The Eosinophil in Infection

Abstract

First described by Paul Ehrlich in 1879, who noted its characteristic staining by acidophilic dyes, for many years, the eosinophil was considered to be an end-effector cell associated with helminth infections and a cause of tissue damage. Over the past 30 years, research has helped to elucidate the complexity of the eosinophil's function and establish its role in host defense and immunity. Eosinophils express an array of ligand receptors which play a role in cell growth, adhesion, chemotaxis, degranulation, and cell-to-cell interactions. They play a role in activation of complement via both classical and alternative pathways. Eosinophils synthesize, store and secrete cytokines, chemokines, and growth factors. They can process antigen, stimulate T cells, and promote humoral responses by interacting with B cells. Eosinophils can function as antigen presenting cells and can regulate processes associated with both T1 and T2 immunity. Although long known to play a role in defense against helminth organisms, the interactions of eosinophils with these parasites are now recognized to be much more complex. In addition, their interaction with other pathogens continues to be investigated. In this paper, we review the eosinophil's unique biology and structure, including its characteristic granules and the effects of its proteins, our developing understanding of its role in innate and adaptive immunity and importance in immunomodulation, and the part it plays in defense against parasitic, viral, fungal and bacterial infections. Rather than our worst enemy, the eosinophil may, in fact, be one of the most essential components in host defense and immunity.

Parasitism in Goats: Husbandry Management, Range Management, Gut Immunity and Therapeutics

“…The higher number of eosinophils suggest sensitization of cellular response to infecting larvae [35]. Previous and updated works on the topic suggest that eosinophilia during helminths infections plays a critical role in providing protective immunity [36,37]. Results from various studies have shown that antigens of developmental stages in parasites are very important for early immunodiagnostics.…”

“…After a concerted effect on the Th3 cells, they show crosstalk signaling that activated Mast cells, eosinophils and release of various cytokines [48,49]. Presently, presence of early eosinophils is characterized with proinflammatory granulocyte that plays a key role in protection against parasitic invasion [36]. This creates a mainstay for the protective immune response to parasites as well as to allergic diseases [29].…”

“…Moreover, dendritic cells driven Th3 cells become sensitive to Myelin Basic Protein (MBP) that releases IL 10 and Transforming Growth Factor β (TGF β) [51]. Thus the presence of parasite enterprises to the autoantigen, resulting in inhibition of the process [28][29][30][31][32][33][34][35][36][37][38][39][40][41][42]. It is further demonstrated that parasitic infection depletes some important generalized and specialized transcriptional factors that are essential to transcription.…”

Involvement of the α/β Isoform of p38 MAP Kinase in Chemotactic Responses of Human Eosinophils to Eotaxin (CCL11) and RANTES (CCL5)

“…Eosinophils are initiator and effector cells of Th2-mediated immunity (Ravin and Loy, 2016). They are associated with key components of inflammation in a variety of chronic diseases affecting the airways (Eng and DeFelice, 2016), heart (Séguéla et al, 2015) and gastrointestinal system (Hogan et al, 2013).…”

“…They are associated with key components of inflammation in a variety of chronic diseases affecting the airways (Eng and DeFelice, 2016), heart (Séguéla et al, 2015) and gastrointestinal system (Hogan et al, 2013). Eosinophils are characterized by secretory granules that contain multiple cytotoxic proteins (Ravin and Loy, 2016). Additionally, eosinophils produce reactive oxygen metabolites, lipid mediators and cytokines, all of which are capable of causing severe host tissue damage in eosinophilic inflammation (Barnes, 2011).…”