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Evaluation of host immune responses to pulmonary cryptococcosis using a temperature-sensitive C. neoformans calcineurin A mutant strain.
Microb Pathog. 2005 Feb-Mar; 38(2-3):113-23.MP

Abstract

Cryptococcus neoformans is an opportunistic fungal pathogen that threatens individuals with impaired cell-mediated immunity (CMI). Presently, there are no standardized vaccines available to prevent cryptococcal infections and conventional anti-fungal drug therapy does not induce host immune reactivity and thus cannot efficiently resolve C. neoformans infections in immunocompromised individuals. The present study was designed to characterize pulmonary immune responses following infection with an avirulent temperature-sensitive (ts) mutant, calcineurin A1 (cna1) compared to the pathogenic C. neoformans strain H99 and its potential to induce protective anti-cryptococcal immunity. Host CMI responses in cna1-inoculated mice were observed to be dose-dependent, and comprise increases in pulmonary macrophages and CD4(+) T lymphocytes. However, cytokine analysis demonstrated a mixed pulmonary cytokine response (increases in IL-4, and MCP-1) with no induction of IFN-gamma. Also, pre-immunization with the ts cna1 mutant did not result in protection from a subsequent secondary pulmonary infection with the pathogenic C. neoformans strain H99. Taken together, these results suggest that host pulmonary CMI responses to the ts cna1 mutant that is eventually eliminated from the host without the induction of IFN-gamma appear to be dose-dependent, diverse, and require further stimulation to induce C. neoformans-specific Th1-type cytokine responses to resolve subsequent experimental pulmonary cryptococcal infections.

Authors+Show Affiliations

Department of Medicine/Division of Infectious Diseases, Duke University Medical Center, Duke South, Stead Bldg, Box 3353, Durham, NC 27710, USA. floyd.wormley@duke.eduNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

15748813

Citation

Wormley, Floyd L., et al. "Evaluation of Host Immune Responses to Pulmonary Cryptococcosis Using a Temperature-sensitive C. Neoformans Calcineurin a Mutant Strain." Microbial Pathogenesis, vol. 38, no. 2-3, 2005, pp. 113-23.
Wormley FL, Cox GM, Perfect JR. Evaluation of host immune responses to pulmonary cryptococcosis using a temperature-sensitive C. neoformans calcineurin A mutant strain. Microb Pathog. 2005;38(2-3):113-23.
Wormley, F. L., Cox, G. M., & Perfect, J. R. (2005). Evaluation of host immune responses to pulmonary cryptococcosis using a temperature-sensitive C. neoformans calcineurin A mutant strain. Microbial Pathogenesis, 38(2-3), 113-23.
Wormley FL, Cox GM, Perfect JR. Evaluation of Host Immune Responses to Pulmonary Cryptococcosis Using a Temperature-sensitive C. Neoformans Calcineurin a Mutant Strain. Microb Pathog. 2005 Feb-Mar;38(2-3):113-23. PubMed PMID: 15748813.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Evaluation of host immune responses to pulmonary cryptococcosis using a temperature-sensitive C. neoformans calcineurin A mutant strain. AU - Wormley,Floyd L,Jr AU - Cox,Gary M, AU - Perfect,John R, PY - 2004/11/11/received PY - 2004/12/27/revised PY - 2004/12/27/accepted PY - 2005/3/8/pubmed PY - 2005/7/29/medline PY - 2005/3/8/entrez SP - 113 EP - 23 JF - Microbial pathogenesis JO - Microb Pathog VL - 38 IS - 2-3 N2 - Cryptococcus neoformans is an opportunistic fungal pathogen that threatens individuals with impaired cell-mediated immunity (CMI). Presently, there are no standardized vaccines available to prevent cryptococcal infections and conventional anti-fungal drug therapy does not induce host immune reactivity and thus cannot efficiently resolve C. neoformans infections in immunocompromised individuals. The present study was designed to characterize pulmonary immune responses following infection with an avirulent temperature-sensitive (ts) mutant, calcineurin A1 (cna1) compared to the pathogenic C. neoformans strain H99 and its potential to induce protective anti-cryptococcal immunity. Host CMI responses in cna1-inoculated mice were observed to be dose-dependent, and comprise increases in pulmonary macrophages and CD4(+) T lymphocytes. However, cytokine analysis demonstrated a mixed pulmonary cytokine response (increases in IL-4, and MCP-1) with no induction of IFN-gamma. Also, pre-immunization with the ts cna1 mutant did not result in protection from a subsequent secondary pulmonary infection with the pathogenic C. neoformans strain H99. Taken together, these results suggest that host pulmonary CMI responses to the ts cna1 mutant that is eventually eliminated from the host without the induction of IFN-gamma appear to be dose-dependent, diverse, and require further stimulation to induce C. neoformans-specific Th1-type cytokine responses to resolve subsequent experimental pulmonary cryptococcal infections. SN - 0882-4010 UR - https://www.unboundmedicine.com/medline/citation/15748813/Evaluation_of_host_immune_responses_to_pulmonary_cryptococcosis_using_a_temperature_sensitive_C__neoformans_calcineurin_A_mutant_strain_ DB - PRIME DP - Unbound Medicine ER -