TY - JOUR
T1 - Growth hormone modulates Trypanosoma cruzi infection in vitro
AU - Mora-Criollo, Patricia
AU - Basu, Reetobrata
AU - Qian, Yanrong
AU - Costales, Jaime A.
AU - Guevara-Aguirre, Jaime
AU - Grijalva, Mario J.
AU - Kopchick, John J.
N1 - Publisher Copyright:
© 2022 Elsevier Ltd
PY - 2022/6
Y1 - 2022/6
N2 - Objective: Chagas disease (CD) is caused by the protozoan parasite, Trypanosoma cruzi. It affects 7 to 8 million people worldwide and leads to approximately 50,000 deaths per year. In vitro and in vivo studies had demonstrated that Trypanosoma cruziinfection causes an imbalance in the hypothalamic-pituitary-adrenal (HPA) axis that is accompanied by a progressive decrease in growth hormone (GH) and prolactin (PRL) production. In humans, inactivating mutations in the GH receptor gene cause Laron Syndrome (LS), an autosomal recessive disorder. Affected subjects are short, have increased adiposity, decreased insulin-like growth factor-I (IGF[sbnd]I), increased serum GH levels, are highly resistant to diabetes and cancer, and display slow cognitive decline. In addition, CD incidence in these individuals is diminished despite living in highly endemic areas. Consequently, we decided to investigate the in vitro effect of GH/IGF-I on T. cruzi infection. Design: We first treated the parasite and/or host cells with different peptide hormones including GH, IGF[sbnd]I, and PRL. Then, we treated cells using different combinations of GH/IGF-I attempting to mimic the GH/IGF-I serum levels observed in LS subjects. Results: We found that exogenous GH confers protection against T. cruzi infection. Moreover, this effect is mediated by GH and not IGF[sbnd]I. The combination of relatively high GH (50 ng/ml) and low IGF-I (20 ng/ml), mimicking the hormonal pattern seen in LS individuals, consistently decreased T. cruzi infection in vitro. Conclusions: The combination of relatively high GH and low IGF-I serum levels in LS individuals may be an underlying condition providing partial protection against T. cruzi infection.
AB - Objective: Chagas disease (CD) is caused by the protozoan parasite, Trypanosoma cruzi. It affects 7 to 8 million people worldwide and leads to approximately 50,000 deaths per year. In vitro and in vivo studies had demonstrated that Trypanosoma cruziinfection causes an imbalance in the hypothalamic-pituitary-adrenal (HPA) axis that is accompanied by a progressive decrease in growth hormone (GH) and prolactin (PRL) production. In humans, inactivating mutations in the GH receptor gene cause Laron Syndrome (LS), an autosomal recessive disorder. Affected subjects are short, have increased adiposity, decreased insulin-like growth factor-I (IGF[sbnd]I), increased serum GH levels, are highly resistant to diabetes and cancer, and display slow cognitive decline. In addition, CD incidence in these individuals is diminished despite living in highly endemic areas. Consequently, we decided to investigate the in vitro effect of GH/IGF-I on T. cruzi infection. Design: We first treated the parasite and/or host cells with different peptide hormones including GH, IGF[sbnd]I, and PRL. Then, we treated cells using different combinations of GH/IGF-I attempting to mimic the GH/IGF-I serum levels observed in LS subjects. Results: We found that exogenous GH confers protection against T. cruzi infection. Moreover, this effect is mediated by GH and not IGF[sbnd]I. The combination of relatively high GH (50 ng/ml) and low IGF-I (20 ng/ml), mimicking the hormonal pattern seen in LS individuals, consistently decreased T. cruzi infection in vitro. Conclusions: The combination of relatively high GH and low IGF-I serum levels in LS individuals may be an underlying condition providing partial protection against T. cruzi infection.
KW - Chagas disease
KW - Growth hormone
KW - IGF-I
KW - Laron syndrome
KW - Prolactin
KW - Trypanosoma cruzi
UR - http://www.scopus.com/inward/record.url?scp=85129557960&partnerID=8YFLogxK
U2 - 10.1016/j.ghir.2022.101460
DO - 10.1016/j.ghir.2022.101460
M3 - Article
C2 - 35490602
AN - SCOPUS:85129557960
SN - 1096-6374
VL - 64
JO - Growth Hormone and IGF Research
JF - Growth Hormone and IGF Research
M1 - 101460
ER -