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Introduction: In today's world, which is progressively oriented towards science and technology and facing a growing demand for skilled professionals, it becomes essential to identify the factors that encourage individuals to pursue careers in STEM fields (Science, Technology, Engineering and Mathematics). Previous research has shown that affective-motivational factors, math performance and gender influence STEM occupational and academic choices in adulthood. However, few studies examined how these factors may influence STEM choices as early as middle school. This study aims to assess how math anxiety, math self-efficacy, math performance and gender influence STEM school choices during middle school., Methods: We longitudinally assessed a group of 109 students (Year 6) over three school years, with measurements taken on three different occasions., Results: Findings indicated that individuals who made an STEM school choice experienced lower math anxiety, higher self-efficacy and math performance and were predominantly male. Furthermore, the results indicated that both math anxiety in Year 7 and self-efficacy in Year 6 made the most substantial unique contributions to the STEM school choice., Conclusion: Math anxiety and math self-efficacy seem to be both crucial in influencing middle school students' STEM choices, offering new perspectives for early interventions aimed at promoting more informed school choices., (© 2024 The Author(s). British Journal of Educational Psychology published by John Wiley & Sons Ltd on behalf of British Psychological Society.)

Previous research has suggested that math anxiety may contribute to poor math performance by interfering with working memory. However, only a limited number of studies investigated the mediating role of working memory in the math anxiety-math performance link in school-aged children. Unlike math anxiety, ego-resiliency is a personality resource that promotes the management of challenges and has been positively associated with math performance and negatively with anxiety. Nevertheless, there is still limited understanding regarding the specific role of ego-resiliency in math learning and how it relates to math anxiety. This study aimed to investigate conjunctly the interplay between primary school children's ego-resiliency, math anxiety, working memory, and performance on two different math tasks (i.e., arithmetic task and word problem-solving task), after controlling for general anxiety and age. The study involved 185 Italian children from grades 3 to 5. Serial multi-mediational analyses revealed that: (1) ego-resiliency has a positive indirect effect on math achievement through two paths - math anxiety, and math anxiety and working memory; (2) the study replicated previous findings showing that working memory partially mediated the relationship between math anxiety and math performance; (3) similar patterns of results were found for both math skills. The study identifies ego-resiliency as a possible protective factor in the development of math anxiety and suggests that ego-resiliency could be worth considering when designing interventions aimed at reducing negative emotions towards mathematics., (© 2024. The Author(s).)

According to the processing efficiency theory (PET), math anxiety would interfere with working memory resources, negatively affecting mathematical abilities. To date, few studies have explored how the interaction between math anxiety and working memory would affect different types of math tasks, especially in primary school children. Therefore, the purpose of this study was to explore whether the interplay between math anxiety and working memory would influence performance in numerical operations (i.e., math fluency task) and mathematical reasoning (i.e., math reasoning task) in a group of primary school children (N = 202). Results showed that visuospatial working memory appeared to moderate the relationship between math anxiety and math performance when the math fluency task was considered, indicating that participants with higher levels of working memory were more negatively affected by math anxiety. No interaction effect was found for the math reasoning task in which students' scores were explained only by visuospatial working memory. The findings suggest that math anxiety and visuospatial working memory interact to influence performance in the math fluency task and that this effect may vary depending on the strategies used to complete the task. On the other hand, results on the math reasoning task showed that visuospatial working memory continues to have a positive effect on the math performance independently of math anxiety. The implications in the educational setting are discussed, pointing to the importance of monitoring and intervention studies on affective factors., (Copyright © 2023 Elsevier Inc. All rights reserved.)

School closures because of the COVID-19 emergency forced a rapid transition to distance learning worldwide. In this study, we investigated teachers' experiences with distance learning during the first Italian lockdown. A sample of 270 primary and secondary teachers answered a semi-structured questionnaire administered between April and May 2020. Didactic modalities, students' and teachers' difficulties with distance learning, and teachers' feelings during school closure were investigated through open-ended questions. Content analysis indicated that most teachers adopted both synchronous and asynchronous modalities, which resembled the traditional classroom learning environment. Moreover, technological weaknesses (lack of proper digital equipment and poor digital skills) and lack of interactions appeared to be the main threats to the quality of distance learning. The implementation of distance learning in primary schools emerged as more challenging than in secondary education. Furthermore, most teachers experienced negative feelings during online teaching. However, 13% of the sample reported a sense of resilience and opportunity. Particularly, older teachers reported more resilience compared with younger teachers, indicating the importance of experience in managing stressful teaching events. Overall, findings suggest that-in this novel educational environment-teachers' role has changed significantly, placing strong emphasis on the ability to encourage communication, discussion, and contact with students. Future work should focus on how information and communications technology could sustain meaningful interactions between students and teachers, especially in primary education., Competing Interests: Conflict of interestThe authors declare that they have no conflict of interest., (© The Author(s), under exclusive licence to Springer Nature B.V. 2022, Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.)

Children's performance in arithmetic word problems (AWPs) predicts their academic success and their future employment and earnings in adulthood. Understanding the nature and difficulties of interpreting and solving AWPs is important for theoretical, educational, and social reasons. We investigated the relation between primary school children's performance in different types of AWPs and their basic cognitive abilities (reading comprehension, fluid intelligence, inhibition, and updating processes). The study involved 182 fourth- and fifth-graders. Participants were administered an AWP-solving task and other tasks assessing fluid intelligence, reading comprehension, inhibition, and updating. The AWP-solving task included comparison problems incorporating either the adverb more than or the adverb less than, which demand consistent or inconsistent operations of addition or subtraction. The results showed that consistent problems were easier than inconsistent problems. Efficiency in solving inconsistent problems is related to inhibition and updating. Moreover, our results seem to indicate that the consistency effect is related to updating processes' efficiency. Path analyses showed that reading comprehension was the most important predictor of AWP-solving accuracy. Moreover, both executive functions-updating and inhibition-had a distinct and significant effect on AWP accuracy. Fluid intelligence had both direct and indirect effects, mediated by reading comprehension, on the overall measure of AWP performance. These domain-general factors are important factors in explaining children's performance in solving consistent and inconsistent AWPs., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Tuberculosis (TB), caused by Mycobacterium tuberculosis (Mtb) is one of the most prevalent lung infections of humans and kills ~1.7 million people each year. TB pathophysiology is complex with a central role played by granuloma where a delicate balance takes place to both constrain bacilli and prevent excessive inflammation that may destroy lung functions. Neutrophils reach the lung in waves following first encounter with bacilli and contribute both to early Mtb elimination and late deleterious inflammation. The hypoxic milieu where cells and bacilli cohabit inside the granuloma favors metabolism changes and the impact on TB infection needs to be more thoroughly understood. At the cellular level while the key role of the alveolar macrophage has long been established, behavior of neutrophils in the hypoxic granuloma remains poorly explored. This review will bring to the front new questions that are now emerging regarding neutrophils activity in TB. Are different neutrophil subsets involved in Mtb infection and how? How do neutrophils and close relatives contribute to shaping the granuloma immune environment? What is the role of hypoxia and hypoxia induced factors inside granuloma on neutrophil fate and functions and TB pathophysiology? Addressing these questions is key to the development of innovative host-directed therapies to fight TB.

Achieving the control of bovine tuberculosis (bTB) would require the discovery of an efficient combined immunodiagnostic and vaccine strategy. Since in vivo experiments on cattle are not ethically and economically acceptable there is a need for a cost-effective animal model capable of reproducing, as closely as possible, the physiopathology of bTB to (i) better characterize the cellular and molecular features of bTB immunopathogenesis and (ii) screen preclinical vaccine candidates. To develop such a model, we focused on the C3HeB/FeJ Kramnik's mouse forming hypoxic, encapsulated granulomas with a caseous necrotic center following Mycobacterium tuberculosis infection. Our work represents the first investigation on C3HeB/FeJ interaction with M. bovis, the main agent of bTB. Detailed histopathological analysis of C3HeB/FeJ lung lesions development following aerogenous M. bovis infection unraveled a bimodal evolution of the pathology. The C3HeB/FeJ recapitulated all the hallmarks of classical bovine lung granulomas but also developed, to some extend, lethal necrotic large lesions characterized by high mycobacterial and neutrophil load, and an inefficient collagen-driven lesion encapsulation. Interestingly these rapidly invasive pneumonia lesions, occurring in a constant percentage of the mice, shared all features with some exacerbated lung lesions that we and others have observed in lungs of cattle naturally or experimentally infected with M. bovis. Together, our findings demonstrate the relevance of the C3HeB/FeJ mouse as a comprehensive model to study bTB immunopathology that could be used for further vaccine therapies in the future.

During chronic infection with Mycobacterium tuberculosis (Mtb), bacilli multiplication is constrained within lung granulomas until excessive inflammation destroys the lung. Neutrophils are recruited early and participate in granuloma formation, but excessive neutrophilia exacerbates the tuberculosis disease. Neutrophils thus appear as potential targets for therapeutic interventions, especially in patients for whom no antibiotic treatment is possible. Signals that regulate neutrophil recruitment to the lung during mycobacterial infection need to be better understood. We demonstrated here, in the mouse model, that neutrophils were recruited to the lung in two waves after intranasal infection with virulent Mtb or the live attenuated vaccine strain Bacillus Calmette Guérin (BCG). A first wave of neutrophils was swiftly recruited, followed by a subsequent adaptive wave that reached the lung together with IFN-γ- and IL-17A-producing T cells. Interestingly, the second neutrophil wave did not participate to mycobacteria control in the lung and established contacts with T cells. The adaptive wave was critically dependent on the expression of IL-17RA, the receptor for IL-17A, expressed in non-hematopoietic cells. In absence of this receptor, curtailed CXCL-1 and 5 production in the lung restrained neutrophil recruitment. CXCL-1 and 5 instillation reconstituted lung neutrophil recruitment in BCG-infected IL17RA-/- mice.

Neutrophils participate in the control of mycobacterial infection both by directly eliminating bacilli and by interacting with macrophages and dendritic cells (DCs). Despite host defenses, slow-growing mycobacteria can persist in the host for decades, mostly inside macrophages and DCs, and eventually destroy tissues after exacerbated inflammation. IL-17A-driven neutrophil recruitment may participate in this process. We report that mouse bone marrow-derived DCs infected with live Mycobacterium bovis Bacillus Calmette-Guérin (BCG) produced large amounts of CXCL1 and CXCL2, and attracted neutrophils. After physical contact with DCs infected with live BCG, the neutrophils produced large quantities of the immunosuppressive cytokine IL-10 via the MyD88 and spleen tyrosine kinase pathways. The CD11b integrin was involved in this neutrophil-DC interaction and allowed IL-10 production. TCR OVA transgenic mice immunized with a BCG strain producing OVA mounted an OVA-specific Th17 and Th1 CD4 response. Interestingly, IL-10-producing neutrophils specifically shut down IL-17A production by Th17 CD4 cells, but not IFN-γ production by Th1 cells. This was due to Th17 CD4 cell-restricted expression of the receptor for IL-10. After neutrophil depletion, total mouse lung cells produced less IL-10 but more IL-17A; IFN-γ production was not affected. Therefore, we suggest that during mycobacterial infection, regulatory neutrophils are instructed by infected reservoir DCs to produce IL-10 that specifically targets IL-10Rα-expressing Th17 CD4 T cells. This could be important to control the otherwise exuberant Th17 response.

Mycobacterium tuberculosis modulates host immune responses through proteins and complex glycolipids. Here, we report that the glycosylphosphatidylinositol anchor phosphatidyl-myo-inositol hexamannosides PIM(6) or PIM(2) exert potent anti-inflammatory activities. PIM strongly inhibited the Toll-like receptor (TLR4) and myeloid differentiation protein 88 (MyD88)-mediated release of NO, cytokines, and chemokines, including tumor necrosis factor (TNF), interleukin 12 (IL-12) p40, IL-6, keratinocyte-derived chemokine, and also IL-10 by lipopolysaccharide (LPS)-activated macrophages. This effect was independent of the presence of TLR2. PIM also reduced the LPS-induced MyD88-independent, TIR domain-containing adaptor protein inducing interferon beta (TRIF)-mediated expression of co-stimulatory receptors. PIM inhibited LPS/TLR4-induced NFkappaB translocation. Synthetic PIM(1) and a PIM(2) mimetic recapitulated these in vitro activities and inhibited endotoxin-induced airway inflammation, TNF and keratinocyte-derived chemokine secretion, and neutrophil recruitment in vivo. Mannosyl, two acyl chains, and phosphatidyl residues are essential for PIM anti-inflammatory activity, whereas the inosityl moiety is dispensable. Therefore, PIM exert potent antiinflammatory effects both in vitro and in vivo that may contribute to the strategy developed by mycobacteria for repressing the host innate immunity, and synthetic PIM analogs represent powerful anti-inflammatory leads.

Acute cigarette smoke exposure of the airways (two cigarettes twice daily for three days) induces acute inflammation in mice. In this study, we show that airway inflammation is dependent on Toll-like receptor 4 and IL-1R1 signaling. Cigarette smoke induced a significant recruitment of neutrophils in the bronchoalveolar space and pulmonary parenchyma, which was reduced in TLR4-, MyD88-, and IL-1R1-deficient mice. Diminished neutrophil influx was associated with reduced IL-1, IL-6, and keratinocyte-derived chemokine levels and matrix metalloproteinase-9 activity in the bronchoalveolar space. Further, cigarette smoke condensate (CSC) induced a macrophage proinflammatory response in vitro, which was dependent on MyD88, IL-1R1, and TLR4 signaling, but not attributable to LPS. Heat shock protein 70, a known TLR4 agonist, was induced in the airways upon smoke exposure, which probably activates the innate immune system via TLR4/MyD88, resulting in airway inflammation. CSC-activated macrophages released mature IL-1beta only in presence of ATP, whereas CSC alone promoted the TLR4/MyD88 signaling dependent production of IL-1alpha and pro-IL-1beta implicating cooperation between TLRs and the inflammasome. In conclusion, acute cigarette exposure results in LPS-independent TLR4 activation, leading to IL-1 production and IL-1R1 signaling, which is crucial for cigarette smoke induced inflammation leading to chronic obstructive pulmonary disease with emphysema.

Recent studies on endotoxin/lipopolysaccharide (LPS)-induced acute inflammatory response in the lung are reviewed. The acute airway inflammatory response to inhaled endotoxin is mediated through Toll-like receptor 4 (TLR4) and CD14 signalling as mice deficient for TLR4 or CD14 are unresponsive to endotoxin. Acute bronchoconstriction, tumour necrosis factor (TNF), interleukin (IL)-12 and keratinocyte-derived chemokine (KC) production, protein leak and neutrophil recruitment in the lung are abrogated in mice deficient for the adaptor molecules myeloid differentiation factor 88 (MyD88) and Toll/Interleukin-1 receptor (TIR)-domain-containing adaptor protein (TIRAP), but independent of TIR-domain-containing adaptor-inducing interferon-beta (TRIF). In particular, LPS-induced TNF is required for bronchoconstriction, but dispensable for inflammatory cell recruitment. Lipopolysaccharide induces activation of the p38 mitogen-activated protein kinase (MAPK). Inhibition of pulmonary MAPK activity abrogates LPS-induced TNF production, bronchoconstriction, neutrophil recruitment into the lungs and broncho-alveolar space. In conclusion, TLR4-mediated, bronchoconstriction and acute inflammatory lung pathology to inhaled endotoxin are dependent on TLR4/CD14/MD2 expression using the adapter proteins TIRAP and MyD88, while TRIF, IL-1R1 or IL-18R signalling pathways are dispensable. Further downstream in this axis of signalling, TNF blockade reduces only acute bronchoconstriction, while MAPK inhibition abrogates completely endotoxin-induced inflammation.

Mycobacterium tuberculosis lipomannans (LMs) modulate the host innate immune response. The total fraction of Mycobacterium bovis BCG LM was shown both to induce macrophage activation and pro-inflammatory cytokines through Toll-like receptor 2 (TLR2) and to inhibit pro-inflammatory cytokine production by lipopolysaccharide (LPS)-activated macrophages through a TLR2-independent pathway. The pro-inflammatory activity was attributed to tri- and tetra-acylated forms of BCG LM but not the mono- and di-acylated ones. Here, we further characterize the negative activities of M. bovis BCG LM on primary murine macrophage activation. We show that di-acylated LMs exhibit a potent inhibitory effect on cytokine and NO secretion by LPS-activated macrophages. The inhibitory activity of mycobacterial mannose-capped lipoarabino-mannans on human phagocytes was previously attributed to their binding to the C-type lectins mannose receptor or specific intracellular adhesion molecule-3 grabbing nonintegrin (DC-SIGN). However, we found that di-acylated LM inhibition of LPS-induced tumor necrosis factor secretion by murine macrophages was independent of TLR2, mannose receptor, or the murine ortholog SIGNR1. We further determined that tri-acyl-LM, an agonist of TLR2/TLR1, promoted interleukin-12 p40 and NO secretion through the adaptor proteins MyD88 and TIRAP, whereas the fraction containing tetra-acylated LM activated macrophages in a MyD88-dependent fashion, mostly through TLR4. TLR4-dependent pro-inflammatory activity was also seen with M. tuberculosis LM, composed mostly of tri-acylated LM, suggesting that acylation degree per se might not be sufficient to determine TLR2 versus TLR4 usage. Therefore, LM acylation pattern determines the anti-inflammatory versus pro-inflammatory effects of LM through different pattern recognition receptors or signaling pathways and may represent an additional mean of regulating the host innate immunity by mycobacteria.

MyD88, the common adapter involved in TLR, IL-1, and IL-18 receptor signaling, is essential for the control of acute Mycobacterium tuberculosis (MTB) infection. Although TLR2, TLR4, and TLR9 have been implicated in the response to mycobacteria, gene disruption for these TLRs impairs only the long-term control of MTB infection. Here, we addressed the respective role of IL-1 and IL-18 receptor pathways in the MyD88-dependent control of acute MTB infection. Mice deficient for IL-1R1, IL-18R, or Toll-IL-1R domain-containing adaptor protein (TIRAP) were compared with MyD88-deficient mice in an acute model of aerogenic MTB infection. Although primary MyD88-deficient macrophages and dendritic cells were defective in cytokine production in response to mycobacterial stimulation, IL-1R1-deficient macrophages exhibited only a reduced IL-12p40 secretion with unaffected TNF, IL-6, and NO production and up-regulation of costimulatory molecules CD40 and CD86. Aerogenic MTB infection of IL-1R1-deficient mice was lethal within 4 wk with 2-log higher bacterial load in the lung and necrotic pneumonia but efficient pulmonary CD4 and CD8 T cell responses, as seen in MyD88-deficient mice. Mice deficient for IL-18R or TIRAP controlled acute MTB infection. These data demonstrate that absence of IL-1R signal leads to a dramatic defect of early control of MTB infection similar to that seen in the absence of MyD88, whereas IL-18R and TIRAP are dispensable, and that IL-1, together with IL-1-induced innate response, might account for most of MyD88-dependent host response to control acute MTB infection.