Background: Major Depressive Disorder (MDD) is a debilitating mental health condition with complex etiology, and recent research has focused on pro-inflammatory cytokines and chemokines as potential contributors to its pathogenesis. However, studies investigating the roles of TNF-α and MCP-4 in MDD within the Bangladeshi population are scarce. This study aimed to assess the association between serum TNF-α and MCP-4 levels and the severity of MDD, exploring their potential as risk indicators for MDD development.Methods: This case-control study enrolled 58 MDD patients from Bangabandhu Sheikh Mujib Medical University (BSMMU) Hospital, Dhaka, Bangladesh, alongside 30 age, sex, and BMI-matched healthy controls. MDD diagnosis followed DSM-5 criteria and disease severity using the 17-item Hamilton Depression Rating Scale (Ham-D). We measured serum TNF-α and MCP-4 levels using ELISA assays according to the supplied protocols.Results: The study revealed significantly elevated serum TNF-α levels in MDD patients (47±6.6 pg/ml, mean±SEM) compared to controls (28.06±1.07 pg/ml). These increased TNF-α levels positively correlated with Ham-D scores (Pearson’s r = 0.300, p = 0.038), suggesting a potential association between peripheral TNF-α levels and MDD pathology. Additionally, MDD patients exhibited significantly higher serum MCP-4 levels (70.49±6.45 pg/ml) than controls (40.21±4.08 pg/ml). However, serum MCP-4 levels showed a significant negative correlation (r = -0.270, P = 0.048) with Ham-D scores in MDD patients, indicating a more complex role for MCP-4 in MDD pathogenesis.Conclusion: This study highlights that Bangladeshi MDD patients exhibit heightened inflammatory and immune responses compared to controls, supporting the cytokine hypothesis in MDD pathogenesis. Serum TNF-α, but not MCP-4, shows promise as a potential biomarker for assessing the risk of MDD development, which could aid in early detection. Future investigations involving larger populations and longitudinal studies are essential to confirm the utility of these cytokines as biomarkers for MDD.

Expelling antibiotic molecules out of the cell wall through multiple efflux pumps is one of the potential mechanisms of developing resistance against a wide number of antibiotics in Staphylococcus aureus. The aim of this study was to investigate the association between the antibiotic susceptibility profile and the prevalence of different efflux pump genes i.e., norA, norB, norC, mepA, sepA, mdeA, qacA/B, and smr in the clinical isolates of S. aureus. Sixty clinical isolates were collected from a tertiary level hospital in Bangladesh. The disc diffusion method using ten antibiotics of different classes was used to discern the susceptibility profile. polymerase chain reaction (PCR) was employed to observe the resistance patterns and to detect the presence of plasmid and chromosomal encoded genes. Among the clinical isolates, 60% (36 out of 60) of the samples were Methicillin-resistant Staphylococcus aureus (MRSA), whereas 55% (33 out of 60) of the bacterial samples were found to be multi-drug resistant. The bacteria showed higher resistance to vancomycin (73.33%), followed by ciprofloxacin (60%), cefixime (53.33%), azithromycin (43.33%), and amoxicillin (31.67%). The prevalence of the chromosomally-encoded efflux genes norA (91.67%), norB (90%), norC (93.33%), mepA (93.33%), sepA (98.33%), and mdeA (93.33%) were extremely high with a minor portion of them carrying the plasmid-encoded genes qacA/B (20%) and smr (8.33%). Several genetic combinations of efflux pump genes were revealed, among which norA + norB + norC + mepA + sepA + mdeA was the most widely distributed combination among MRSA and MSSA bacteria that conferred resistance against ciprofloxacin and probably vancomycin. Based on the present study, it is evident that the presence of multiple efflux genes potentiated the drug extrusion activity and may play a pivotal role in the development of multidrug resistance in S. aureus.

Background: Diabetic Neuropathy (DN) is a prevalent complication of diabetes linked to chronic inflammation. Interleukin-6 (IL-6) and Interleukin-10 (IL-10) are key cytokines implicated in DN pathogenesis. This study investigates the association of IL6 and IL10 gene polymorphisms and serum levels with DN in the Bangladeshi population. Materials and methods: A case-control study was conducted with 225 participants: diabetic patients with DN (n = 75), diabetic patients without DN (n = 75), and healthy controls (n = 75). Genomic DNA was extracted for genotyping IL-6 (rs1800796) and IL-10 (rs1800896) SNPs via PCR. Serum cytokine levels were measured using ELISA. Results: Serum IL-6 levels were significantly higher in the DN group than in the other study groups (p < 0.0001), with the highest levels observed among individuals with the IL-6 rs1800796 CC genotype. In unadjusted analyses, the IL-6 CC genotype was associated with increased odds of DN compared with healthy controls (OR = 4.813, 95% CI: 1.752–13.85, p = 0.0040), as was the IL-10 GG genotype (OR = 2.679, 95% CI: 1.000–6.751, p = 0.0373). However, neither IL-6 nor IL-10 genotype remained independently associated with DN after multivariable adjustment. Serum IL-10 levels did not differ significantly among the study groups (p = 0.0948). Combined genotype analyses showed several nominal associations, although these findings were exploratory. Serum IL-6 showed promising discriminatory ability in distinguishing patients with DN from the other study groups, whereas IL-10 demonstrated limited discriminatory performance. Conclusion: These findings support further investigation of serum IL-6 as a potential candidate biomarker for diabetic neuropathy, whereas the independent contribution of the investigated IL-6 and IL-10 polymorphisms remains uncertain. Larger prospective studies with independent external validation are required before clinical application can be considered.

Background Diabetic Neuropathy (DN) is a prevalent complication of diabetes linked to chronic inflammation. Interleukin-6 (IL-6) and Interleukin-10 (IL-10) are key cytokines implicated in DN pathogenesis. This study investigates the association of IL6 and IL10 gene polymorphisms and serum levels with DN in the Bangladeshi population. Materials and methods A case-control study was conducted with 225 participants: diabetic patients with DN (n = 75), diabetic patients without DN (n = 75), and healthy controls (n = 75). Genomic DNA was extracted for genotyping IL-6 (rs1800796) and IL-10 (rs1800896) SNPs via PCR. Serum cytokine levels were measured using ELISA. Results Serum IL-6 levels were significantly higher in the DN group than in the other study groups (p < 0.0001), with the highest levels observed among individuals with the IL-6 rs1800796 CC genotype. In unadjusted analyses, the IL-6 CC genotype was associated with increased odds of DN compared with healthy controls (OR = 4.813, 95% CI: 1.752–13.85, p = 0.0040), as was the IL-10 GG genotype (OR = 2.679, 95% CI: 1.000–6.751, p = 0.0373). However, neither IL-6 nor IL-10 genotype remained independently associated with DN after multivariable adjustment. Serum IL-10 levels did not differ significantly among the study groups (p = 0.0948). Combined genotype analyses showed several nominal associations, although these findings were exploratory. Serum IL-6 showed promising discriminatory ability in distinguishing patients with DN from the other study groups, whereas IL-10 demonstrated limited discriminatory performance. Conclusion These findings support further investigation of serum IL-6 as a potential candidate biomarker for diabetic neuropathy, whereas the independent contribution of the investigated IL-6 and IL-10 polymorphisms remains uncertain. Larger prospective studies with independent external validation are required before clinical application can be considered.