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1.
FEBS Open Bio ; 11(2): 446-455, 2021 02.
Article in English | MEDLINE | ID: mdl-33332733

ABSTRACT

Porphyromonas gingivalis (Pg) is a periodontopathic pathogen that may affect MUC5AC-related mucus hypersecretion along airway epithelial cells. Here, we attempted to establish whether Pg virulence factors (lipopolysaccharide, FimA fimbriae, gingipains) affect MUC5AC in immortalized and primary bronchial cells. We report that MUC5AC gene expression and protein levels are affected by Pg culture supernatant, but not by lipopolysaccharide or FimA fimbriae. Cells treated with either Pg single (Kgp or Rgp) or double (Kgp/Rgp) mutants had altered levels of MUC5AC gene expression and protein levels, and MUC5AC staining of double mutant-treated mouse lung cells showed that MUC5AC protein levels were unaffected. Taken together, we propose that Pg gingipains may be the primary virulence factor that influences both MUC5AC gene expression and protein levels.


Subject(s)
Mucin 5AC/metabolism , Periodontal Diseases/complications , Porphyromonas gingivalis/immunology , Respiratory Tract Infections/immunology , Animals , Bronchi/immunology , Bronchi/metabolism , Bronchi/pathology , Disease Models, Animal , Epithelial Cells/immunology , Epithelial Cells/metabolism , Fimbriae Proteins/metabolism , Fimbriae, Bacterial/metabolism , Gingipain Cysteine Endopeptidases/metabolism , Host-Pathogen Interactions , Humans , Male , Mice , Mucin 5AC/analysis , Periodontal Diseases/immunology , Periodontal Diseases/microbiology , Porphyromonas gingivalis/metabolism , Primary Cell Culture , Respiratory Mucosa/immunology , Respiratory Mucosa/metabolism , Respiratory Tract Infections/microbiology , Respiratory Tract Infections/pathology , Specific Pathogen-Free Organisms , Virulence Factors/metabolism
2.
Cell Physiol Biochem ; 53(1): 49-61, 2019.
Article in English | MEDLINE | ID: mdl-31169991

ABSTRACT

BACKGROUND/AIMS: The most prevalent infectious disease, chronic periodontitis which leads to alveolar bone destruction and subsequent tooth loss, develops due to proinflammatory cytokine production induced by periodontopathic bacteria. Chronic obstructive pulmonary disease (COPD), a non-infectious disease, is the third leading cause of death globally. This condition exacerbates frequently, and which is attributable to proinflammatory cytokine production induced by infection by respiratory microorganisms such as Streptococcus pneumoniae. Although a positive association has recently been revealed between chronic periodontitis and COPD, how periodontitis contributes to the pathogenesis of COPD remains unclear. Therefore, we hypothesized that some periodontopathic bacteria are involved in the exacerbation of COPD through the induction of proinflammatory cytokine production by respiratory epithelial cells. In this connection, COPD develops in the airways; however, because most periodontopathic bacteria are anaerobic, they are unlikely to exhibit stable virulence in the lower respiratory organs in humans. Hence, we aimed to elucidate whether exposure to heat-inactivated periodontopathic bacteria induces proinflammatory cytokine production by several human respiratory epithelial cell lines and in the lower respiratory organs and serum in mice. METHODS: Real-time polymerase chain reaction and enzyme-linked immunosorbent assay (ELISA) were used to investigate in vitro induction by heat-inactivated periodontopathic bacteria and S. pneumoniae for mRNA expression and protein production of interleukin (IL)-8 and IL-6 by human respiratory epithelial cell lines. ELISA was also used to determine in vivo induction of cytokine production in the lower respiratory organs and serum of intratracheally heat-inactivated Fusobacterium nucleatum-inoculated mice. RESULTS: Some, but not all, periodontopathic bacteria, especially F. nucleatum, strongly induced IL-8 and IL-6 production by BEAS-2B bronchial epithelial cells. In addition, F. nucleatum induced IL-8 production by A549 alveolar epithelial cells as well as IL-8 and IL-6 production by Detroit 562 pharyngeal epithelial cells. Furthermore, F. nucleatum induced considerably higher cytokine production than S. pneumoniae. This was also observed in the entire lower respiratory organs and serum in mice. CONCLUSION: Exposure to increased number of F. nucleatum potentially induces proinflammatory cytokine production by human bronchial and pharyngeal epithelial cells, which may trigger exacerbation of COPD.


Subject(s)
Fusobacterium nucleatum/pathogenicity , Interleukin-6/metabolism , Respiratory System/microbiology , Animals , Bronchi/cytology , Cell Line , Epithelial Cells/cytology , Epithelial Cells/metabolism , Epithelial Cells/microbiology , Humans , Interleukin-6/blood , Interleukin-6/genetics , Interleukin-8/blood , Interleukin-8/genetics , Interleukin-8/metabolism , Male , Mice , Mice, Inbred C57BL , Respiratory System/metabolism , Streptococcus pneumoniae/pathogenicity
3.
J Oral Sci ; 60(3): 321-328, 2018.
Article in English | MEDLINE | ID: mdl-30249933

ABSTRACT

Recently, reports regarding a foreign body in the maxillary sinus have considerably increased, with the majority being iatrogenic cases resulting from dental treatment. This study involves an extensive review of the Japanese literature, including 112 papers from 1978 to 2017. These papers documented total 407 cases of a foreign body in the maxillary sinus. Among the 392 cases for which treatment details were available, the Caldwell-Luc approach was used for 216, the alveolar approach for 116, extraction using nasal endoscopy for 15, and extraction using oral endoscopy for eight. Spontaneous passage occurred in 19 cases, follow-up with medication was used in 17, and "other" was noted in one. This study determined that surgical removal remains the most common method for treating both tooth roots and other foreign bodies and that the Caldwell-Luc approach is used in majority of the surgeries. No marked differences were noted among the removal methods used in relation to the foreign body type.


Subject(s)
Foreign Bodies/therapy , Maxillary Sinus , Endoscopy , Humans , Iatrogenic Disease , Japan
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