High expression of co-stimulatory and adhesion molecules are observed on eosinophils during human Schistosoma mansoni infection

Abstract

Herein we have focused attention on major phenotypic features of peripheral blood eosinophils from chronic Schistosoma mansoni-infected patients. For this purpose, detailed immunophenotypic profiles of a range of cell surface markers were performed, including activation markers (CD23/CD69/CD25/HLA-DR), co-stimulatory molecules (CD28/CD80/CD86), chemokine receptors (CXCR1/CXCR2/CCR3/CCR5) besides L-selectin-CD62L and adhesion molecules (CD18/CD54). Our major findings pointed out increased frequency of CD23 + -cells, besides decreased percentages of CD69 + -eosinophils, suggesting a chronic activation status with low frequency of early activated eosinophils in chronic S. mansoni-infected patients (INT) in comparison to non-infected individuals (NI). Moreover, a dichotomic expression of beta-chemokine receptors was observed during human schistosomiasis mansoni with higher CCR5 and lower levels of CCR3 observed between groups. Enhanced expression of co-stimulatory receptors (CD28/CD86) and adhesion molecules (CD54/CD18), besides striking lower frequency of L-selectin + were reported for eosinophils from INT group as compared to NI. Interestingly, the frequency of CD62L + -eosinophils and a range of cell activation related molecules pointed out an opposite pattern of association in NI and INT, where only INT patients that display lower frequency of CD62L + -eosinophils (first CD62L tertile) kept the unusual relationship between the expression of L-selectin and the CD23 activation marker. These findings suggest that distinct dynamic of activation markers expressed by eosinophils may occur during chronic S. mansoni infection.Key words: schistosomiasis -eosinophils -activation markers -L-selectin Eosinophils have been shown to play a major role in the immune response to helminthic infections (Butterworth et al. 1979, Hamann et al. 1987. In this context, transendothelial migration is essential for eosinophil recruitment from blood vessels into inflammatory tissues. At the inflammatory site, further interaction with invading parasites occurs via adherence with subsequent larval damage mediated by release of eosinophil toxic granular effector molecules, proinflammatory lipids, and cytokines (Greene et al. 1981, Medina-De la Garza et al. 1990, Strote et al. 1990, Brattig et al. 1991, Wildenburg et al. 1994. The prerequisite for adherence of effector eosinophils to parasite's larval stages is their sequential activation and chemotactic attraction that favor the eosinophils tethering. The migration of mature activated eosinophils from circulatory pools into the inflammatory foci depends on specific upregulation of adhesion molecules and chemokine receptors, which direct transmigration through a positive chemotactic gradient. This phenomenon seems to represent the key element for eosinophils recruitment that lead to accumulation of these proinflammatory cells that surround the parasite in its microenvironment (Pearlman 1997, Tachimoto et al. 2000.The profile of cell surface molecules expression on mature eosinophils resembles...

Bronchoalveolar lavage as a tool for evaluation of cellular alteration during Aelurostrongylus abstrusus infection in cats

“…In the present study, eosinophils comprised the vast majority of cells 30 days after infection. In previous studies, eosinophilia is reported to be a key factor in many helminthic infections (Silveira-Lemos et al 2006, Barçante et al 2008. Among infectious agents, helminth parasites are regarded as master manipulators of the host immune system, often inducing a long-lasting asymptomatic form of infection.…”

“…In this context, transendothelial migration is essential to eosinophil recruitment from blood vessels into inflammated tissues. At the site of inflammation, further interaction with invading parasites occurs via adherence with subsequent larval damage mediated by the release of effector molecules from the toxic granules of eosinophils (Silveira- Lemos et al 2006).…”

CCR5 and CCR5Δ32 in bacterial and parasitic infections: Thinking chemokine receptors outside the HIV box

“…CCR5‐deficient mice show more severe Schistosoma infection and mortality rate than CCR5 wild‐type mice, suggesting a protective role of CCR5 against aggressive granuloma formation during the course of infection (Souza et al, 2011). Studies with humans linked Schistosoma infection to increased CCR5 expression or CCR5 + cell frequencies (Kleppa et al, 2014; Secor et al, 2003; Silveira‐Lemos, Teixeira‐Carvalho, Martins‐Filho, Oliveira, & Corrêa‐Oliveira, 2006). Importantly, since CCR5 is the main HIV co‐receptor, such an increase in the number of receptors on the surface of immune cells enhances the susceptibility to HIV infection in Schistosoma ‐infected patients.…”

Schistosoma mansoni infection is associated with decreased risk of respiratory allergy symptoms and low production of CCL2

“…In asthma, higher levels of sCD23 have been described [20,21]. In S. mansoni infection, an increase in the frequency of eosinophils and B cell expressing mCD23 has been reported [22,23]. Increased mCD23 expression in B cells and high levels of sCD23 were shown to correlate with eosinophilia and resistance to infection by S. mansoni, but not with parasite-specific IgE [23].…”