Recent work revealed that Dar is an enlargement of rectal epithelial cells K/K′, F, U and B [42]. Genetic analysis has shown that host-encoded sugar transporters and acyltransferases are required for microbial attachment to the anus and induction of the Dar phenotype [43]. In addition, the swelling response requires an extracellular-regulated kinase (ERK) signalling pathway, as does inflammation in mammalian cells [43,44]. These results provided a cellular explanation

for the Dar phenotype, and revealed for the first time a role for the rectal epithelium in the host response to infection. Interestingly, forward genetic screens for mutants defective in the swelling response to M. nematophilum identified the HOX gene egl-5. EGL-5 is required in the rectal epithelial cells for the transcription of the ERK homologous Panobinostat concentration gene mpk-1[45]. S. aureus infection also causes a swelling response in the anal region, although in this case the involvement

of the rectal epithelial cells is still conjecture. Despite having a defective transcriptional host response to S. aureus infection, egl-5 mutants are not defective in the swelling response to S. aureus[9]. In contrast, the β-catenin gene bar-1, PLX4032 which acts upstream of egl-5 during Wnt signal transduction, is required both for the swelling response and the transcriptional host response to S. aureus infection (J. E. Irazoqui and F. M. Ausubel, unpublished). Thus, even if the same cells were involved in the responses to M. nematophilum Thalidomide and S. aureus, the signalling pathways required for cell swelling are distinct. Further work is required to identify the components of each different pathway. Several genes induced during infection with S. aureus or P. aeruginosa are expressed in the rectal gland, a group of cells directly apposed to the rectum that are thought to secrete molecules into the rectal lumen [9,10] (J. E. Irazoqui and F. M. Ausubel, unpublished). This is consistent with a potential role for rectal gland cells in secretion of immune defence molecules into the rectal lumen. Further study is required to test this hypothesis. Although it is clear that C.

elegans lacks a bona fide circulatory system with sessile professional phagocytes, C. elegans does have phagocytes that reside in its body cavity, the pseudocoelom. Three pairs of static coelomocytes are located in ventral anterior, ventral posterior and dorsal posterior locations, where they constitutively endocytose pseudocoelomic fluid [46]. The coelomocytes have been proposed to function in immune surveillance, although direct experimental evidence is lacking [46]. The collagenous cuticle that encases the C. elegans body provides a highly impermeable physical barrier with the environment. However, some bacteria have learned to exploit this surface to their advantage. Forward genetic analysis has identified components of the cuticle required for M. nematophilum binding and for Yersinia biofilm formation [47,48].