Association of Pneumococcal Carriage and Expression of Foxp3+ Regulatory T Cells and Th17 Cells in the Adenoids of Children.
BACKGROUND
Pneumococcal carriage in the nasopharynx is a primary means of transmission and a necessary prerequisite for pneumococcal disease.


OBJECTIVE
We analyzed the relationship between expressions of Foxp3+ regulatory T (Treg) cells and Th17 cells, and pneumococcal carriage in the adenoids of children who were either positive or negative for pneumococci.


METHODS
We collected adenoidal tissue and nasopharyngeal swab samples from children undergoing an adenoidectomy. Adenoidal mononuclear cells were isolated, cultured and then stimulated with culture concentrated supernatant (CCS) obtained from a D39 bacterial strain.


RESULTS
Foxp3+ Treg cells were upregulated and Th17 cells were downregulated in populations of adenoidal mononuclear cells obtained from the pneumococcus-positive group. Following CCS stimulation, the increment in Foxp3+ Treg cells in the pneumococcus-positive group was significantly greater than that in the pneumococcus-negative group, while the increment in Th17 cells was less as compared to that in the pneumococcus-negative group. These results were consistent with variations in levels of Foxp3 mRNA and retinoic acid receptor-related orphan receptor-γt mRNA in adenoidal mononuclear cells. Levels of IL-17A and IL-6 in adenoid tissue were higher in the pneumococcus-negative group, and the levels of TGF-β in adenoid tissue were lower in the pneumococcus-negative group compared to the pneumococcus-positive group. Pneumococcal carriage in children was closely associated with the expressions of Foxp3+ Treg and Th17 cells in the adenoid.


CONCLUSIONS
Upregulation of Foxp3+ Treg cells might downregulate the production of Th17 cells in the adenoid, resulting in decreased scavenging of Streptococcus pneumoniae and chronic pneumococcal carriage.
Chongqing International Science and Technology Cooperation Center for Child Development and Disorders, Key Laboratory of Child Development and Disorders, Key Laboratory of Pediatrics in Chongqing, Ministry of Education, Chongqing Medical University, Chongqing, China.
Xiao-Li
XL
Jiang
Guang-Li
GL
Zhang
Ting
T
Yang
Bao-Hui
BH
Yang
Li-Jia
LJ
Wang
Qing-Hong
QH
Wang
Zheng-Xiu
ZX
Luo
En-Mei
EM
Liu
Zhou
Z
Fu
D000234:Adenoids / Q000276:immunology / Q000382:microbiology*; D002353:Carrier State; D002648:Child; D002675:Child, Preschool; D005260:Female; D051858:Forkhead Transcription Factors / Q000235:genetics / Q000276:immunology; D006801:Humans; D020381:Interleukin-17 / Q000276:immunology; D015850:Interleukin-6 / Q000276:immunology; D008297:Male; D009305:Nasopharynx / Q000276:immunology / Q000382:microbiology; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3 / Q000235:genetics / Q000276:immunology; D011008:Pneumococcal Infections / Q000276:immunology / Q000382:microbiology*; D012333:RNA, Messenger / Q000378:metabolism*; D013296:Streptococcus pneumoniae / Q000276:immunology / Q000302:isolation & purification*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology* / Q000378:metabolism; D058504:Th17 Cells / Q000276:immunology*; D016212:Transforming Growth Factor beta / Q000276:immunology
C418974:FOXP3 protein, human; D051858:Forkhead Transcription Factors; C508717:IL17A protein, human; C508600:IL6 protein, human; D020381:Interleukin-17; D015850:Interleukin-6; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3; D012333:RNA, Messenger; C539900:RORC protein, human; D016212:Transforming Growth Factor beta