Immune Responses to Subcellular Antigens of Histoplasma Capsulatum

1988 ◽  
pp. 431-444
Author(s):  
Ram P. Tewary ◽  
R. B. Kohler ◽  
L. J. Wheat
Keyword(s):  
Immune Responses ◽  
Histoplasma Capsulatum

scholarly journals Erythropoietin Exacerbates Inflammation and Increases the Mortality ofHistoplasma capsulatum-Infected Mice

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Gisele Aparecida Locachevic ◽  
Priscilla Aparecida Tartari Pereira ◽  
Adriana Secatto ◽  
Caroline Fontanari ◽  
Alyne Fávero Galvão ◽  
...  
Keyword(s):  
Immune Responses ◽  
Fungal Infection ◽  
Lung Inflammation ◽  
Histoplasma Capsulatum ◽  
Fungal Infections ◽  
Cell Formation ◽  
Fungal Burden ◽  
Animal Survival ◽  
The Impact ◽  
First Time

Erythropoietin (EPO) is a key hormone involved in red blood cell formation, but its effects on nonerythroid cells, such as macrophages, have not been described. Macrophages are key cells in controlling histoplasmosis, a fungal infection caused byHistoplasma capsulatum(Hc). Considering that little is known about EPO’s role during fungal infections and its capacity to activate macrophages, in this study we investigated the impact of EPO pretreatment on the alveolar immune response duringHcinfection. The consequence of EPO pretreatment on fungal infection was determined by evaluating animal survival, fungal burden, activation of bronchoalveolar macrophages, inflammatory mediator release, and lung inflammation. Pretreatment with EPO diminished mononuclear cell numbers, increased the recruitment of F4/80+/CD80+and F4/80+/CD86+cells to the bronchoalveolar space, induced higher production of IFN-γ, IL-6, MIP-1α, MCP-1, and LTB4, reduced PGE2concentration, and did not affect fungal burden. As a consequence, we observed an increase in lung inflammation with extensive tissue damage that might account for augmented mouse mortality after infection. Our results demonstrate for the first time that EPO treatment has a deleterious impact on lung immune responses during fungal infection.

scholarly journals HistoplasmaVirulence and Host Responses

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
Mircea Radu Mihu ◽  
Joshua Daniel Nosanchuk
Keyword(s):  
Immune System ◽  
Immune Responses ◽  
Respiratory Disease ◽  
Histoplasma Capsulatum ◽  
Current Knowledge ◽  
Complex Interaction ◽  
Host Responses ◽  
Adaptive Immune Responses ◽  
Disease Extent ◽  
Adaptive Immune

Histoplasma capsulatumis the most prevalent cause of fungal respiratory disease. The disease extent and outcomes are the result of the complex interaction between the pathogen and a host's immune system. The focus of our paper consists in presenting the current knowledge regarding the multiple facets of the dynamic host-pathogen relationship in the context of the virulence arsenal displayed by the fungus and the innate and adaptive immune responses of the host.

scholarly journals Celecoxib Improves Host Defense through Prostaglandin Inhibition duringHistoplasma capsulatumInfection

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Priscilla Aparecida Tartari Pereira ◽  
Bruno Caetano Trindade ◽  
Adriana Secatto ◽  
Roberto Nicolete ◽  
Camila Peres-Buzalaf ◽  
...  
Keyword(s):  
Immune Responses ◽  
Host Defense ◽  
Mononuclear Cells ◽  
Histoplasma Capsulatum ◽  
Lung Parenchyma ◽  
Phagocytic Capacity ◽  
Immune Modulators ◽  
Adaptive Immune ◽  
Mediators Of Inflammation

Prostaglandins act as mediators of inflammation and, similar to cytokines, function as immune modulators during innate and adaptive immune responses. Therefore, using a pharmacological inhibitor, celecoxib, we investigated the role of prostaglandins in host defense againstHistoplasma capsulatuminfection in C57BL/6 mice. Our results showed that treatment with celecoxib inhibited cyclooxygenase 2, reduced the total fungal burden, and reduced the concentration of PGE2, cytokines, lymphocytes, neutrophils, and mononuclear cells in the bronchoalveolar space and lung parenchyma. In addition, celecoxib treatment increased the synthesis of nitric oxide, IFN-γ, LTB4, and the phagocytic capacity of alveolar macrophages. Moreover, celecoxib treatment increased the survival of mice after infection with a lethal inoculum ofH. capsulatum. These results suggest that prostaglandins alter the host immune response and play an important role in the pathogenesis of histoplasmosis. Thus, the inhibition of prostaglandins could be a valuable immunomodulatory strategy and antifungal therapy for histoplasmosis treatment.

scholarly journals CD40-CD40 Ligand Interactions Augment Survival of Normal Mice, but Not CD40 Ligand Knockout Mice, Challenged Orally withSalmonella dublin

1999 ◽  
Vol 67 (10) ◽  
pp. 5253-5257 ◽  
Author(s):  
Ian Marriott ◽  
Elaine K. Thomas ◽  
Kenneth L. Bost
Keyword(s):  
Immune Responses ◽  
Knockout Mice ◽  
Histoplasma Capsulatum ◽  
Cd40 Ligand ◽  
Protective Role ◽  
Intracellular Pathogen ◽  
Ligand Interactions ◽  
Ligand Expression

ABSTRACT Interactions between CD40 expressed on macrophages and CD40 ligand expressed on T lymphocytes can be an important signal for optimal macrophage activation. Previous studies have demonstrated that the optimal response against certain intracellular pathogens (e.g.,Crytosporidium and Leishmania spp.) by macrophages requires CD40-CD40 ligand interactions. However, this finding is not universal, since two recent reports utilizing CD40 knockout mice have shown no such contribution to the protective immune response against Mycobacterium tuberculosis orHistoplasma capsulatum. We demonstrate here that CD40-CD40 ligand interactions are significant events in the protective response against the intracellular pathogen Salmonella dublin in normal mice but not for animals genetically deficient in CD40 ligand expression. Treating BALB/c mice exogenously with a CD40 agonist (i.e., soluble trimeric CD40 ligand) increased resistance against a lethal, orally administered dose of S. dublin. Conversely, in vivo administration of a monoclonal antibody against CD40 ligand to block endogenous CD40-CD40 ligand interactions resulted in a decreased resistance to salmonellosis. In contrast, CD40 ligand knockout mice demonstrated no increased susceptibility to salmonellosis. In vitro treatment of Salmonella-infected macrophages from BALB/c mice with soluble trimeric CD40 ligand resulted in an elevated production of interleukin 12p70 by these cells, suggesting a mechanism whereby CD40-CD40 ligand interactions might enhance protective immune responses to this pathogen. Taken together, these studies strongly suggest that CD40-CD40 ligand interactions in normal mice play an important protective role in immune responses against the gram-negative, intracellular pathogen S. dublin.

Specific humoral immune responses in 12 cases of food sensitization to sesame seed

1997 ◽  
Vol 27 (11) ◽  
pp. 1285-1291 ◽  
Author(s):  
M. N. KOLOPP-SARDA ◽  
D. A. MONERET-VAUTRIN ◽  
B. GOBERT ◽  
G. KANNY ◽  
M. BRODSCHII ◽  
...  
Keyword(s):  
Immune Responses ◽  
Sesame Seed ◽  
Humoral Immune ◽  
Humoral Immune Responses ◽  
Food Sensitization
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