Molecular Targets in Campylobacter Infections

Abstract

Human campylobacteriosis results from foodborne infections with Campylobacter bacteria such as Campylobacter jejuni and Campylobacter coli, and represents a leading cause of bacterial gastroenteritis worldwide. After consumption of contaminated poultry meat, constituting the major source of pathogenic transfer to humans, infected patients develop abdominal pain and diarrhea. Post-infectious disorders following acute enteritis may occur and affect the nervous system, the joints or the intestines. Immunocompromising comorbidities in infected patients favor bacteremia, leading to vascular inflammation and septicemia. Prevention of human infection is achieved by hygiene measures focusing on the reduction of pathogenic food contamination. Molecular targets for the treatment and prevention of campylobacteriosis include bacterial pathogenicity and virulence factors involved in motility, adhesion, invasion, oxygen detoxification, acid resistance and biofilm formation. This repertoire of intervention measures has recently been completed by drugs dampening the pro-inflammatory immune responses induced by the Campylobacter endotoxin lipo-oligosaccharide. Novel pharmaceutical strategies will combine anti-pathogenic and anti-inflammatory effects to reduce the risk of both anti-microbial resistance and post-infectious sequelae of acute enteritis. Novel strategies and actual trends in the combat of Campylobacter infections are presented in this review, alongside molecular targets applied for prevention and treatment strategies.

Metabolomic signatures of intestinal colonization resistance against Campylobacter jejuni in mice

“…Without microbial nutrient competition, these amino acids are utilized by C. jejuni for the multiplication required for gut colonization. C. jejuni utilize transporters and other uptake systems to acquire essential amino acids, including cysteine, serine, aspartate, asparagine, glutamate, glutamine, threonine, and proline ( Velayudhan et al, 2004 ; Hofreuter et al, 2006 ; Leon-Kempis Mdel et al, 2006 ; Heimesaat et al, 2023 ). Most importantly, cysteine has been shown to be essential for C. jejuni 81-176 growth in vitro ( Vorwerk et al, 2014 ; Hitchcock et al, 2022 ).…”

Molecular Pathology of Campylobacter

“…Neutrophils move from the basolateral to the apical side of the epithelium within colonic crypts, which are reliant on 12-lipoxygenase (12-LOX), a host-derived enzyme, and n-formyl peptides from bacterial sources (Murphy et al 2011). The interaction between C. jejuni and neutrophils causes complementopsonized cells to be phagocytosed, leading to the generation of reactive oxygen species (ROS), which directly kills the bacterium and causes localized tissue damage (WALAN et al 1992;Heimesaat et al 2023). Along with phagocytosis and direct cell death, a large number of neutrophil-derived antimicrobial proteins are released into the surrounding tissue, and they build up in the feces of individuals with a C. jejuni infection.…”

A broad host phage, CP6, for combating multidrug-resistant Campylobacter prevalent in poultry meat

“…Campylobacter , especially Campylobacter jejuni and Campylobacter coli , are major foodborne bacterial pathogens that can cause human gastroenteritis worldwide ( Kaakoush et al, 2015 ). The transmission of Campylobacter to humans occurs primarily through the food chain, and contaminated poultry meat is considered the major source of pathogenic transfer to humans ( García-Sánchez et al, 2018 ; Rasschaert et al, 2020 ; EI-Saadony et al, 2023 ; Heimesaat et al, 2023 ). Previous studies from around the world have estimated that 50 to 80% of all campylobacteriosis cases can be attributed to the poultry reservoir Asuming-Bediako et al, 2019 , Hailu et al, 2021 , Skarp et al, 2016 , Van Gerwe, 2012 .…”