Table 1.

Advances in our understanding of Campylobacter jejuni

Inflammatory pathways

Innate immunity leads to persistent inflammation; adaptive immunity is required to clear infection [5]

C. jejuni infection leads to Th1 polarization [6]

C. jejuni activates MyD88 via TLR2 leading to induction of IL-6 [7]

TLR4-MyD88 and TLR4-TRIF activate dendritic cells in C. jejuni infection [8]

Innate and T-cell immunity lead to release of IFN-g, IL-17A and IL-22 to promote protection against C. jejuni [9]

C. jejuni infection disrupts TLR9 signaling, abrogating protection to DSS-induced colitis [10]

TLR2 is protective while TLR4 leads to inflammation [11]

SIGIRR-deficient mice represent a murine model of C. jejuni enterocolitis [12■]

Bacterial virulence factors

C. jejuni survives within vacuoles and produces CDT leading to cell death [13]

Alterations in C. jejuni virulence factors allow for different tissue colonization [14]

Role of microbiota

Limited defined enteric flora allows for persistent colonization with C. jejuni [5]

Reconstitution of mice with ‘murine flora’ vs ‘human flora’ confers protection to C. jejuni [15]

‘Westernized diet’ vs ‘conventional diet’ leads to heightened susceptibility to C. jejuni [15]

’Week old mice are easily colonized by C. jejuni [16]

Elevated E. coli levels allow for colonization and infection with C. jejuni [17]

Treatment with ampicillin leads to decreased E. faecalis, which allows for C. jejuni colonization [18■■]

Implications of Campylobacter in disease

Elevated inflammation makes infant mice more susceptible to C. jejuni [16]

Malnutrition increases risk for C. jejuni infection and infection is associated with growth stunting and decreased weight gain [19]

Early intestinal infections and malnutrition predispose to cognitive deficits and growth stunting [20]

Campylobacter is one of the most frequently identified pathogens in the first 2 years of life among 8 sites in the MAL-ED studies and is most

commonly associated with bloody diarrhea [20]

High C. jejuni burden is associated with lower length-for-age scores [4■■]

Heightened systemic inflammation is correlated with higher mortality for children with acute severe malnutrition; C. jejuni was one of the most frequently identified pathogens [21■]

Postinfectious complications

C. jejuni infection in rats leads to SIBO, and those developing SIBO were more likely to have stool changes (P-IBS) [22]

A significant number of C. jejuni infections lead to postinfectious sequelae [23]

Advances in diagnostics

PCR is highly sensitive and can determine pathogen burden for Campylobacter [24]

CDT, cytolethal distending toxin; P-IBS, postinfectious irritable bowel syndrome; SIBO, small intestinal bacterial overgrowth; SIGIRR, single IgG IL-1-related receptor.