Defense and adaptation: the complex inter-relationship between Campylobacter jejuni and mucus

Abstract

Mucus colonization is an essential early step toward establishing successful infection and disease by mucosal pathogens. There is an emerging literature implicating specific mucin sub-types and mucin modifications in protecting the host from Campylobacter jejuni infection. However, mucosal pathogens have evolved sophisticated mechanisms to breach the mucus layer and C. jejuni in particular appears to harbor specific adaptations to better colonize intestinal mucus. For example, components of mucus are chemotactic for C. jejuni and the rheological properties of mucus promote motility of the organism. Furthermore, recent studies demonstrate that mucins modulate the pathogenicity of C. jejuni in a species-specific manner and likely help determine whether these bacteria become pathogenic (as in humans), or adopt a commensal mode of existence (as in chickens and other animals). This review focuses on recent advances in understanding the complex interplay between C. jejuni and components of the mucus layer.

Keywords: Campylobacter; chickens; motility; mucins; mucus; pathogenicity.

Figure 1

Fluorescence microscopy image of C. jejuni colonization of E12 mucus. E12 cells were grown for 14 days in transwell inserts and infected with C. jejuni. The filter was excised and wrapped between two pieces of frozen liver and sections probed with DAPI (A) to reveal cell nuclei and (B) anti-Campylobacter antibodies. Mag: ×400.

Figure 2

Purified chicken intestinal mucins attenuate C. jejuni invasion depending on the region of the chicken gut from which mucins were isolated (Alemka et al., , reproduced with permission). C. jejuni was pre-incubated with mucins prior to infecting HCT-8 cells. Cae, mucin from the cecum; SI, small intestinal mucins; LI, large intestinal mucins. *Denotes significant difference compared to control. Cae p < 0.05, p < 0.005 for SI and LI. Hundred percentage mucin represents 1 mg/ml.

Figure 3

Hypothetical model of how mucus and mucins modulate the pathogenicity of C. jejuni in a species-specific manner: in mucus C. jejuni displays chemotaxis and flagellar motility toward components of mucin. The characteristic spiral shape and the ability of C. jejuni to replicate in mucus suggests an adaptation of these bacteria to the mucus milieu. Interaction with human mucin enhances bacterial binding and internalization into underlying epithelial cells. In chickens, mucin glycoproteins prevent C. jejuni association with intestinal epithelial cells, possibly by interfering with their transit through the inner mucus layer and/or onto the appropriate host cell receptors.