Neonatal sepsis is the term used to describe a severe form of morbidity and mortality causing systemic illness that has a viral, bacterial, or fungal source, is accompanied by hemodynamic abnormalities, and results in clinical findings. Clinical signs can range from mild localized or systemic disease to subclinical infection [17, 18].

In the current study, we reported significant differences between cases and controls regarding gestational age, Apgar score at 1 min, respiratory rate, heart rate, head circumference, and height (P value < 0.005, each) which is in agreement with Belachew and Tewabe, 2020 who revealed the relationship between neonates with sepsis and each of low birth weight and preterm state explaining that preterm babies have immature immune systems so it could not fight infection [1]. Also, Gutbir et al. (2020) showed that an Apgar score with a low score had a higher risk of infection [19]. Interestingly, Pawar et al. (2018) exhibited that neonatal infection is associated with low weight and poor head growth [20]

MiRNAs, which are short non-coding RNAs, control a variety of biological activities. There is growing evidence that miRNAs are critical for immune regulation in autoimmune and infectious illnesses [21, 22].

Several biomarkers have been investigated to help in sepsis diagnosis and prognosis, although they have limits in severe and early cases [23, 24]. Serum miRNAs have attracted a lot of attention as indicators recently for the diagnosis and prognosis of sepsis. External cells release miRNAs into the serum, which remain stable in the bloodstream. This is because they are simple to detect [25].

Human miR-182-5p, which is transcribed from the cluster of the miR-183 family and is found at the 7q32 region of chromosome 7, has been widely studied in human malignancies. MiR-182-5p has been described as an oncogene in the majority of common forms of human malignancies, but it also has tumor-suppressive properties in human lung, gastric, and posterior uveal melanoma adenocarcinomas [26, 27].

In the current study, we showed that individuals with neonatal sepsis had markedly lower serum expression levels of miR-1825p compared to healthy controls.

The presenting results are in compliance with a prior study that established that miR-182-5p expression level is reduced by hypoxia, a critical pathologic condition in sepsis [28]. Additionally, miR-182-5p overexpression improved cell survival by protecting human retinal microvascular endothelial cells from hypoxia [28].

Along the lines of current results, Gregory et al. (2018) proved that In vitro miR-182 transfection protects against intracellular bacterial infection. Additionally, they demonstrated that miR-182 overexpression in primary human macrophages could protect against pro-inflammatory and autophagic responses to infection [29].

As well, it was noted that the downregulation of miR-182 contributed to the proliferation of renal cell carcinoma via over-expression of its target gene flotillin 1(FLOT1) [30], which was, on the other hand, proved to play an important role in pediatric sepsis [31].

Besides, According to research, lncRNA cardiac hypertrophy-related factor causes miR-182-5p to be negatively regulated, which raises the level of autophagy-related 7 (ATG7) and accelerates autophagy in myocardial I/R injury. It is interesting to note that ATG7 has been demonstrated to control autophagy, a pathogenic process involved in sepsis-induced acute kidney damage [32].

In this study, we discovered that patients with neonatal sepsis had considerably lower serum expression levels of miR-590-3p than healthy newborns. Some research has studied the function of miR-590-3p in inflammatory responses. Also, by targeting lipoprotein lipase, miR-590 reduced the levels of the pro-inflammatory cytokines monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1b (IL-1b) [33].

Also, sepsis reduced the expression of miR-590-3p, which may lessen the injury to cardiomyocytes caused by lipopolysaccharide (LPS) as demonstrated by Liu et al. Furthermore, in LPS-induced cardiomyocytes, miR-590-3p also decreased the expression of Tumor necrosis factor receptor (TNFR)-associated factor 6 (TRAF6) [11].

Our results are compatible with a prior study that reported that miR-590-3p was reduced in mice treated with (LPS) and mice injected with ad-miR-590-3p showed reduction of inflammatory responses via reduction of renal TRAF6 expression and nucleic nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB)-p65, suggesting that Inflammatory responses to septic challenges may be negatively regulated by miR-590-3p, which may cause better survival results [12].

Moreover, miR-590-3p was reported to be reduced in systemic lupus erythematosus (SLE) and lupus mice, according to Huang et al. (2022). Additionally, they demonstrated that 590-3p reduced Th17 cells by inhibiting autophagy activity [34]. Consequently, miR-590-3p may represent a new strategy for the management and treatment of SLE and other autoimmune diseases related to Th17 [34].

However, our result disagreed with Li et al. (2021) who proved that miR-590-3p was elevated in mice with sepsis [35].