Related Experiment Video
Updated: Jun 12, 2026
An In vitro Model to Study Immune Responses of Human Peripheral Blood Mononuclear Cells to Human Respiratory Syncytial Virus Infection
Published on: December 10, 2013
Gender differences and inflammation: an in vitro model of blood cells stimulation in prepubescent children
Georges Ja Casimir1, Fabienne Heldenbergh, Laurence Hanssens
1Department of Pulmonology and Allergology, Université Libre de Bruxelles (ULB), University Children's Hospital Queen Fabiola, Avenue J,J, Crocq 15, Brussels, 1020, Belgium. georges.casimir@huderf.be.
Insights
Male children and Turner
Area of Science:
- Immunology
- Genetics
- Pediatrics
Background:
- Gender significantly impacts inflammatory disease presentation and complication frequency, with females often experiencing more severe outcomes.
- Chronic inflammation may lead to greater organ damage in females, suggesting underlying biological differences.
Purpose of the Study:
- To investigate cellular-level gender dimorphism in cytokine production.
- To explore the role of X chromosome monosomy in immune responses.
Main Methods:
- Evaluated cytokine production (IL-1, IL-6, PGE-2, TNF-alpha) in healthy children and Turner's syndrome (TS) patients.
- Used lipopolysaccharide (LPS) and Pokeweed Mitogen (PWM) to stimulate whole blood cultures.
- Analyzed data from 57 subjects, including boys, girls, and TS patients.
Main Results:
- Confirmed higher cytokine production in males compared to females, contrasting with some in vivo findings.
- Observed that TS patients largely mirrored male immune reactivity patterns.
- Identified Interleukin-6 (IL-6) as potentially having a stronger modulating function in males.
Conclusions:
- The observed gender dimorphism in immune response may persist independently of hormonal status.
- Suggests that X chromosome gene products, escaping X inactivation in females and absent in males/TS, could influence immune responses.
- Highlights the need for further research into genetic influences on sex-based immune differences.
Background:
Gender influences clinical presentations and markers in inflammatory diseases. In many chronic conditions, frequency of complications is greater in females, suggesting that continuous inflammatory reaction may induce greater damage in targeted organs and functions.
Methods:
To investigate gender dimorphism at a cellular level, we evaluated the production of cytokines implicated in inflammatory processes (IL -1, IL- 6, PGE-2 and TNF alpha), in healthy prepubescent children of both sex and Turner's syndrome (TS) patients (genotype XO). We used stimulation by LPS (0.2 and 1 ng/ml) and Pokeweed Mitogen (PWM) on overnight cultures from whole blood samples, collected in 57 subjects: 22 girls/26 boys (5-96 months), and 9 TS patients (6-15 years). The primary outcome was to evaluate if gender influences the production of cytokines, with potential relation to X chromosome monosomy. Secondary endpoints were to relate different cytokines level productions and conditions.
Results:
We confirm the male over female increased cytokine productions already observed in adults. This is contrasting with numerous observations obtained in vivo about increased production of inflammatory markers in females (CRP, ESR and neutrophil counts), as we recently reported in children. Relative variations of the dimorphism according to stimulus, its concentration and cytokine type are discussed, presenting IL6 with a modulating function that could be more potent in males. TS subjects follow mostly the male pattern of reactivity, sustaining the role of some gene expression differing with X chromosome monosomy and disomy.
Conclusions:
Persistence of the latter dimorphism throughout life casts doubts on its direct relationship with individual hormonal status, as already documented by others in vitro, and supports the need for alternative hypothesis, such as the influence of X chromosome gene products escaping X inactivation in females and absent in subjects with X monosomy (males, TS).
