## 1 Introduction  
Type 2 diabetes mellitus (T2 DM) is considered an inflammatory disease associated with the development of insulin resistance [1]. Globally, the prevalence of diabetes in adults is expected to rise from 8.8% (424.9 million people) to 9.9% (628.6 million people) by 2045 [2]. This rising trend in T2 DM can be attributed to ageing, a rapid increase in urbanization, as well as an increase in obesogenic environments [3]. Haematological parameters such as red blood cells (RBC), white blood cells (WBC), platelets (PLT), and other variables such as blood glucose and insulin levels are commonly used as clinical indicators of health and disease [4]. Changes detected in these parameters could provide an insight into the onset and spread of degenerative impediments in diabetes mellitus (DM) [5]. White blood cells are known to be fixed biomarkers of inflammation in metabolic diseases and in T2 DM and its complications [6]. Studies have shown an increase in peripheral WBC (e.g., neutrophils, eosinophils and basophils) with no difference in monocytes counts in T2 DM patients [7]. In addition, peripheral increased WBC count is known to be associated with insulin resistance, stroke, T2 DM, coronary artery disease (CAD), diabetes micro and macrovascular complications [8]. Therefore, haematological markers may play a complementary role for the assessment of changes in form, number, size and maturity of various blood cells and the evaluation and management of T2 DM patients [9]. Studies have shown that T2 DM is linked with inflammation and the induction of T helper 1 (Th1) immune responses, M1 macrophages (MACs) activation and the production of pro-inflammatory cytokines such as interleukin IL-1 \(\beta\), interferon gamma (IFN-\(\gamma\)), Tumour Necrosis Factor alpha (TNF-\(\alpha\)), and Interleukin-6 (IL-6), which regulate the destruction of pancreatic Beta (\(\beta\)) cells, as well as insulin resistance in glucoregulatory tissues [10]. One of the numerous pathophysiological mechanisms underlying the progression of T2 DM is the development of chronic, low-level inflammation, which is characterized by a pronounced exaggerated pro-inflammatory cytokines and chemokines [11]. The outbreak of inflammatory metabolic diseases such as T2 DM has increased, especially in high-income countries and the absence of exposure to helminth infections has been hypothesized to be one mechanism to explain this markedly high prevalence [12; 13]. Helminth infections affect approximately one-quarter of the world's total population and are widespread in lower- to middle-income countries [14; 15]. Previous studies have reported that the prevalence of helminth infections was remarkably lower in patients with T2 DM compared to non-diabetic individuals [16; 17], hence confirming the protective effect of helminids against T2 DM. Helminth infections are known for their ability to regulate harmful inflammatory responses and support local and systemic metabolic homeostasis [18]. Previous studies indicated that helminth infections are usually characterized by the induction of Type 2 immune responses, with an increase in Type 2 and regulatory cytokines [11]. Moreover, it has been reported that enlistment and growth of regulatory T cells (Tregs), as well as modulation of inflammation, is enhanced by helminth infections [19]. Furthermore, it has been established that infections of mice with different species of parasitic helminids is associated with remarkably high type 2 innate lymphoid cells (ILC2s), eosinophils, alternatively activated macrophages (M2 MACs), and T helper 2 (Th2) cytokines, which result in the restoration of glucose levels and ameliorate insulin sensitivity [20]. Several studies have shown the immunomodulatory effect of other helminth species on T2 DM [11; 17; 18]. Tissue dwelling larvae of nematodes such as _Trichinella_ spp. are known to induce hypoglycemia [21]; however, there is paucity of information on the effect of this nematode species and the pathophysiology of a host with T2 DM.