B-1 cells upregulate CD8 T lymphocytes and increase proinflammatory cytokines serum levels in oral encephalitozoonosis

Santos, Denise Langanke dos; Alvares-Saraiva, Anuska Marcelino; Xavier, José Guilherme; Spadacci-Morena, Diva Denelle; Peres, Giovani Bravin; Rocha, P.R.D.; Pérez, Elizabeth; Lallo, Maria Anete

doi:10.1016/j.micinf.2017.11.004

Cited by 15 publications

(22 citation statements)

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“…bacteria such as Streptococcus pneumoniae [33], viruses such as the Influenza virus [34], or fungi [35,36]. In line with these studies, our group demonstrated that XID mice were more susceptible to encephalitozoonosis than BALB/c mice, suggesting that the pathogenicity caused by E. cuniculi depends on the relationship between the multiplication of parasites and the host immune response [15,16]. In addition, da Costa et al [15] showed that BALB/c mice infected with E. cuniculi showed an increase in the number of macrophages and plasma levels of IFN-γ, which was responsible for the activation of macrophages and elimination of the pathogens.…”

Section: Nevertheless B-1 Cells Are Critical For the Early Control Osupporting

confidence: 58%

“…The proportion of macrophages in XID APerC (approximately 60%) was significantly higher than that in BALB/c APerC (approximately 20%), regardless of microsporidial infection ( Figure 6A). Since the BALB/c culture also contains B-1 cells that adhere together with the macrophages in the first incubation [15,16], this result was expected. After infection, the percentage of macrophages in XID APerC was 80%, which is higher than that observed in uninfected cultures, Figure 6C).…”

Section: B-1 Cells Are Associated With M1 Macrophage Profilementioning

confidence: 80%

“…In recent studies from our group, we demonstrated that B-1 cell deficient XID mice were more susceptible to experimental encephalitozoonosis than BALB/c mice, evidenced histologically with more prominent inflammatory lesions and fungal burden [15,16]. Although the mechanism of action of B-1 cells in the resistance of BALB/c mice to encephalitozoonosis is not fully understood, a significant increase in the population of peritoneal macrophages was reported in BALB/c mice infected with E. cuniculi [15].…”

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confidence: 85%

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B-1 cell-mediated modulation of m1-macrophage profile can ameliorate microbicidal functions and disrupt the evasion mechanisms ofEncephalitozoon cuniculi

Pereira

Alvares-Saraiva

Konno

et al. 2019

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Highlights E. cuniculi phagocytosis and microbicidal activity by macrophages increases in the presence of B-1 cells  M1 macrophage profiles were predominant in the presence of B-1 cells  Extrusion of the polar tubule of E. cuniculi occur inside M2 macrophages in cultures without B-1 cells  B-1 cells derived phagocytes (B-1CDP) identified with microbicidal activity against spores of E. cuniculi AbstractHere, we have investigated the possible effect of B-1 cells on the activity of peritoneal macrophages in E. cuniculi infection. In the presence of B-1 cells, peritoneal macrophages had an M1 profile with showed increased phagocytic capacity and index, associated with the intense microbicidal activity, increased proinflammatory cytokines production and a higher percentage of apoptotic death. The absence of B-1 cells was associated with a predominance of the M2 macrophages, indicating reduced phagocytic capacity and index, microbicidal activity, proinflammatory cytokine production, and apoptotic death, but equal death rate. In addition, in the M2 macrophages, spores of phagocytic E. cuniculi with polar tubular extrusion were observed, which is an important mechanism of evasion of the immune response. The results showed the importance of B-1 cells in the modulation of macrophage function against E. cuniculi infection, increasing microbicidal activity, and reducing the fungal mechanisms involved in the evasion of the immune response. Author SummaryThe adaptive immune response plays a key role against Encephalitozoon cuniculi, an opportunistic fungus for T cells immunodeficient patients. The role of B cells and antibody play in natural resistance to Encephalitozoon cuniculi remains unresolved. Previously, we demonstrated that B-1 deficient mice (XID), an important component of innate immunity, were more susceptible to encephalitozoonosis, despite the increase in the number of CD4 + and CD8 + T lymphocytes. Here we observed that the absence of B-1 cells was associated with a larger population of M2 macrophages, an anti-inflammatory profile, which had lower microbicidal 3 activity and phagocytic E. cuniculi spores were seen with the extrusion of the polar tubule, which is an important mechanism of evasion of the immune response. The results showed the importance of B-1 cells in the modulation of macrophage function against E. cuniculi infection, increasing microbicidal activity, and reducing the fungal mechanisms involved in the evasion of the immune response. IntroductionMicrosporidia are obligate intracellular spore-forming microorganisms that can infect a wide range of vertebrate and invertebrate species. These fungi have been recognized as human pathogens and are particularly harmful to immunodeficient patients infected with HIV. Since then, interest among researchers of in vitro culture techniques has increased, with more people studying their biology and immune response against them [1].Encephalitozoon cuniculi is one of the most common microsporidian species, in humans or animals. It is considered to be an emerg...

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Section: Nevertheless B-1 Cells Are Critical For the Early Control Osupporting

confidence: 58%

Section: B-1 Cells Are Associated With M1 Macrophage Profilementioning

confidence: 80%

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confidence: 85%

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B-1 cell-mediated modulation of m1-macrophage profile can ameliorate microbicidal functions and disrupt the evasion mechanisms ofEncephalitozoon cuniculi

Pereira

Alvares-Saraiva

Konno

et al. 2019

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“…These populations include mostly HIV infected and patients in chemotherapy [4,5]. In decreased immune response, the pathogen development and spreads are facilitate determining cells death [6,7,8,9]. However, a previous study in mice infected with E. cuniculi showed that even in animals treated with albendazole the pathogen could reinfect, characterizing a latent infection [10].…”

Section: Introductionmentioning

confidence: 99%

“…Cellular immunity is critical for survival of E. cuniculi infected host, and CD8 + T lymphocytes are crucial for the targeted death of infected cells, avoiding pathogen dissemination [11,12,13,14]. Depending the infection route, CD4 + T lymphocytes are required for efficient immune response against E. cuniculi , as showed in oral infection [9]. Although B cells produce antibodies against E. cuniculi , its effective role may be incipient and not enough for avoiding the pathogen from progressively infecting other cells [15,16].…”

Section: Introductionmentioning

confidence: 99%

Cyclophosphamide immunosuppressed Xid mice model clarify the protective role of B cells in experimental encephalitozoonosis

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21Encephalitozoon cuniculi is an intracellular pathogen that stablishes a balanced relationship 22 with immunocompetent individuals, which is dependent of T lymphocytes activity. We 23 previously showed X-linked immunodeficiency (XID -B cell deficient) mice are more 24 susceptible to encephalitozoonosis and B-1 cells presence influences in the immune response. 25 Because XID mice are deficient both in B-1 and B-2 cells, here we investigate the role of these 26 cells against E. cuniculi infection using cyclophosphamide (Cy) immunosuppressed murine 27 model to exacerbate the infection. XID mice presented lethargy and severe symptoms, 28 associated with encephalitozoonosis and there was an increase in the peritoneal populations of 29 CD8 + and CD4 + T lymphocytes and macrophages and also in the proinflammatory cytokines 30 IFN-γ, TNF-α and IL-6. In BALB/c mice, no clinical signs were observed and there was an 31 increase of T lymphocytes and macrophages in the spleen, showing an effective immune 32 response. B-2 cells transfer to XID mice resulted in reduction of symptoms and lesion area with 33 increase of B-2 and CD4 + T populations in the spleen. B-1 cells transfer increased the peritoneal 34 populations of B-2 cells and macrophages and also reduced the symptoms. Therefore, the 35 immunodeficiency of B cells associated to Cy immunosuppression condition leads to 36 disseminated and severe encephalitozoonosis in XID mice with absence of splenic immune 37 response and ineffective local immune response, evidencing the B-1 and B-2 cells role against 38 microsporidiosis.39 40 lymphocytes 42 43 3 44 Author summary 45 46 The adaptive immune response plays a key role against Encephalitozoon cuniculi, an 47 opportunistic fungus for T cells immunodeficient patients. The role of B cells and antibody play 48 in natural resistance to Encephalitozoon cuniculi remains unresolved. Previously, we 49 demonstrated that B-1 deficient mice (XID), an important component of innate immunity, were 50 more susceptible to encephalitozoonosis, despite the increase in the number of CD4 + and CD8 + 51 T lymphocytes. In order to better understand the role of B-1 and B-2 cells and the relationship 52 with the other cells of the immune response in encephalitozoonosis, we infected with E. cuniculi 53 in cyclophosphamide immunosuppressed mice. Here we demonstrate that infected XID mice 54 showed reduction of T cells and macrophages and increase of proinflammatory cytokines 55 associated with disseminated and severe encephalitozoonosis with presence of abdominal 56 effusion and lesions in multiple organs. This pattern of infection observed in mice with genetic 57 deficiency in T cells, so we suggest that the absence of B-1 cells affects the cytotoxic capacity 58 of these lymphocytes. When we transfer B-2 cells to XID mice, the lesion areas caused by the 59 fungus, the populations of T lymphocytes in the peritoneum and the proinflammatory cytokines 60 decrease, indicating a better resolution of the infection. We speculate that B-1 and B-2 cells...

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B-1 cell response in immunity against parasites

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B-1 cells upregulate CD8 T lymphocytes and increase proinflammatory cytokines serum levels in oral encephalitozoonosis

Cited by 15 publications

References 48 publications

B-1 cell-mediated modulation of m1-macrophage profile can ameliorate microbicidal functions and disrupt the evasion mechanisms ofEncephalitozoon cuniculi

B-1 cell-mediated modulation of m1-macrophage profile can ameliorate microbicidal functions and disrupt the evasion mechanisms ofEncephalitozoon cuniculi

Cyclophosphamide immunosuppressed Xid mice model clarify the protective role of B cells in experimental encephalitozoonosis

B-1 cell response in immunity against parasites

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