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Alcohol and Murine Acquired Immunodeficiency Syndrome Suppression of Resistance to Cryptosporidium parvum Infection during Modulation of Cytokine Production
Author(s) -
Alak John I. B.,
Shahbazian Masoud,
Huang Dennis S.,
Wang Yuejian,
Darban Hamid,
Jenkins Edward M.,
Watson Ronald R.
Publication year - 1993
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1993.tb00795.x
Subject(s) - cryptosporidium parvum , biology , immunology , cytokine , splenocyte , tumor necrosis factor alpha , retrovirus , interferon gamma , concanavalin a , virology , microbiology and biotechnology , immune system , virus , biochemistry , in vitro
The effects of inoculation of LP‐BM5 murine leukemia retrovirus and chronic ethanol (5% v/v) ingestion on immunomodulation and Cryptosporidium parvum infection in C57BL/6 female mice were evaluated. The intestinal mucosae of retrovirally immunosuppressed animals were heavily colonized by Cryptosporidium parasites, and oocysts shedding in the feces persisted throughout the duration of the study. Mortality was exacerbated by murine retrovirus infection alone and exacerbated with concomitant chronic alcohol feeding (42.8 and 69.4%). Chronic ethanol ingestion decreased production of interferon‐γ and soluble interleukin‐2 receptor released in supernatants of splenocytes when stimulated with concanavalin A, compared with the control group. Decreased production of interferon‐γ and interleukin‐2 receptor was further exacerbated due to retrovirus infection. Tumor necrosis factor production by splenocytes stimulated with lipopolysaccharide, however, was significantly increased because of retrovirus infection. LP‐BM5 retrovirus infection alone as well as with concomitant ethanol feeding altered cytokine production, which might have led to immunodeficiency. These changes may help explain the enhanced persistence of Cryptosporidiosis.