ABSTRACT
INTRODUCTION: CCR5 receptor exerts an important role in the host immune response. Osteomyelitis is an inflammatory process and Staphylococcus aureus is the principal causative agent of this bone injury complication. A deletion of 32bp (CCR5Δ32) in the CCR5 gene seems to protect against HIV-1, S.aureus and other infections. However, the CCR5Δ32 allele has been associated with an increased risk for other diseases. OBJECTIVE: To investigate the function of CCR5 and to gather data about the relationship of the CCR5Δ32 mutation and the risk of developing osteomyelitis as a complication in patients with bone traumas. METHODS: In a study of 153 patients with bone traumas the presence of the CCRΔ32 mutation was determined by PCR. RESULTS: In this study, the CCR5Δ32 allele was present only in the heterozygous form. Osteomyelitis was more frequent in the wild type carriers (94.87%; 37/39) and most of the CCR5Δ32 carriers (87.5%; 14/16) did not present with osteomyelitis. CONCLUSION: The CCR5Δ32 could be associated with protection against osteomyelitis caused by S. aureus, corroborating the data from Alonzo & Torres study, in which CCR5 receptor is required for S. aureus leukotoxin ED (LukED) cytotoxicity.
Subject(s)
Alleles , Mutation , Osteomyelitis/etiology , Receptors, CCR5/genetics , Adult , Aged , Brazil , Female , Genetic Predisposition to Disease , Genotype , Humans , Male , Middle Aged , Odds Ratio , Osteomyelitis/immunologyABSTRACT
Cervical cancer incidence has grown worldwide, with it being a more significant problem in developing countries. Invasive squamous cell cervical cancers are preceded by a long phase of preinvasive disease, known as cervical intraepithelial neoplasia. Cervical cancer can develop when the virus takes advantage of any TP53 gene dysfunction of the host organism. TP53 is responsible for encoding the tumor suppressor p53 phosphoprotein, which helps preserve genome integrity. Currently, many studies have focused on genetic polymorphisms as an important contribution to cancer susceptibility, but few related to cervical intraepithelial neoplasia (CIN). Thus, the present study aimed to see whether patients with suspected CIN had TP53 gene polymorphisms that might have contributed to the development of neoplasia. This study included 133 women who were referred to the Cervical Pathology Clinic of the Maternity School Assis Chateaubriand MEAC for suspected cervical lesions. Polymorphism genotyping was carried out by the PCR-RFLP technique using DNA extracted from patients' blood. The most frequent genotype in both CIN(+) and CIN(-) patients was Arg/Pro TP53 codon 72 and A1A1 for 16-bp Del in intron 3. No risk of cervical cancer was found for the polymorphisms studied. However, a significant association was found when the two polymorphisms were combined: patients with the A1A1/ArgPro genotype were statistically more frequent in the CIN(-) group (p = 0.042), while A2A2-A1A2/ProArg was significantly more frequent in the CIN(+) group. The results of our study suggest that combined analysis of TP53 polymorphisms Arg72Pro and 16-bp Ins/Del may help to monitor the development of CIN in Brazilian women.
