Abstract
The intestinal epithelium deploys multiple defense systems against microbial infection to sense bacterial components and danger alarms, as well as to induce intracellular signal transduction cascades that trigger both the innate and the adaptive immune systems, which are pivotal for bacterial elimination. However, many enteric bacterial pathogens, including Shigella, deliver a subset of virulence proteins (effectors) via the type III secretion system (T3SS) that enable bacterial evasion from host immune systems; consequently, these pathogens are able to efficiently colonize the intestinal epithelium. In this review, we present and select recently discovered examples of interactions between Shigella and host immune responses, with particular emphasis on strategies that bacteria use to manipulate inflammatory outputs of host-cell responses such as cell death, membrane trafficking, and innate and adaptive immune responses.
Highlights
Shigella is a causative agent of bacillary dysentery, which leads to severe bloody and mucous diarrhea
When bacteria invade and multiply within host cells, they release bacterial components [e.g., lipopolysaccharide (LPS) and peptidoglycan (PGN)] and T3SS components, and further cause infection-associated cellular damage. These are recognized as pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs) by recognition receptors, such as toll-like receptors (TLRs), nucleotide-binding oligomerization domain-like receptors (NLRs), AIM2-like receptors (ALRs), and RIG-like receptors, and trigger host immune responses against bacterial infection
Shigella exploits calpain activation and mitochondrial function to suppress the innate immune response without inducing host-cell death [36]. These results indicate that Shigella deploys a sophisticated strategy that controls the delicate balance of hostcell death until Shigella has succeeded in primary colonization and proliferation within epithelial cells
Summary
Shigella is a causative agent of bacillary dysentery, which leads to severe bloody and mucous diarrhea (shigellosis). Shigella injects a subset of effectors (secreted virulence proteins) via a type III secretion system (T3SS) (protein delivery system) into host cells, allowing the bacterium to invade, multiply within the intestinal epithelium, and subvert cellular and immune functions during bacterial internalization [1, 2]. When Shigella cells are ingested via the oral route, the bacteria move down to the colon and rectum, and preferentially enter the M cells overlying the follicle-associated epithelium of the Peyer’s patches [3, 4] (Figure 1). Shigella cells that are released from dying macrophages subsequently enter the surrounding epithelium via the basolateral surface. The Shigella cells are surrounded by a vacuolar membrane, but the bacteria rapidly disrupt this membrane and
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