Abstract
BackgroundTumor necrosis factor alpha (TNF-α) −308 G>A promoter polymorphism might be associated with excessive production of the proinflammatory cytokine TNF-α, modulating host response to pulmonary infections. Our objective was to evaluate the association of TNF-α gene −308 G>A polymorphism with susceptibility to, and severity of, community-acquired pneumonia (CAP).ResultsThis was a cross-sectional study including 45 Egyptian children hospitalized for CAP in addition to 45 healthy children who served as a control group. Pneumonia severity was assessed on admission by the World Health Organization (WHO) guidelines; Pediatric Respiratory Severity Score (PRESS) score; Predisposition, Infection, Response and Organ failure (PIROm) score; and Respiratory Index of Severity in Children (RISC) score. Genotyping of TNF-α polymorphism was performed to all individuals by polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP). Patients were monitored till hospital discharge. Frequency of AG genotype was lower among patients compared with control [odds ratio (OR) and 95% confidence interval (CI) = 0.13 (0.03–0.63); p = 0.012]. Prevalence of genotypes AA+AG was lower among patients compared with controls [OR and 95% CI = 0.34 (0.12–0.99); p = 0,048]. The “A” allele prevalence was higher among controls, but no significant association was found with CAP [OR and 95% CI = 0.58 (0.25–1.35); p = 0.21]. When PRESS score was used to classify patients into “severe pneumonia” and “non-severe pneumonia,” no significant association of any of the alleles or genotypes with CAP severity was found.ConclusionTNF-α −308 G>A polymorphism confers protection from pediatric CAP but is not associated with indicators of CAP severity. Larger studies are needed to confirm these findings in pediatric patients from different ethnicities.
Highlights
Tumor necrosis factor alpha (TNF-α) −308 G>A promoter polymorphism might be associated with excessive production of the proinflammatory cytokine TNF-α, modulating host response to pulmonary infections
The frequency of “A” allele was lower among patients but no significant association was found with community-acquired pneumonia (CAP) [odds ratio (OR) and 95% confidence interval (CI) = 0.58 (0.25–1.35); p = 0.21]
In addition to the effect of TNF-α polymorphism on CAP susceptibility, we evaluated a potential influence of the polymorphism on CAP severity
Summary
Tumor necrosis factor alpha (TNF-α) −308 G>A promoter polymorphism might be associated with excessive production of the proinflammatory cytokine TNF-α, modulating host response to pulmonary infections. Our objective was to evaluate the association of TNF-α gene −308 G>A polymorphism with susceptibility to, and severity of, community-acquired pneumonia (CAP). It was later discovered that TNF-α has a wide range of biological effects on host defense against pathogenic agents. It can induce cell survival, El Gendy et al Egyptian Pediatric Association Gazette (2020) 68:5 proliferation, and differentiation. It can cause both apoptosis and necrosis under certain conditions [6]
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.