule. Our vaccination protocol also confers increased protection in wild-type mice vaccinated and then treated with cyclophosphamide; an immunosuppressive drug described to strongly increase the susceptibility of mice to A. baumannii infection. Finally, we demonstrate that HK LAC-4 can induce the activation of human monocyte-derived dendritic cells and T lymphocytes from PBMCs of healthy donors, suggesting that it may activate the human adaptive immune system and induce a protective memory response against A. baumannii.ConclusionsOverall, our results demonstrate that administration of HK bacteria can induce protective immunity against A. baumannii in both immuno-competent and immuno-compromised mice and that these HK bacteria can activate the human adaptive immune system.

SUMMARYChagas disease (CD) is caused by the protozoan parasite Trypanosoma cruzi (Tc), infecting 6-7 million people. It is transmitted by insect vectors, orally, through infected tissues, or congenitally. Tc infection can progress toward chronic cardiac and/or digestive severe and fatal CD in 20%-40% of patients. Tc exhibits an important genetic and phenotypic intraspecies diversity and a preponderant clonal population structure. The impact of multiclonal coinfections has been little studied in CD patients. Relationships between the currently used discrete typing unit (DTU)-based classification of Tc lineages and the occurrence of the different clinical forms of CD, its congenital transmission, as well as the efficacy of trypanocidal molecules (benznidazole and nifurtimox) could not be established. In this review, we revisit the different aspects of Tc diversity and analyze the impact of infections with multiple clones and their variants on the dynamic and pathogenesis of CD and its maternal-fetal transmission. We propose to call "cruziome" all the Tc clones and their variants infecting a given host and provide strong evidence that (i) multiclonal Tc infections are likely the rule rather than the exception; (ii) each "cruziome" is associated with a unique combination of virulence factors, tissular tropisms, and host immune responses; (iii) accordingly, some particularly harmful "cruziomes" likely trigger the occurrence and progression of CD and might also favor the congenital transmission of parasites. We propose that our concept of "cruziome" should be taken into consideration because of its practical consequences in epidemiological studies, laboratory diagnosis, clinical management, and treatment of CD.

Immune evasion strategies of Brucella, the etiologic agent of brucellosis, a global zoonosis, remain partially understood. The omentum, a tertiary lymphoid organ part of visceral adipose tissue, has never been explored as a Brucella reservoir. We report that B. abortus infects and replicates within murine omental macrophages. Throughout the chronic phase of infection, the omentum accumulates macrophages, monocytes and neutrophils. The maintenance of PD-L1+Sca-1+ macrophages, monocytes and neutrophils in the omentum depends on the wadC-encoded determinant of Brucella LPS. We demonstrate that PD-L1+Sca-1+ murine omental neutrophils produce high levels of IL-1RA leading to T cell hyporesponsiveness. These findings corroborate brucellosis patient analysis of whole blood displaying upregulation of PDL1 and Ly6E genes, and of serum exhibiting high levels of IL-1RA. Overall, the omentum, a reservoir for B. abortus, promotes bacterial persistence and causes CD4+ and CD8+ T cell immunosuppression by IL-1RA secreted by PD-L1+Sca-1+ neutrophils.

Live attenuated vaccines (LAVs) whose virulence would be controlled at the tissue level could be a crucial tool to effectively fight intracellular bacterial pathogens, because they would optimize the induction of protective immune memory while avoiding the long-term persistence of vaccine strains in the host. Rational development of these new LAVs implies developing an exhaustive map of the bacterial virulence genes according to the host organs implicated. We report here the use of transposon sequencing to compare the bacterial genes involved in the multiplication of Brucella melitensis, a major causative agent of brucellosis, in the lungs and spleens of C57BL/6 infected mice. We found 257 and 135 genes predicted to be essential for B. melitensis multiplication in the spleen and lung, respectively, with 87 genes common to both organs. We selected genes whose deletion is predicted to produce moderate or severe attenuation in the spleen, the main known reservoir of Brucella, and compared deletion mutants for these genes for their ability to protect mice against challenge with a virulent strain of B. melitensis. The protective efficacy of a deletion mutant for the plsC gene, implicated in phospholipid biosynthesis, is similar to that of the reference Rev.1 vaccine but with a shorter persistence in the spleen. Our results demonstrate that B. melitensis faces different selective pressures depending on the organ and underscore the effectiveness of functional genome mapping for the design of new safer LAV candidates.

Brucellae are facultative intracellular Gram-negative coccobacilli that chronically infect various mammals and cause brucellosis. Human brucellosis is among the most common bacterial zoonoses and the vast majority of cases are attributed to B. melitensis. Using transposon sequencing (Tn-seq) analysis, we showed that among 3369 predicted genes of the B. melitensis genome, 861 are required for optimal growth in rich medium and 186 additional genes appeared necessary for survival of B. melitensis in RAW 264.7 macrophages in vitro. As the mucosal immune system represents the first defense against Brucella infection, we investigated the early phase of pulmonary infection in mice. In situ analysis at the single cell level indicates a succession of killing and growth phases, followed by heterogenous proliferation of B. melitensis in alveolar macrophages during the first 48 hours of infection. Tn-seq analysis identified 94 additional genes that are required for survival in the lung at 48 hours post infection. Among them, 42 genes are common to RAW 264.7 macrophages and the lung conditions, including the T4SS and purine synthesis genes. But 52 genes are not identified in RAW 264.7 macrophages, including genes implicated in lipopolysaccharide (LPS) biosynthesis, methionine transport, tryptophan synthesis as well as fatty acid and carbohydrate metabolism. Interestingly, genes implicated in LPS synthesis and β oxidation of fatty acids are no longer required in Interleukin (IL)-17RA-/- mice and asthmatic mice, respectively. This demonstrates that the immune status determines which genes are required for optimal survival and growth of B. melitensis in vivo.

In hindsight, the early response of liberal governments to the SARS-CoV-2 pandemic was chaotic and generally inefficient. Though one might be tempted to attribute these failures to the incompetence of certain political decision-makers, we propose another explanation. Global threats require a coordinated international response, which is only possible if the threat is perceived in the same way by all, and if government priorities are similar. The effectiveness of the response also relies on massive adhesion of citizens to the measures imposed, which in turn requires trust in government. Our hypothesis is that certain fundamental features of liberalism complicate such global and collective responses: neutrality of the state and primacy of the individual over collective society. Liberalism considers that institutions and public policy must not be designed to favor any specific conception of the common good. That which is best for all is usually determined by a “competition of opinions,” which frequently leads to scientific expertise being considered as only one opinion among many. Liberalism also imposes strict respect for individual freedoms and private interests and tends to reject any form of collectivism or dictate imposed by the common good. In order to solve these structural problems and improve society's management of global threats, we make several proposals, such as the introduction of a minimal and consensual definition of the common good and the promotion of a health policy guided by One Health-like concepts. Overall, our analysis suggests that because political ideologies provide their own definitions of the common good and the place of scientific knowledge in the governance process and can thus affect the response to global threats, they should be urgently taken into consideration by public health experts.

Mycobacterium tuberculosis ( Mtb ), the pathogen causing human tuberculosis, has evolved multiple strategies to successfully prevent clearance by immune cells and to establish dissemination and long-term survival in the host. The modulation of host immunity to maximize pathogen elimination while minimizing inflammation-mediated tissue damage may provide another tool to fight drug-resistant Mtb strains. Metabolic reprogramming of phagocytes can dramatically influence the intracellular colonization by Mtb and the key players involved in this process remain a matter of debate. Here, we demonstrate that aconitate decarboxylase 1 (Acod1; also known as immune-responsive gene 1, IRG1), which converts cis-aconitate into the metabolite itaconate, is a major player in controlling the acute phase of Mtb infection. Exposure of IRG1-deficient mice to a virulent Mtb strain (H37Rv) was lethal, while M. bovis BCG and the H37Ra attenuated Mtb strain induced neither lethality nor severe lung immunopathology. Lungs of IRG1-deficient mice infected by Mtb H37Rv displayed large areas of necrotizing granulomatous inflammation and neutrophil infiltration, accompanied by reduced levels of B and T lymphocytes and increased levels of alveolar and interstitial macrophage populations, compared to their wild type counterparts. Next, we show that IRG1, beyond its recruitment to Mtb -containing vacuoles, restricts Mtb replication and lipid droplets accumulation in phagocytes, hallmarks of a tight interplay between the bacillus and the host. Altogether, IRG1 confines the host response to create a favourable phagocytic environment for Mtb controlled intracellular replication. ### Competing Interest Statement The authors have declared no competing interest.

Cyclic-di-GMP plays crucial role in the cell cycle regulation of the alpha-Proteobacterium Caulobacter crescentus. Here we investigated its role in the alpha-Proteobacterium Brucella abortus, a zoonotic intracellular pathogen. Surprisingly, deletion of all predicted cyclic-di-GMP synthesizing or degrading enzymes did not drastically impair the growth of B. abortus, nor its ability to grow inside cell lines. As other Rhizobiales, B. abortus displays unipolar growth from the new cell pole generated by cell division. We found that the phosphodiesterase PdeA, the ortholog of the essential polar growth factor RgsP of the Rhizobiale Sinorhizobium meliloti, is required for rod shape integrity but is not essential for B. abortus growth. Indeed, the radius of the pole is increased by 31 +/- 1.7% in a Delta pdeA mutant, generating a coccoid morphology. A mutation in the cyclic-di-GMP phosphodiesterase catalytic site of PdeA does not generate the coccoid morphology and the Delta pdeA mutant kept the ability to recruit markers of new and old poles. However, the presence of PdeA is required in an intra-nasal mouse model of infection. In conclusion, we propose that PdeA contributes to bacterial morphology and virulence in B. abortus, but it is not crucial for polarity and asymmetric growth.

[...]que jamais, une politique sanitaire europeenne reposant sur un cadre conceptuel scientifique s’avere indispensable pour prevenir et faire face aux futures pandemies tout comme aux consequences du changement climatique et de la pollution atmospherique. Dans le cas des epidemies, One Health favorise une politique proactive en surveillant les zones identifiees comme a risque et en regulant l’usage des sols, les conditions d’elevage et de transport des animaux. Pour atteindre cet objectif, comme dans le domaine de la promotion de la sante, le plaidoyer est fondamental : les acteurs de terrain tout comme les associations ont la responsabilite d’informer, d’alerter sur ces sujets et de participer a induire, le plus rapidement possible car le temps nous est compte, un changement de comportement de l’humain face a la nature.

Global Health Promotion 1757-9759; Vol 28(3): 3 –5; 1035070 Copyright © The Author(s) 2021, Reprints and permissions: http://www.sagepub.co.uk/journalsPermissions.nav DOI: https://doi.org/ 0.1 /17579759211035070 journals.sagepub.com/home/ghp The pandemic caused by the novel Coronavirus SARS-CoV-2 has highlighted the astounding speed with which epidemics are spreading in a highly interconnected world and the weakness of governments in responding to them. Reported in China on November 16, 2019, the COVID-19 epidemic was declared a pandemic on March 11, 2020 by the World Health Organization (WHO). During the first nine months, in the absence of specific treatments and vaccines, governments were reduced to practicing lockdowns and imposing social distancing in order to avoid saturation of hospitals. Although the development and validation of several effective and safe vaccines in a single year is a remarkable achievement (the average research time being eight years (1)), vaccinating the world’s population is proving to be a daunting task and will require well over a year. In addition, the emergence of variants of SARS-CoV-2 (2) potentially capable of eluding natural immunity and vaccines makes constant monitoring of this virus necessary. Finally, the human and economic cost of the COVID-19 pandemic is already catastrophic and will undoubtedly mark the 21st century. As of May 1, 2021, nearly 3.2 million individuals have died of COVID-19, and the existence of long (3) and disabling forms of the virus, as well as the impact of the containment and distancing measures put in place on precariousness, education, and mental health, suggests a much higher human cost in the medium and long term. In the US alone, the economic cost of the pandemic is estimated at US$3 trillion (4) or even US$16 trillion (5). The COVID-19 pandemic has also served as a reminder of the crucial importance of governance and international cooperation in the face of global threats. While scientific information about SARSCoV-2 was quickly and widely shared throughout the pandemic, the way the US and European governments responded to it was deemed chaotic and ineffective by many scientific experts (6,7) as well as by the WHO (8). Faced with a global threat, the US has developed national and sometimes even regional responses, without the slightest coordination. In Europe, countries such as Germany, France, and Belgium have adopted partial or total containment policies while others, such as the United Kingdom, have opted for a health policy of ‘complacency’ and betting on the development of herd immunity, which makes no sense between neighboring countries whose borders remain open. More than ever, a European health policy based on a scientific conceptual framework is proving essential to prevent and deal with future pandemics as well as the consequences of climate change and air pollution. It is worth recalling that the latter is the cause, alone, of 9 million deaths each year (WHO figure), much more than malaria, tuberculosis, and the human immunodeficiency virus (HIV) combined. Indeed, if the precise origin of SARS-CoV-2 remains uncertain, it is well demonstrated that of the 335 emerging infectious agents detected between 1940 and 2004, more than 60.3% are zoonoses, infections transmitted by animals (9). Contrary to what some economists (10) claim, these events cannot be interpreted as ‘black swans’ (11), or unexpected events having a cause external to our economic system. Agricultural activities are associated with 25% of all outbreaks of infectious agents and almost 50% of emerging zoonoses (12). For example, influenza viruses infecting humans originate from viruses infecting wild birds, which infect poultry and pig farms, then breeders, and gradually adapt to them (13). The link between the emergence of new infectious agents and the invasion of natural ecosystems has been well demonstrated, 1035070PED0010.1177/17579759211035070English EditorialE. Muraille research-article2021

Al 1 de mayo del 2021, cerca de 3.2 millones de personas habían fallecido de la COVID-19 y su existencia prolongada (3) e incapacitante, así como el impacto de las medidas de confinamiento y de distanciación sobre la precariedad, la educación y la salud mental, dejan suponer un costo humano considerablemente mayor a mediano y a largo plazo. Esta interdependencia entre salud humana, salud animal y el estado de los ecosistemas es la base del concepto Una Salud (One Health) que hoy constituye el marco conceptual de la estrategia de agencias de salud pública nacionales e internacionales como la OMS, la Organización Mundial de la Salud Animal y la Organización de las Naciones Unidas para la Alimentación y la Agricultura. En 1984, Medicina veterinaria y salud humana, obra de uno de los padres de la epidemiología moderna, el veterinario Calvin Schwab, dejaba ya en evidencia la interconexión entre la salud animal y humana.

The newborns of women infected with the parasite Trypanosoma cruzi (the agent of Chagas disease) can be infected either before birth (congenitally), or after birth (as e.g., by vector route). Congenital Chagas disease can induce high levels of neonatal morbidity and mortality. Parasite-infected pregnant women transmit antibodies to their fetus. Antibodies, by opsonizing parasites, can promote phagocytosis and killing of T. cruzi by cells expressing FcγR, on the mandatory condition that such cells are sufficiently activated in an inflammatory context. Antibody-dependent enhancement (ADE) is a mechanism well described in viral infections, by which antibodies enhance entry of infectious agents into host cells by exploiting the phagocytic FcγR pathway. Previously reported Chagas disease studies highlighted a severe reduction of the maternal-fetal/neonatal inflammatory context in parasite-transmitting pregnant women and their congenitally infected newborns. Otherwise, experimental observations brought to light ADE of T. cruzi infection (involving FcγR) in mouse pups displaying maternally transferred antibodies, out of an inflammatory context. Herein, based on such data, we discuss the previously unconsidered possibility of a role of ADE in the trans-placental parasite transmission, and/or the development of severe and mortal clinical forms of congenital/neonatal Chagas disease in newborns of T. cruzi-infected mothers.

Perturbation of the endoplasmic reticulum (ER), a central organelle of the cell, can have critical consequences for cellular homeostasis. An elaborate surveillance system known as ER quality control ensures that cells can respond and adapt to stress via the unfolded protein response (UPR) and that only correctly assembled proteins reach their destination. Interestingly, several bacterial pathogens hijack the ER to establish an infection. However, it remains poorly understood how bacterial pathogens exploit ER quality-control functions to complete their intracellular cycle. Brucella spp. replicate extensively within an ER-derived niche, which evolves into specialized vacuoles suited for exit from infected cells. Here we present Brucella-secreted protein L (BspL), a Brucella abortus effector that interacts with Herp, a central component of the ERassociated degradation (ERAD) machinery. We found that BspL enhances ERAD at the late stages of the infection. BspL targeting of Herp and ERAD allows tight control of the kinetics of autophagic Brucella-containing vacuole formation, delaying the last step of its intracellular cycle and cell-to-cell spread. This study highlights a mechanism by which a bacterial pathogen hijacks ERAD components for fine regulation of its intracellular trafficking.

Brucellosis is one of the most widespread bacterial zoonoses worldwide. Here, our aim was to identify the effector mechanisms controlling the early stages of intranasal infection with Brucella in C57BL/6 mice. During the first 48 hours of infection, alveolar macrophages (AMs) are the main cells infected in the lungs. Using RNA sequencing, we identified the aconitate decarboxylase 1 gene (Acod1; also known as Immune responsive gene 1), as one of the genes most upregulated in murine AMs in response to B. melitensis infection at 24 hours post-infection. Upregulation of Acod1 was confirmed by RT-qPCR in lungs infected with B. melitensis and B. abortus. We observed that Acod1-/- C57BL/6 mice display a higher bacterial load in their lungs than wild-type (wt) mice following B. melitensis or B. abortus infection, demonstrating that Acod1 participates in the control of pulmonary Brucella infection. The ACOD1 enzyme is mostly produced in mitochondria of macrophages, and converts cis-aconitate, a metabolite in the Krebs cycle, into itaconate. Dimethyl itaconate (DMI), a chemically-modified membrane permeable form of itaconate, has a dose-dependent inhibitory effect on Brucella growth in vitro. Interestingly, structural analysis suggests the binding of itaconate into the binding site of B. abortus isocitrate lyase. DMI does not inhibit multiplication of the isocitrate lyase deletion mutant ΔaceA B. abortus in vitro. Finally, we observed that, unlike the wt strain, the ΔaceA B. abortus strain multiplies similarly in wt and Acod1-/- C57BL/6 mice. These data suggest that bacterial isocitrate lyase might be a target of itaconate in AMs.

In just a few weeks’ time, leaders across the globe will have to start making decisions about lifting lockdown policies, with considerable social, economic and political consequences. We propose a framework for what is arguably the most difficult health challenge that governments have faced since the beginning of this century: a responsible lockdown exit strategy.

In many infectious diseases, the immune response operates as a double-edged sword. While required for protective immunity, infection-induced inflammation can be detrimental if it is not properly controlled, causing collateral body damage and potentially leading to death. It is in this context that the potent anti-inflammatory cytokine interleukin-10 (IL-10) is required to dampen the pro-inflammatory immune response that hallmarks trypanosomosis. Effective control of this infection requires not just the action of antibodies specific for the parasite's variable surface glycoprotein (VSG) coat antigens, but also a pro-inflammatory immune response mediated mainly by IFNγ, TNF, and NO. However, strict control of inflammation is mandatory, as IL-10-deficient mice succumb from an unrestrained cytokine storm within 10 days of a Trypanosome brucei infection. The relevant cellular source of IL-10 and the associated molecular mechanisms implicated in its trypanosomosis associated production are poorly understood. Using an IL-10 reporter mouse strain (Vert-X), we demonstrate here that NK cells, CD8+ T cells and CD4+ T cells as well as B cells and plasma cells constitute potential cellular sources of IL-10 within the spleen and liver during acute infection. The IL-10 wave follows peak pro-inflammatory cytokine production, which accompanied the control of peak parasitemia. Similar results were observed following conventional experimental needle infection and physiological infections via T. brucei-infected tsetse flies. Our results show that conditional T cell-specific ablation of the IL-10 regulating Prdm1 gene (encoding for the Blimp-1 transcription factor), leads to an uncontrolled trypanosome-induced pro-inflammatory syndrome like the one observed in infected IL-10-deficient mice. This result indicates that the biological role of IL-10-derived from non-T cells, including NK cells, is of minor importance when considering host survival. The cytokine IL-27 that is also considered to be an IL-10 regulator, did not affect IL-10 production during infection. Together, these data suggest that T. brucei activates a Blimp-1-dependent IL-10 regulatory pathway in T cells that acts as a critical anti-inflammatory rheostat, mandatory for host survival during the acute phase of parasitemia.

Live attenuated vaccines play a key role in the control of many human and animal pathogens. Their rational development is usually helped by identification of the reservoir of infection, the lymphoid subpopulations associated with protective immunity as well as the virulence genes involved in pathogen persistence. Here, we compared the course of Brucella melitensis infection in C57BL/6 mice infected via intraperitoneal (i.p.), intranasal (i.n.) and intradermal (i.d.) route and demonstrated that the route of infection strongly impacts all of these parameters. Following i.p. and i.n. infection, most infected cells observed in the spleen or lung were F4/80+ myeloid cells. In striking contrast, infected Ly6G+ neutrophils and CD140a+ fibroblasts were also observed in the skin after i.d. infection. The virB operon encoding for the type IV secretion system is considered essential to deflecting vacuolar trafficking in phagocytic cells and allows Brucella to multiply and persist. Unexpectedly, the ΔvirB Brucella strain, which does not persist in the lung after i.n. infection, persists longer in skin tissues than the wild strain after i.d. infection. While the CD4+ T cell-mediated Th1 response is indispensable to controlling the Brucella challenge in the i.p. model, it is dispensable for the control of Brucella in the i.d. and i.n. models. Similarly, B cells are indispensable in the i.p. and i.d. models but dispensable in the i.n. model. γδ+ T cells appear able to compensate for the absence of αβ+ T cells in the i.d. model but not in the other models. Taken together, our results demonstrate the crucial importance of the route of infection for the host pathogen relationship.

Multi-drug-resistant tuberculosis (TB) is a major public health problem, concerning about half a million cases each year. Patients hardly adhere to the current strict treatment consisting of more than 10 000 tablets over a 2-year period. There is a clear need for efficient and better formulated medications. We have previously shown that nanoparticles made of cross-linked poly-β-cyclodextrins (pβCD) are efficient vehicles for pulmonary delivery of powerful combinations of anti-TB drugs. Here, we report that in addition to being efficient drug carriers, pβCD nanoparticles are endowed with intrinsic antibacterial properties. Empty pβCD nanoparticles are able to impair Mycobacterium tuberculosis (Mtb) establishment after pulmonary administration in mice. pβCD hamper colonization of macrophages by Mtb by interfering with lipid rafts, without inducing toxicity. Moreover, pβCD provoke macrophage apoptosis, leading to depletion of infected cells, thus creating a lung microenvironment detrimental to Mtb persistence. Taken together, our results suggest that pβCD nanoparticles loaded or not with antibiotics have an antibacterial action on their own and could be used as a carrier in drug regimen formulations effective against TB.