title: Acute phase protein induction by experimental inflammation in the salivary gland.
abstract: BACKGROUND
  The submandibular gland (SMG) is a major salivary gland, which plays an important role in maintenance the oral health. In this study, we intended to explore the role of the SMG's defense system of the animals in which experimental inflammation is induced.
  
  
  METHODS
  The levels of mRNAs for inflammation cytokines and acute phase proteins were detected by reverse transcriptase-polymerase chain reaction (RT-PCR).
  
  
  RESULTS
  The mRNAs for acute phase proteins were found to be increased in the SMG and extraorbital and intraorbital lacrimal gland (ELG and ILG) of rats at 24 h after subcutaneous injection of turpentine oil. The induction of mRNA for these inflammatory proteins by turpentine oil was preceded by a transient increase in the level of mRNAs for IL-1beta, IL-6 and TNF-alpha at 6 h after subcutaneous injection of the oil. Such cytokine induction was similarly seen by lipopolysaccharide (LPS) injection, and involvement of Toll-like receptor 4 (TLR4) was strongly suggested from experiment using C3H/HeJ mice, a TLR4-deficient mutant strain.
  
  
  CONCLUSIONS
  The up-regulation of acute phase proteins and inflammation cytokines in the SMG, ELG and ILG by experimental inflammation suggests the existence of a strict defense system via the innate immune system in the SMG and other exocrine gland.
authors.affiliation: Department of Molecular Oral Physiology, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima-shi, Tokushima, 770-8504, Japan.
authors.forename: Chenjuan
authors.initials: C
authors.lastname: Yao
authors.forename: Wei
authors.initials: W
authors.lastname: Wei
authors.forename: Xuefei
authors.initials: X
authors.lastname: Li
authors.forename: Kazuo
authors.initials: K
authors.lastname: Hosoi
mesh_terms: D000209:Acute-Phase Proteins / Q000032:analysis*; D000818:Animals; D015853:Cysteine Proteinase Inhibitors / Q000032:analysis; D016207:Cytokines / Q000032:analysis; D007375:Interleukin-1 / Q000032:analysis; D015850:Interleukin-6 / Q000032:analysis; D007509:Irritants / Q000494:pharmacology; D007704:Kininogens / Q000032:analysis; D007765:Lacrimal Apparatus / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D008562:Membrane Glycoproteins / Q000032:analysis; D051379:Mice; D008809:Mice, Inbred C3H; D008815:Mice, Inbred Strains; D008817:Mice, Mutant Strains; D051381:Rats; D017208:Rats, Wistar; D011956:Receptors, Cell Surface / Q000032:analysis; D012793:Sialadenitis / Q000378:metabolism*; D013364:Submandibular Gland Diseases / Q000378:metabolism*; D013997:Time Factors; D051197:Toll-Like Receptor 4; D051193:Toll-Like Receptors; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D014425:Turpentine / Q000494:pharmacology; D015854:Up-Regulation
chemical_list: D000209:Acute-Phase Proteins; D015853:Cysteine Proteinase Inhibitors; D016207:Cytokines; D007375:Interleukin-1; D015850:Interleukin-6; D007509:Irritants; D007704:Kininogens; D008070:Lipopolysaccharides; D008562:Membrane Glycoproteins; D011956:Receptors, Cell Surface; C495347:Tlr4 protein, rat; D051197:Toll-Like Receptor 4; D051193:Toll-Like Receptors; D014409:Tumor Necrosis Factor-alpha; D014425:Turpentine