A scoping review of supports on college and university campuses for autistic post-secondary students

Given the demand to better address the principles of equity, diversity, inclusion, and accessibility in higher education, research into both barriers and promising practices to support autistic students on post-secondary campuses has advanced significantly in the last decade. The objective of this scoping review is to identify, map, and characterize literature that enumerates and describes supports for autistic post-secondary students. This scoping review was limited to peer-reviewed research published between January 2012 and May 2022, in these databases: Web of Science, PsycINFO, Medline, EMBASE, ERIC, Social Work Abstracts, Social Services Abstracts, and EMCARE. The review aligns to Joanna Briggs Institute methodology for scoping reviews and includes consultation with an expert panel made up of the Autistic Community Partners–four autistic individuals with postsecondary experience who acted as co-researchers. Literature on creating accessible campuses were mapped in three ways: (1) through the four domains of the PASS Taxonomy; (2) ten support categories characterizing types of supports, and (3) nine emergent themes, based on autistic experiences on support and campus navigation, were inductively and iteratively coded throughout process. This review summarizes both areas that have been researched and under-studied areas in the literature that act as contributors or challenges for autistic students on postsecondary campuses. It was also the first scoping review, to our knowledge, to integrate lived experience within the methods and results analysis to describe the current state of the evidence on post-secondary campuses. Mapping the literature in known and emerging categories indicated that broad categories of support are experienced variably by autistic students. Findings provide multiple avenues for future research

Innate Immune Memory and the Host Response to Infection

Unlike the adaptive immune system, the innate immune system has classically been characterized as being devoid of memory functions. However, recent research shows that innate myeloid and lymphoid cells have the ability to retain memory of prior pathogen exposure and become primed to elicit a robust, broad-spectrum response to subsequent infection. This phenomenon has been termed innate immune memory or trained immunity. Innate immune memory is induced via activation of pattern recognition receptors and the actions of cytokines on hematopoietic progenitors and stem cells in bone marrow and innate leukocytes in the periphery. The trained phenotype is induced and sustained via epigenetic modifications that reprogram transcriptional patterns and metabolism. These modifications augment antimicrobial functions, such as leukocyte expansion, chemotaxis, phagocytosis, and microbial killing, to facilitate an augmented host response to infection. Alternatively, innate immune memory may contribute to the pathogenesis of chronic diseases, such as atherosclerosis and Alzheimer\u27s disease

Immunobiology and Application of Toll-Like Receptor 4 Agonists to Augment Host Resistance to Infection

Infectious diseases remain a threat to critically ill patients, particularly with the rise of antibiotic-resistant bacteria. Septic shock carries a mortality of up to ∼40% with no compelling evidence of promising therapy to reduce morbidity or mortality. Septic shock survivors are also prone to nosocomial infections. Treatment with toll-like receptor 4 (TLR4) agonists have demonstrated significant protection against common nosocomial pathogens in various clinically relevant models of infection and septic shock. TLR4 agonists are derived from a bacteria cell wall or synthesized de novo, and more recently novel small molecule TLR4 agonists have also been developed. TLR4 agonists augment innate immune functions including expansion and recruitment of innate leukocytes to the site of infection. Recent studies demonstrate TLR4-induced leukocyte metabolic reprogramming of cellular metabolism to improve antimicrobial function. Metabolic changes include sustained augmentation of macrophage glycolysis, mitochondrial function, and tricarboxylic acid cycle flux. These findings set the stage for the use of TLR4 agonists as standalone therapeutic agents or antimicrobial adjuncts in patient populations vulnerable to nosocomial infections

β-Glucan Induces Distinct and Protective Innate Immune Memory in Differentiated Macrophages

Bacterial infections are a common and deadly threat to vulnerable patients. Alternative strategies to fight infection are needed. β-Glucan, an immunomodulator derived from the fungal cell wall, provokes resistance to infection by inducing trained immunity, a phenomenon that persists for weeks to months. Given the durability of trained immunity, it is unclear which leukocyte populations sustain this effect. Macrophages have a life span that surpasses the duration of trained immunity. Thus, we sought to define the contribution of differentiated macrophages to trained immunity. Our results show that β-glucan protects mice from infection by augmenting recruitment of innate leukocytes to the site of infection and facilitating local clearance of bacteria, an effect that persists for more than 7 d. Adoptive transfer of macrophages, trained using β-glucan, into naive mice conferred a comparable level of protection. Trained mouse bone marrow-derived macrophages assumed an antimicrobial phenotype characterized by enhanced phagocytosis and reactive oxygen species production in parallel with sustained enhancements in glycolytic and oxidative metabolism, increased mitochondrial mass, and membrane potential. β-Glucan induced broad transcriptomic changes in macrophages consistent with early activation of the inflammatory response, followed by sustained alterations in transcripts associated with metabolism, cellular differentiation, and antimicrobial function. Trained macrophages constitutively secreted CCL chemokines and robustly produced proinflammatory cytokines and chemokines in response to LPS challenge. Induction of the trained phenotype was independent of the classic β-glucan receptors Dectin-1 and TLR-2. These findings provide evidence that β-glucan induces enhanced protection from infection by driving trained immunity in macrophages