TY - JOUR
T1 - Influence of Fetuin-A on Chlamydia muridarum Pulmonary Infection
AU - Mahjabeen, Faria
AU - Yu, Jieh Juen
AU - Chambers, James P.
AU - Gupta, Rishein
AU - Arulanandam, Bernard P.
N1 - Publisher Copyright:
© 2022 Faria Mahjabeen et al.
PY - 2022
Y1 - 2022
N2 - Fetuin-A is an acute phase glycoprotein shown to counter in a regulatory manner proinflammatory cytokine production to maintain homeostasis during inflammation. We report here that in wild-type mice 12 days after Chlamydia muridarum (Cm) intranasal challenge, fetuin-A content in the lungs decreased 46%, while INF-γ increased 44%, consistent with a negative regulatory role of fetuin-A in inflammation. Importantly, the observed increased IFN-γ production was abrogated in fetuin-A-deficient AHSG mice suggesting that IFN-γ induction following Cm infection is fetuin-A dependent. Assessment of expression of genes associated with inflammation revealed fetuin-A-dependent upregulation of TBX21 (a Th1 cell-specific transcription factor) in the lungs of Cm-infected WT mice that correlated with IFN-γ induction. Additionally, the effect of fetuin-A deficiency in mounting an adaptive immune response to Cm infection was demonstrated using a splenocyte recall assay. Although preliminary in nature, these findings are suggestive of fetuin-A involvement following Cm pulmonary infection and underscores the need to investigate further the role of fetuin-A in the immune response and the consequences of its gene deletion.
AB - Fetuin-A is an acute phase glycoprotein shown to counter in a regulatory manner proinflammatory cytokine production to maintain homeostasis during inflammation. We report here that in wild-type mice 12 days after Chlamydia muridarum (Cm) intranasal challenge, fetuin-A content in the lungs decreased 46%, while INF-γ increased 44%, consistent with a negative regulatory role of fetuin-A in inflammation. Importantly, the observed increased IFN-γ production was abrogated in fetuin-A-deficient AHSG mice suggesting that IFN-γ induction following Cm infection is fetuin-A dependent. Assessment of expression of genes associated with inflammation revealed fetuin-A-dependent upregulation of TBX21 (a Th1 cell-specific transcription factor) in the lungs of Cm-infected WT mice that correlated with IFN-γ induction. Additionally, the effect of fetuin-A deficiency in mounting an adaptive immune response to Cm infection was demonstrated using a splenocyte recall assay. Although preliminary in nature, these findings are suggestive of fetuin-A involvement following Cm pulmonary infection and underscores the need to investigate further the role of fetuin-A in the immune response and the consequences of its gene deletion.
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U2 - 10.1155/2022/6082140
DO - 10.1155/2022/6082140
M3 - Article
AN - SCOPUS:85129623458
SN - 1687-918X
VL - 2022
JO - International Journal of Microbiology
JF - International Journal of Microbiology
M1 - 6082140
ER -