The intracellular Nod-like proteins or receptors are a family of sensors of intracellularly encountered microbial motifs and 'danger signals' that have emerged as being critical components of the innate immune responses and of inflammation in mammals. Several Nod-like receptors, including Nod1, Nod2, NALP3, Ipaf and Naip, are strongly associated with host responses to intracellular invasion by bacteria or the intracellular presence of specific bacterial products. An additional key function of Nod-like receptors is in inflammatory conditions, which has been emphasized by the identification of several different mutations in the genes encoding Nod1, Nod2 and NALP3 that are associated with susceptibility to inflammatory disorders. Those and other issues related to the Nod-like receptor family are discussed here.

Recent evidence has suggested that signals other than those from Toll-like receptors (TLRs) could contribute to the elicitation of antigen-specific immunity. Therefore, we examined the role of the Nod-like receptor (NLR) family member, Nod1, in the generation of adaptive immune responses. Our findings show that innate immune sensing of peptidoglycan by Nod1 is key for priming antigen-specific T cell immunity and subsequent antibody responses in vivo. Nod1 stimulation alone was sufficient to drive antigen-specific immunity with a predominant Th2 polarization profile. In conjunction with TLR stimulation, however, Nod1 triggering was required to instruct the onset of Th1 and Th2 as well as Th17 immune pathways. Cells outside of the hematopoietic lineage provided the early signals necessary to orchestrate the development of Nod1-dependent immune responses. These findings highlight Nod1 as a key innate immune trigger in the local tissue microenvironment that drives the development of adaptive immunity.

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A model permitting the establishment of persistentHelicobacter pylori infection in mice was recently described. To evaluate murine immune responses to H. pylori infection, specific-pathogen-free Swiss mice (n = 50) were intragastrically inoculated with 1.2 × 107 CFU of a mouse-adapted H. pylori isolate (strain SS1). Control animals (n= 10) received sterile broth medium alone. Animals were sacrificed at various times, from 3 days to 16 weeks postinoculation (p.i.). Quantitative culture of gastric tissue samples from inoculated mice demonstrated bacterial loads of 4.0 × 104 to 8 × 106 CFU per g of tissue in the animals. Infected mice had H. pylori-specific immunoglobulin M (IgM) and IgG antibodies in serum (at day 3 p.i.) and IgG and IgA antibodies in their gastric contents (weeks 4 and 16 p.i.) and saliva (week 16 p.i.). Mucosal IgM antibodies were not detected. Histological examination of the gastric mucosae from control and infected mice revealed mild chronic gastritis, characterized by the presence of polymorphoneutrophil cell infiltrates and submucosal lymphoid aggregates, in infected animals at 16 weeks p.i. Differences in the quantities of IgG1 and IgG2a subclass antibodies detected in the sera of mouse strains (Swiss, BALB/c, and C57BL/6) infected by H. pylori suggested that host factors influence the immune responses induced against this bacterium in the host. In conclusion, immune responses to H. pylori infection in mice, like those in chronically infected humans, appear to be ineffective in resolving the infection.

The motility of four strains of Campylobacter jejuni in solutions of varying viscosity was measured and compared to that of a number of conventional rod-shaped bacteria (CRSB). All the bacteria tested showed an initial increase in velocity in the low viscosity solutions--between 1 and 3 centipoise (1 P = 0.1 Pa s). However, only the campylobacters were actively motile in highly viscous solutions with velocities ranging from 60 to 100 micron s-1. All strains of C. jejuni tested showed three separate peaks of motility as the viscosity of the solution was increased. A higher proportion of C. jejuni cells exhibited longer path lengths when the viscosity of the surrounding medium was increased from 1.4 to 57 cP. The findings of the study suggest that C. jejuni has a motility suited to movement in a viscous environment, and that this ability might provide the organism with an ecological advantage when in intestinal mucus. It is proposed that the mechanism of motility changes depending on the viscosity of the supporting environment.