The Host Cellular Immune Response to Infection by Campylobacter Spp. and Its Role in Disease

Abstract

Campylobacter spp. are the leading cause of bacterial-derived gastroenteritis worldwide, impacting ninety-six million individuals annually. Unlike other bacterial pathogens of the gastrointestinal tract, Campylobacter spp. lack many of the classical virulence factors that are often associated with the ability to induce disease in humans, including an array of canonical secretion systems and toxins. As such, the clinical manifestations of human campylobacteriosis and its resulting gastrointestinal pathology are believed to be primarily due to the host immune response toward the bacterium. Further, while gastrointestinal infection is usually self-limiting, numerous post-infectious disorders can occur, including the development of Guillan-Barré syndrome, reactive arthritis, and irritable bowel syndrome. Because gastrointestinal disease likely results from the host immune response, the development of these post-infectious disorders may be due to dysregulation or misdirection of the same inflammatory response. As a result, it is becoming increasingly important to the Campylobacter field, and human health, that the cellular immune responses toward Campylobacter be better understood, including which immunological events are critical to the development of disease and the post-infectious disorders mentioned above. In this review, we will collectively cover the cellular immune responses across susceptible hosts to C. jejuni infection, along with the tissue pathology and post-infectious disorders which may develop.

Foodborne pathogens in the plastisphere: Can microplastics in the food chain threaten microbial food safety?

“…Amongst the PRRs, Toll-like receptors (TLR) and nucleotide oligomerization domain-like receptors (NLR) specifically bind to lipopolysaccharides (LPS), also called endotoxins. These bind to PRRs thereby generating immune responses, and are typically present in the cell wall of Gram-negative bacteria including E. coli, V. cholerae and C. jejunum (Baker-Austin et al, 2018;Callahan et al, 2021;Kaper et al, 2004). Hence, PRRs play a key role in pathogen recognition and the induction of innate effectors and inflammation (Wells et al, 2011).…”

“…In contrast to nanoplastics (NPs), which may be taken up inside the cell by transcellular transport, the predominant route for MPs is paracellular transport through tight and adherent junctions between epithelial cells (Fournier et al, 2021). Some pathogens such as V. cholerae and C. jejuni are able to increase paracellular transport by secreting proteases and altering the expression levels of junction proteins (Baker-Austin et al, 2018;Callahan et al, 2021). Similarly, pathogenic E. coli injects different effectors in the cell cytoplasm, which also impairs tight junction stability.…”

“…Yet, a pathogen may evade such destruction, and hence promote intracellular growth, by stimulating endocytosis in non-phagocytic cell types of the intestinal epithelium through specific mechanisms. This is followed by a cascade of immune reactions and eventually leads to cell death (Callahan et al, 2021). Endocytosis is also the main transport route of cholera toxin from V. cholerae (Baker-Austin et al, 2018) by GM1-ganglioside receptor binding.…”

“…As reviewed by (Kaper et al, 2004), enteropathogenic E. coli have a whole wide set of strain-specific tools which interfere with basic cell functions. C. jejuni injects invasive antigens and produces cytolethal distending toxins to induce cell cycle effects, apoptosis and inflammatory responses (Callahan et al, 2021). Furthermore, B. cereus (Jovanovic et al, 2021), S. aureus (Rajkovic, 2012) and C. perfringens secrete pore-forming toxins which cause apoptosis, necrosis and necroptosis by targeting the cell membrane (Navarro et al, 2018).…”

Battle for the histones: a secreted bacterial sirtuin from Campylobacter jejuni activates neutrophils and induces inflammation during infection

“…Campylobacter species are the leading cause of bacterial-derived gastroenteritis worldwide, infecting a projected ninety million individuals (Man, 2011; World Health Organization, 2015). While infection is often self-limiting in immunocompetent individuals, numerous post-infectious disorders can develop, including Guillain-Barré syndrome (GBS), irritable bowel syndrome (IBS), and reactive arthritis (ReA) (Callahan et al, 2021a; Reti et al, 2015). In addition to the prevalence of infection and these various outcomes, the high incidence of antibiotic resistance has led both the Centers for Disease Control and World Health Organization to classify Campylobacter spp.…”