title: MyD88 deficiency alters expression of antimicrobial factors in mouse salivary glands.
abstract: The surfaces of oral mucosa are protected from infections by antimicrobial proteins and natural immunoglobulins that are constantly secreted in saliva, serving as principal innate immune defense in the oral cavity. MyD88 is an important adaptor protein for signal transduction downstream of Toll-like receptors and TACI, receptors for regulation of innate immunity and B cell responses, respectively. Although MyD88-mediated signaling has a regulatory role in the intestinal mucosal immunity, its specific role in the oral cavity has remained elusive. In the present study, we assessed the influence of MyD88 deficiency on the oral innate defense, particularly the expression of antimicrobial proteins in salivary glands and production of salivary basal immunoglobulins, in mice. Microarray analysis of the whole tissues of submandibular glands revealed that the expression of several genes encoding salivary antimicrobial proteins, such as secretory leukocyte peptidase inhibitor (SLPI), S100A8, and lactotransferrin, was reduced due to MyD88 deficiency. Histologically, SLPI-expressing acinar cells were evidently decreased in the glands from MyD88 deficient mice compared to wild-type mice. Flow cytometric analysis revealed that B cell populations, including B-1 cells and IgA+ plasma cells, residing in submandibular glands were increased by MyD88 deficiency. The level of salivary anti-phosphorylcholine IgA was elevated in MyD88 deficient mice compared to wild-type mice. Thus, this study provides a detailed description of the effect of MyD88 deficiency on expression of several salivary antimicrobial factors in mice, illustrating the role for MyD88-mediated signaling in the innate immune defense in the oral cavity.
authors.affiliation: Department of Oral Microbiology, Division of Oral Infections and Health Sciences, Asahi University School of Dentistry, Gifu, Japan.
authors.forename: Takeshi
authors.initials: T
authors.lastname: Into
authors.affiliation: Department of Oral Anatomy, Division of Oral Structure, Function and Development, Asahi University School of Dentistry, Gifu, Japan.
authors.forename: Toshiya
authors.initials: T
authors.lastname: Takigawa
authors.affiliation: Laboratory of Genomics and Proteomics, National Center for Geriatrics and Gerontology (NCGG), Aichi, Japan.
authors.forename: Shumpei
authors.initials: S
authors.lastname: Niida
authors.affiliation: Laboratory of Oral Molecular Microbiology, Department of Oral Pathobiological Science, Hokkaido University Graduate School of Dental Medicine, Hokkaido, Japan.
authors.forename: Ken-ichiro
authors.initials: K
authors.lastname: Shibata
mesh_terms: D000818:Animals; D001402:B-Lymphocytes / Q000378:metabolism; D040501:Calgranulin A / Q000235:genetics* / Q000378:metabolism; D023082:Defensins / Q000235:genetics / Q000378:metabolism; D005434:Flow Cytometry; D020869:Gene Expression Profiling; D007070:Immunoglobulin A / Q000378:metabolism; D007781:Lactoferrin / Q000235:genetics* / Q000378:metabolism; D008297:Male; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008856:Microscopy, Fluorescence; D053594:Myeloid Differentiation Factor 88 / Q000172:deficiency / Q000235:genetics*; D020411:Oligonucleotide Array Sequence Analysis; D010950:Plasma Cells / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D009418:S100 Proteins / Q000235:genetics / Q000378:metabolism; D012469:Salivary Glands / Q000166:cytology / Q000378:metabolism*; D053481:Secretory Leukocyte Peptidase Inhibitor / Q000235:genetics* / Q000378:metabolism
chemical_list: D040501:Calgranulin A; D023082:Defensins; D007070:Immunoglobulin A; C507780:Myd88 protein, mouse; D053594:Myeloid Differentiation Factor 88; D009418:S100 Proteins; C086145:S100a8 protein, mouse; D053481:Secretory Leukocyte Peptidase Inhibitor; C506815:Slpi protein, mouse; D007781:Lactoferrin