While the intestinal immune system coexists[DPM1] with commensal bacterial flora through immunological tolerance, invading microorganisms are recognized and properly eliminated. However, it remains unknown what kinds of cells in the intestine initiate immune responses and how they activate host immunity. Recently, we identified a subset of CD11c^hiCD11b^hi lamina propria (LP) dendritic cells (DCs) as TLR5-expressing cells, which have the ability to activate adaptive immune responses. The LPDCs induced antigen-specific Th17 cells as well as Th1 cells in a TLR5-dependent manner. In addition, they acted on naïve B cells to induce their development to immunoglobulin A (IgA)⁺ plasma cells in response to flagellin, and such IgA⁺ plasma cell generation took place in a gut-associated lymphoid tissue (GALT)-independent fashion. Our findings demonstrate unique properties of LPDCs and the importance of TLR5 for adaptive immunity in the intestine. We also generated and examined mutant mice of ATG16L1. ATG16L1 is a component of autophagy machinery and has been reported to be a candidate gene responsible for susceptibility to Crohn's disease. We discuss a novel role for autophagy in the regulation of the inflammatory immune responses in the intestine.

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The bacterial community of the bowel of humans and other animals derives carbon and energy sources from the diet and secretions of the host. The metabolic products generated by the community, and the antigens and other molecules associated with the bacterial cells, interact with the bowel mucosa. Some bacterial products are absorbed from the bowel and affect the systemic organs of the body. The interactions that occur within the bacterial community and between the community and food components and host tissues comprise a highly interactive web. It is concluded that this interactive matrix characteristic of the bowel ecosystem may be studied by detailed autecological and synecological experiments. The results of these studies could be used to construct a general blueprint of the healthy bowel and might reveal biomarkers predictive of health or disease.

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An assay method was established for estimation of dry-resistance of Salmonella. Environmental isolates of Salmonella enterica spp., including S. Enteritidis were grown to the logarithmic phase, washed and re-suspended in saline or Luria-Bertani (LB) medium, followed by drying overnight in an automatic dry-keeper at room temperature. The dried bacteria were recovered by mixing with ice-cold PBS, suspended, and examined for viability by colony-forming activity. A pathogenic clone of S. Enteritidis, SECl#15-1, was not viable in saline alone but maintained its viability in LB medium, suggesting it requires nutrients for the acquisition of dry-resistance. Addition of lactoferrin or apolactoferrin to the bacterial suspension in 20% LB medium prior to the dry-protocol decreased the viability of SECl#15-1 in a dose-dependent manner. However, lactoferrin showed no effect on the growth of SECl#15-1 in liquid culture with LB or M9 medium, suggesting that it exerts bactericidal effects under dry but not under wet conditions. Besides, Salmonella spp. other than S. Emteritidis, such as S. Typhimurium, S. Oranienburg, S. Weltevreden, S. Johannesburg, and S. Infantis, also showed dry-resistance, which was significantly inhibited by lactoferrin and almost entirely by apolactoferrin. These results suggest that lactoferrin inhibits the acquisition of dry-resistance by Salmonella spp., suggesting that there is a possible use for lactoferrin in the control of Salmonella food-poisoning as an additive in dry food.

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